Podcasts about nephropathy

Guest: Richard Lafayette, MD, FACP Insights into the complement system are critical to our understanding of the pathogenesis of immunoglobin A (IgA) nephropathy.1 That's why Dr. Richard Lafayette is here to share what we currently know about the complement system and its role in IgA nephropathy. Dr. Lafayette is a nephrologist at Stanford University Medical Center in California. References: Medjeral-Thomas NR, O'Shaughnessy MM. Adv Chronic Kidney Dis. 2020 Mar;27(2):111-119. doi: 10.1053/j.ackd.2019.12.004 319698 12/23

Guest: Jai Radhakrishnan, MD The most widely accepted mechanism for the pathogenesis of immunoglobin A (IgA) nephropathy is referred to as the “four-hit model,” which is a sequence of four events that can occur.1-3 Here to break down each of those four stages is Dr. Jai Radhakrishnan, a nephrologist at Columbia University Medical Center in New York. References: Knoppova B, Reily C, King RG, et al. J Clin Med. 2021;10(19):4501. doi:10.3390/jcm10194501 Maillard N, Wyatt RJ, Julian BA, et al. J Am Soc Nephrol. 2015;26(7):1503-1512. doi:10.1681/ASN.2014101000 Chang S, Li X-K. Front Med (Lausanne). 2020;7:92. doi:10.3389/fmed.2020.00092 319698 12/23

A new Kidney360 study describes the association between the pre-vaccination microscopic hematuria or proteinuria and post vaccination gross hematuria.

Join experts Drs Matthew Sparks and Laurence Beck as they discuss the diagnosis and management of membranous nephropathy, a rare kidney disease. Relevant disclosures can be found with the episode show notes on Medscape (https://www.medscape.com/viewarticle/991606). The topics and discussions are planned, produced, and reviewed independently of advertisers. This podcast is intended only for US healthcare professionals. Resources Chronic Kidney Disease (CKD) https://emedicine.medscape.com/article/238798-overview Membranous Glomerulonephritis https://emedicine.medscape.com/article/239799-overview M-type Phospholipase A2 Receptor as Target Antigen in Idiopathic Membranous Nephropathy https://pubmed.ncbi.nlm.nih.gov/19571279/ The Endocytic Receptor Megalin and Its Associated Proteins in Proximal Tubule Epithelial Cells https://pubmed.ncbi.nlm.nih.gov/25019425/ PLA2R Autoantibodies and PLA2R Glomerular Deposits in Membranous Nephropathy https://pubmed.ncbi.nlm.nih.gov/21323563/ Genome-Wide Association Studies (GWAS) https://www.genome.gov/genetics-glossary/Genome-Wide-Association-Studies Thrombospondin Type-1 Domain-Containing 7A in Idiopathic Membranous Nephropathy https://pubmed.ncbi.nlm.nih.gov/25394321/ New 'Antigens' in Membranous Nephropathy https://pubmed.ncbi.nlm.nih.gov/33380523/ Nephrotic Syndrome https://emedicine.medscape.com/article/244631-overview NAACCR Item #3812: B Symptoms https://staging.seer.cancer.gov/naaccr/item/eod_public/2.1/3812/ Video-Assisted Thoracoscopy https://www.ncbi.nlm.nih.gov/books/NBK532952/ Direct Oral Anticoagulants: A Quick Guide https://pubmed.ncbi.nlm.nih.gov/30416551/ Focal Segmental Glomerulosclerosis https://emedicine.medscape.com/article/245915-overview IgA Nephropathy https://emedicine.medscape.com/article/239927-overview DOAC Compared With Warfarin for VTE in Patients With Obesity: A Retrospective Cohort Study Conducted Through the VENUS Network https://pubmed.ncbi.nlm.nih.gov/36757644/ Is It Lupus Nephritis? A Path to Diagnosis and Treatment https://www.medscape.com/viewarticle/991602 Noninvasive Diagnosis of PLA2R-Associated Membranous Nephropathy: A Validation Study https://pubmed.ncbi.nlm.nih.gov/34782349/ Noninvasive Diagnosis of Primary Membranous Nephropathy Using Phospholipase A2 Receptor Antibodies https://pubmed.ncbi.nlm.nih.gov/30665573/ Proteinuria Medication https://emedicine.medscape.com/article/238158-medication Sodium-Glucose Transport Protein 2 (SGLT2) Inhibitors https://www.ncbi.nlm.nih.gov/books/NBK576405/ Dapagliflozin in Patients With Chronic Kidney Disease https://pubmed.ncbi.nlm.nih.gov/32970396/ Empagliflozin in Patients With Chronic Kidney Disease https://pubmed.ncbi.nlm.nih.gov/36331190/ Long-Term Follow-Up of Cyclical Cyclophosphamide and Steroids Versus Tacrolimus and Steroids in Primary Membranous Nephropathy https://pubmed.ncbi.nlm.nih.gov/34622104/ Strategies Towards Antigen-Specific Treatments for Membranous Nephropathy https://pubmed.ncbi.nlm.nih.gov/35185913/ Transplant Candidate https://kdigo.org/guidelines/transplant-candidate/

Experts Drs Matthew A. Sparks and Dana V. Rizk discuss the pathology, presentation, and management of IgA nephropathy. Looking for the latest on clinical trials and approved treatments? Tune in! Relevant disclosures can be found with the episode show notes on Medscape (https://www.medscape.com/viewarticle/991603). The topics and discussions are planned, produced, and reviewed independently of advertisers. This podcast is intended only for US healthcare professionals. Resources Chronic Kidney Disease (CKD) https://emedicine.medscape.com/article/238798-overview IgA Nephropathy https://emedicine.medscape.com/article/239927-overview Polycystic Kidney Disease https://emedicine.medscape.com/article/244907-overview Biomarkers for IgA Nephropathy on the Basis of Multi-Hit Pathogenesis https://pubmed.ncbi.nlm.nih.gov/29740706/ Galactose-Deficient IgA1 as a Candidate Urinary Marker of IgA Nephropathy https://pubmed.ncbi.nlm.nih.gov/35683557/ Immunological Drivers of IgA Nephropathy: Exploring the Mucosa-Kidney Link https://pubmed.ncbi.nlm.nih.gov/34821031/ Nephrotic Syndrome https://emedicine.medscape.com/article/244631-overview Podocytopathies https://pubmed.ncbi.nlm.nih.gov/32792490/ Minimal-Change Disease https://emedicine.medscape.com/article/243348-overview IgA Vasculitis (Henoch-Schönlein Purpura) https://emedicine.medscape.com/article/984105-overview Sodium-Glucose Transport Protein 2 (SGLT2) Inhibitors https://www.ncbi.nlm.nih.gov/books/NBK576405/ Dapagliflozin in Patients With Chronic Kidney Disease https://pubmed.ncbi.nlm.nih.gov/32970396/ Empagliflozin in Patients With Chronic Kidney Disease https://pubmed.ncbi.nlm.nih.gov/36331190/ A Controlled Trial of Fish Oil in IgA Nephropathy. Mayo Nephrology Collaborative Group https://pubmed.ncbi.nlm.nih.gov/7935657/ Fish Consumption, Omega 3 Fatty Acids and Cardiovascular Disease. The Science and the Clinical Trials https://pubmed.ncbi.nlm.nih.gov/19326716/ Tonsillectomy in a European Cohort of 1,147 Patients With IgA Nephropathy https://pubmed.ncbi.nlm.nih.gov/26586175/ Sparsentan in Patients With IgA Nephropathy: A Prespecified Interim Analysis From a Randomised, Double-Blind, Active-Controlled Clinical Trial https://pubmed.ncbi.nlm.nih.gov/37015244/ Intensive Supportive Care Plus Immunosuppression in IgA Nephropathy https://pubmed.ncbi.nlm.nih.gov/26962737/ Effect of Oral Methylprednisolone on Clinical Outcomes in Patients With IgA Nephropathy: The TESTING Randomized Clinical Trial https://pubmed.ncbi.nlm.nih.gov/28763548/ Targeted-Release Budesonide Versus Placebo in Patients With IgA Nephropathy (NEFIGAN): A Double-Blind, Randomised, Placebo-Controlled Phase 2b Trial https://pubmed.ncbi.nlm.nih.gov/28363480/ Results From Part A of the Multi-Center, Double-Blind, Randomized, Placebo-Controlled NefIgArd Trial, Which Evaluated Targeted-Release Formulation of Budesonide for the Treatment of Primary Immunoglobulin A Nephropathy https://pubmed.ncbi.nlm.nih.gov/36270561/ Crescents and IgA Nephropathy: A Delicate Marriage https://pubmed.ncbi.nlm.nih.gov/35806856/ Crescentic, Proliferative IgA Nephropathy: Clinical and Histological Response to Methylprednisolone and Intravenous Cyclophosphamide https://pubmed.ncbi.nlm.nih.gov/12808169/ Hydroxychloroquine Inhibits Macrophage Activation and Attenuates Renal Fibrosis After Ischemia-Reperfusion Injury https://pubmed.ncbi.nlm.nih.gov/33936063/ New Treatment Strategies for IgA Nephropathy: Targeting Plasma Cells as the Main Source of Pathogenic Antibodies https://pubmed.ncbi.nlm.nih.gov/35628935/

Did you know that immunoglobulin A nephropathy has very recently seen 2 treatments first licensed for its management? Credit available for this activity expires: 6/29/24 Earn Credit / Learning Objectives & Disclosures: https://www.medscape.org/viewarticle/993766?ecd=bdc_podcast_libsyn_mscpedu

A macrovascular complication of diabetes, diabetic nephropathy is progressive, chronic kidney disease seen in patients with both type 1 and type 2 diabetes mellitus, usually after at least 10 years of hyperglycemia (high blood glucose levels). The three main lesions that are seen in the kidney in patients with diabetes are glomerular lesions, vascular lesions, and pyelonephritis. This brick will focus primarily on the first two of these three lesions; diabetic pyelonephritis is covered in a separate brick. After listening to this AudioBrick, you should be able to: Define diabetic nephropathy. Outline the timeline of progression of diabetic nephropathy (DN) by urine, serum, and histologic criteria. Describe the diagnosis of diabetic nephropathy. Outline the prevention of diabetic nephropathy and, once it is established, how to slow its progression. Describe the management of diabetic nephropathy. You can also check out the original brick from our Renal collection, which is available for free. Learn more about Rx Bricks by signing up for a free USMLE-Rx account: www.usmle-rx.com You will get 5 days of full access to our Rx360+ program, including nearly 800 Rx Bricks.  After the 5-day period, you will still be able to access over 150 free bricks, including the entire collections for General Microbiology and Cellular and Molecular Biology. *** If you enjoyed this episode, we'd love for you to leave a review on Apple Podcasts.  It helps with our visibility, and the more med students (or future med students) listen to the podcast, the more we can provide to the future physicians of the world. Follow USMLE-Rx at: Facebook: www.facebook.com/usmlerx Blog: www.firstaidteam.com Twitter: https://twitter.com/firstaidteam Instagram: https://www.instagram.com/firstaidteam/ YouTube: www.youtube.com/USMLERX Learn how you can access over 150 of our bricks for FREE: https://usmlerx.wpengine.com/free-bricks/

The kidney is one of the organs necessary to filter blood, composed of tiny functional units that separate waste products from molecules the body should retain. Chronic kidney disease is a significant international problem, with up to 10% of the population requiring treatment, and extreme cases requiring dialysis and/or transplantation with significant personal and public health costs. In today's episode we speak with Dr. Andrew King, Chief Scientific Officer of Chinook Therapeutics.  We discuss rare diseases of the kidney, such as disorders that lead to nephropathy, proteinuria, and oxalic acid deposition, along with how the next generation of drugs work to target these issues. www.chinooktx.com

Host: Jonathan Barratt, PhD A new class of drugs are looking at the ability to reduce proteinuria and protect the loss of kidney function. So what do clinicians need to know about the treatment landscape for IgA nephropathy? Tune in with Dr. Jonathan Barratt, The Mayer Professor of Renal Medicine at the University of Leicester in the United Kingdom.

Host: Jonathan Barratt, PhD Genetic studies have shown that changes in the gene for APRIL are associated with an increased risk of developing IgA nephropathy. So what should clinicians know about the ARPIL pathway? Dive in with Dr. Jonathan Barratt, The Mayer Professor of Renal Medicine at the University of Leicester in the United Kingdom.

To receive up to 1.0 CME/CE credit please complete the evaluation and request form here:  https://www.ceconcepts.com/igan-ee-podcastThis activity will take learners on a deep dive into the pathophysiology of proteinuric glomerular disease, with an incisive focus on IgA nephropathy (IgAN). Expert faculty will review the totality of emerging evidence for novel therapeutics in IgAN, including an appraisal of consensus guidelines and regulatory updates. Finally, the session will conclude with a case-based segment wherein attendees will get to apply the principles they've learned to real-world clinical scenarios.Supported through an independent educational grant from Travere.

Today's Episode Dr. Raj reviews diabetic nephropathy which is the leading cause of leading cause of end-stage kidney disease. He reviews the causes and treatment options and breaks down a practice question to bring everything together. Enter the 100th Episode Giveaway The contest is running from March 1st, 2023 to April 14th, 2023 and winners will be announced on April 17th, 2023. 6 winners will be chosen from the entries and all you have to do is enter your email address to be entered. We will reach out to the winners after the contest to send them their copy of the book. Please visit the link to see all rules and details and to enter the contest. Link to the giveaway! About Dr. Raj Dr Raj is a quadruple board certified physician and associate professor at the University of Southern California. He was a co-host on the TNT series Chasing the Cure with Ann Curry, a regular on the TV Show The Doctors for the past 7 seasons and has a weekly medical segment on ABC news Los Angeles. More from Dr. Raj www.BeyondThePearls.net The Dr. Raj Podcast Dr. Raj on Twitter Dr. Raj on Instagram Want more board review content? Physiology by Physeo Step 1 Success Stories The InsideTheBoards Study Smarter Podcast The InsideTheBoards Podcast Study on the go for free! Download the Audio QBank by InsideTheBoards for free on iOS or Android. If you want to upgrade, you can save money on a premium subscription by customizing your plan until your test date on our website! Produced by Ars Longa Media To learn more about us and this podcast, visit arslonga.media. You can leave feedback or suggestions at arslonga.media/contact or by emailing info@arslonga.media. Produced by: Christopher Breitigan Executive Producer: Patrick C. Beeman, MD Legal Stuff InsideTheBoards is not affiliated with the NBME, USMLE, COMLEX, or any professional licensing body. InsideTheBoards and its partners fully adhere to the policies on irregular conduct outlined by the aforementioned credentialing bodies. The information presented in this podcast is intended for educational purposes only and should not be construed as professional or medical advice. Learn more about your ad choices. Visit megaphone.fm/adchoices

Hosted by Roberto Pecoits-Filho, ISN Education Working Group Chair this special episode is a discussion on IgA nephropathy with Dana Rizik of UAB Birmingham and Dana Larsen of UCSF of San Francisco. The idea behind a podcrawl is for a variety of podcasts to coordinate on timing and topic to push a theme and get each other's listeners to explore all of the podcasts. One of the first goals behind NephMadness was to build a community and in the early years of Twitter, NephMadness was central to the formation of #NephTwitter and defining the ethos that makes our online community kind, intelligent, vibrant, and interesting. The NephMadness Podcrawl hopes to inspire and grow the nephrology podcast community in the same way. This year along with the Global Kidney Care Podcast the following series will participate:  The Curbsiders gets the skinny on mineralcorticoid receptor antagonists Core IM will be covering Kidney Transplant in their classic Five Pearl format The CardioNerds will be covering the effect of Heart Failure Devices on Kidney Health Freely Filtered will try to understand thrombotic microangiopathy The Cribsiders look at transitions, first the Peditrics to Adult nephrology transition and then from living to death with palliative nephrology  Fellow on Call will be covering Onconephrology The Nephron Segment looks at Transgender Health and CKD 8 podcasts in all one for each region in this year's NephMadnessGo to NephMadness.com/podcrawl to get links to all of the shows

In this episode, we review the high-yield topic of Sickle Cell Nephropathy from the Renal section. Follow Medbullets on social media: Facebook: www.facebook.com/medbullets Instagram: www.instagram.com/medbulletsofficial Twitter: www.twitter.com/medbullets --- Send in a voice message: https://anchor.fm/medbulletsstep1/message

Did you know that 25 to 30 percent of patients with immunoglobulin A nephropathy (IgAN) will progress to end-stage kidney disease within 20 to 25 years of presentation?  Credit available for this activity expires: 1/10/2024 Earn Credit / Learning Objectives & Disclosures: https://www.medscape.org/viewarticle/986542?src=mkm_podcast_addon_986542

Looking for more information on this topic? Check out the IgA Nephropathy and Henoch-Schönlein Purpura brick. If you enjoyed this episode, we'd love for you to leave a review on Apple Podcasts.  It helps with our visibility, and the more med students (or future med students) listen to the podcast, the more we can provide to the future physicians of the world. Follow USMLE-Rx at: Facebook: www.facebook.com/usmlerx Blog: www.firstaidteam.com Twitter: https://twitter.com/firstaidteam Twitter: https://twitter.com/mesage_hub Instagram: https://www.instagram.com/firstaidteam/ YouTube: www.youtube.com/USMLERX Learn more about Rx Bricks by signing up for a free USMLE-Rx account: www.usmle-rx.com You will get 5 days of full access to our Rx360+ program, including over 800 Rx Bricks.  After the 5-day period, you will still be able to access over 150 free bricks, including the entire collections for General Microbiology and Cellular and Molecular Biology.

SGLT2 inhibitors, publishing choices, second and third order effects of interventions, decision support, and patient selection for preventive procedures are the topics John Mandrola, MD, discusses in this week's podcast. This podcast is intended for healthcare professionals only. To read a partial transcript or to comment, visit: https://www.medscape.com/twic I. EMPA Kidney - EMPA-Kidney Seals SGLT2 Inhibitors as 'Foundational' for CKD https://www.medscape.com/viewarticle/984439 - EMPA-Kidney Moves the Needle for SGLT2 Inhibitors in Kidney Disease https://www.medscape.com/viewarticle/983521 - Empagliflozin in Patients with Chronic Kidney Disease https://www.nejm.org/doi/pdf/10.1056/NEJMoa2204233 - Canagliflozin and Renal Outcomes in Type 2 Diabetes and Nephropathy https://www.nejm.org/doi/10.1056/NEJMoa1811744 - Dapagliflozin in Patients with Chronic Kidney Disease https://www.nejm.org/doi/full/10.1056/NEJMoa2024816 - Impact of diabetes on the effects of sodium glucose co-transporter-2 inhibitors on kidney outcomes: collaborative meta-analysis of large placebo-controlled trials https://doi.org/10.1016/S0140-6736(22)02074-8 II. Publishing Choices - Motorcycle Rallies Linked to Spike in Organ Transplants https://www.medscape.com/viewarticle/984623 - Organ Donation and Transplants During Major US Motorcycle Rallies https://jamanetwork.com/journals/jamainternalmedicine/article-abstract/2798550 III. Second and Third Order Effects - Heart Disease Deaths Spiked During COVID After 10-Year Decline https://www.medscape.com/viewarticle/984605 IV. Decision Support - Patient App Aids Decisions on Anticoagulants: ENHANCE-AF https://www.medscape.com/viewarticle/984253 - A Randomized Clinical Trial to Evaluate an Atrial Fibrillation Stroke Prevention Shared Decision‐Making Pathway https://www.ahajournals.org/doi/10.1161/JAHA.122.028562 V. Percutaneous Left Atrial Appendage Closure - Consider Life Expectancy When Referring for LAA Closure? https://www.medscape.com/viewarticle/981117 - Transcatheter Left Atrial Appendage Occlusion: A Multi-Center Real Life Experience https://www.mdpi.com/2077-0383/11/23/6944 - Incidence and Predictors of Early Death in Patients Undergoing Percutaneous Left Atrial Appendage Closure https://www.jacc.org/doi/full/10.1016/j.jacep.2022.06.012 - Indications for Left Atrial Appendage Occlusion in the United States and Associated In-Hospital Outcomes: Results From the NCDR LAAO Registry https://www.ahajournals.org/doi/full/10.1161/CIRCOUTCOMES.121.008418 You may also like: Medscape editor-in-chief Eric Topol, MD, and master storyteller and clinician Abraham Verghese, MD, on Medicine and the Machine https://www.medscape.com/features/public/machine The Bob Harrington Show with Stanford University Chair of Medicine, Robert A. Harrington, MD. https://www.medscape.com/author/bob-harrington Questions or feedback, please contact news@medscape.net

This episode, Dr. Douglas Taren speaks with Mateus de Lima Macena and Dr. Nassib Bezerra Bueno from Universidade Federal de Alagoas, Maceió, Alagoas, Brazil. Their article assesses effects of dietary polyphenols, from food sources or supplements, on the anthropometric, glycemic, renal, inflammatory, and oxidative stress markers in adults with diabetic nephropathy (DN). Join us for this conversation with this month's featured authors.

Dr. Marion Cremoni discusses the findings from her study "Toxic Occupational Exposures and Membranous Nephropathy," on behalf of her colleagues.

FDA Panel votes on the potential removal from the market of Makena; results from an apixaban trial of patients with atrial fibrillation and valvular heart disease; reports of serious ocular complications with monkeypox infection; the novavax vaccine becomes the latest authorized COVID-19 booster; and treatments for nephropathy and ALS have their review period extended.

Video for this podcast: https://mehlmanmedical.com/hy-usmle-acute-tubular-necrosis-vs-tubulointerstitial-nephropathy-in-under-60-seconds Main website: https://mehlmanmedical.com/ Instagram: https://www.instagram.com/mehlman_medical/ Telegram private group: https://mehlmanmedical.com/subscribe/ Telegram public channel: https://t.me/mehlmanmedical Facebook: https://www.facebook.com/mehlmanmedical Podcast: https://anchor.fm/mehlmanmedical Patreon: https://www.patreon.com/mehlmanmedical

Drs Sparks and Neuen discuss the proper use of SGLT2 inhibitors to prevent chronic kidney disease, including how to start them and monitor them and their possible side effects. Relevant disclosures can be found with the episode show notes on Medscape (https://www.medscape.com/viewarticle/971884). The topics and discussions are planned, produced, and reviewed independently of advertiser. This podcast is intended only for US healthcare professionals. Resources SGLT2 Inhibitors in Primary Care: 'All Hands on Deck' for Improving Heart Failure Outcomes https://www.medscape.com/viewarticle/965473 Canagliflozin and Cardiovascular and Renal Events in Type 2 Diabetes https://www.nejm.org/doi/full/10.1056/nejmoa1611925 Canagliflozin and Renal Outcomes in Type 2 Diabetes and Nephropathy https://www.nejm.org/doi/full/10.1056/nejmoa1811744 CKD Epidemiology Collaboration CKD-EPI Consortium https://www.tuftsmedicalcenter.org/research-clinical-trials/institutes-centers-labs/chronic-kidney-disease-epidemiology-collaboration/overview Effect of Finerenone on Chronic Kidney Disease Outcomes in Type 2 Diabetes https://www.nejm.org/doi/full/10.1056/NEJMoa2025845 Net Effects of Sodium-Glucose Co-Transporter-2 Inhibition in Different Patient Groups: A Meta-Analysis of Large Placebo-Controlled Randomized Trials https://www.thelancet.com/journals/eclinm/article/PIIS2589-5370(21)00443-0/fulltext EMPA-KIDNEY (The Study of Heart and Kidney Protection With Empagliflozin) https://www.empakidney.org/ FDA Removes Boxed Warning About Risk of Leg and Foot Amputations for the Diabetes Medicine Canagliflozin (Invokana, Invokamet, Invokamet XR) https://www.fda.gov/drugs/fda-drug-safety-podcasts/fda-removes-boxed-warning-about-risk-leg-and-foot-amputations-diabetes-medicine-canagliflozin

In this conversation, Daniel Belkin and Mitch Belkin speak with Joel Topf, MD, about contrast-associated nephropathy. We discuss Acute Kidney Injury (AKI), the value of creatinine as a marker for AKI, how to evaluate volume status, the evidence around contrast-induced/contrast-associated nephropathy, recommendations on fluids to prevent AKI in patients with Chronic Kidney Disease, and comparing venous and arterial contrast with respect to the risk of AKI.Who is Joel Topf?Dr. Topf is a clinical nephrologist in Detroit, who is a partner and medical director at St Clair Nephrology and an assistant professor at Oakland University William Beaumont School of Medicine. He is the co-creator of NephMadness and NephJC. He hosts multiple podcasts, blogs at pbfluids.com, and tweets @Kidney_boy. References: Joel Topf's Blog Twitter: @Kidney_BoyJoel Topf - Grand Rounds Presentation on Contrast NephropathyThe PRESERVE trialN-Acetylcysteine and Contrast-Induced Nephropathy in Primary AngioplastyPrevention of Contrast-Induced Nephropathy With Sodium BicarbonateCraig Brater 1998 - NEJM review on DiureticsChlorthalidone for Hypertension in Advanced Chronic Kidney DiseaseEffect of Salt Substitution on Cardiovascular Events and Death______________________Follow us @ExMedPod and subscribe to our Youtube channel.Daniel Belkin, MD, and Mitch Belkin, MD, are brothers and resident physicians. The External Medicine Podcast is a podcast exploring nontraditional medical ideas and innovation.  

Diabetes is an important topic in nursing school, and a common diagnosis that you'll help treat in your future patients. In this podcast, I talk about the:Differences between type 1 and type 2 diabetes.Complications such as Neuropathy, Retinopathy, Peripheral Vascular Disease, and Nephropathy.How it's diagnosed (Hgb A1C test)Diabetic medicationsPurpose of insulinTriangle of treatment: Medication, exercise, and dietSigns and Symptoms of hypoglycemia and hyperglycemiaDKA and HHNS conditionsSick Day CareCheck out Picmonic for a great way to memorize the types of insulins. https://www.picmonic.com/viphookup/nursingschoolweekbyweekLGH22

CastSusan ThanabalasingamDana LarsenMythri ShankarSandy SureshReferencesNeal B, Perkovic V, Mahaffey KW, de Zeeuw D, Fulcher G, Erondu N, et al. Canagliflozin and Cardiovascular and Renal Events in Type 2 Diabetes. New England Journal of Medicine. 2017 Aug 17;377(7):644–57.Perkovic V, Jardine MJ, Neal B, Bompoint S, Heerspink HJL, Charytan DM, et al. Canagliflozin and Renal Outcomes in Type 2 Diabetes and Nephropathy. New England Journal of Medicine. 2019 Jun 13;380(24):2295–306.Heerspink HJL, Stefánsson BV, Correa-Rotter R, Chertow GM, Greene T, Hou FF, et al. Dapagliflozin in Patients with Chronic Kidney Disease. New England Journal of Medicine. 2020 Oct 8;383(15):1436–46.Joshi SS, Singh T, Newby DE, Singh J. Sodium-glucose co-transporter 2 inhibitor therapy: mechanisms of action in heart failure. Heart. 2021 Jul 1;107(13):1032–8.Zinman B, Wanner C, Lachin JM, Fitchett D, Bluhmki E, Hantel S, et al. Empagliflozin, Cardiovascular Outcomes, and Mortality in Type 2 Diabetes. New England Journal of Medicine. 2015 Nov 26;373(22):2117–28.ScriptContributors: Susan Thalabalasingam, Mythri Shankar, Dana Larsen, Sandhya SureshHost (Susan):Hey everyone! Welcome to our episode of 2 truths and a lie, an NSMC podcast.Let's go over the ground rules.One at a time each member of our elite education panel will state two truths and one lie about Nephrology.This episode will focus specifically on SGLT2 inhibitors. The other panelist will then discuss which statement they think is The Lie.Our presenter will then educate us all on which statement is incorrect and why.So let's warm up our lie detectors.Let's meet our four players for today.I'm your host Susan Thanabalasingam and I'm a first year internal medicine resident at Queen's University in Kingston, Ontario, Canada. I'm really excited to be your host today and to have an amazing discussion with these wonderful women today! Our second panelist is Dr. Mythri Shankar from India. Hi Dr. Mythri, can you please introduce yourself?Mythri: Hello everyone. I am Dr. Mythri Shankar, Assistant Professor in Nephrology from Institute of Nephro-urology, Bengaluru, India.I am also the Associate Program Director of the NSMC. Glad to be here and I have no conflicts of interest to declare.Our third Panelist Dr. Dana Larsen from the United States of America! Hi Dr. Larsen, can you please introduce yourself? Dana: Hi all! I am Dana Larsen, a second year nephrology fellow at University of California, San Francisco and so grateful to get to be on this podcast with this great group today. I have no conflicts of interest in today's topics. Our fourth Panelist is Dr. Sandhya Suresh from India. Hi Dr. Suresh, can you please introduce yourself?Sandhya: Hi to all my fellow members of the 4th Pod, the Distal convoluted Pod and also… Hi to everyone listening to this podcast. I am Dr. Sandhya Suresh and I'm an early career nephrologist working in a medical college in Southern India. My only declaration here is that I am a flozinator who is continually amazed by everything that the SGLT inhibitors can do. Susan: Great, so let me start, I'll give you 3 statements. My statements all focus on the use of SGLT2i in the non-diabetic CKD setting, which is a cohort that merits special attention when discussing the benefits of SGLT2i use (Susan)SGLT-2 inhibitors are nephroprotective in diabetic and non-diabetic CKD (TRUE)SGLT2 inhibitors decrease proteinuria in non-diabetic CKD (TRUE)SGLT2 inhibitors are indicated for all etiologies of non-diabetic CKD (FALSE) Explanation for 1 → Statement 1 is TRUE. SGLT-2 inhibitors are in fact nephroprotective in BOTH diabetic and non-diabetic CKD. The CREDENCE trial was the first to specifically examine kidney outcomes in patients with diabetic, proteinuric CKD, and it demonstrated significant decrease in risk for kidney failure and cardiovascular events in patients treated with canagliflozin (Perkovic et al, 2019). As the effects were independent of glucose lowering effects, further studies have been conducted in the non-diabetic CKD setting. DAPA-CKD included patients with both diabetic and non-diabetic CKD and found that the use of dapagliflozin was associated with decreased risk of >= 50% decline in eGFR, ESKD or death from renal or cardiovascular causes (Heerspink et al, 2020). Explanation for 2 → Statement 2 is ALSO TRUE. We do in fact have compelling data that proteinuria is reduced with the use of SGLT2i in non-diabetic kidney disease. Pre-specified analyses from the DAPA-CKD trial demonstrated that dapagliflozin significantly reduced proteinuria in both diabetic and non-diabetic CKD, although the effect was larger in the diabetic subset. Because clinical outcomes were similar with dapagliflozin initiation between diabetic and non-diabetic patients, despite this difference in effect size on proteinuria, it has been postulated that the observed nephroprotection may not actually be related to reduction in proteinuria. Explanation for 3 → Statement 3 was the FALSE statement. In DAPA-CKD, included etiologies of non diabetic CKD were FSGS, minimal change disease, chronic pyelonephritis, chronic interstitial nephritis and hypertensive, IgA, membranous, and obstructive nephropathies. However, patients with lupus nephritis, polycystic kidney disease and vasculitis were excluded. The results of EMPA-Kidney are highly anticipated, in part as it includes a larger number of participants without diabetes, in particular those with glomerular disease, which will hopefully give us more answers about whether these patients will also benefit from SGLT2i initiation. EMPA-Kidney does however also exclude patients with PKD (The EMPA-KIDNEY Collaborative Group, 2022). That was fun, I can't wait to hear more from the rest of our panelists. Moving on to Dr. Mythri now, can you please give us your 2 truths and a lie?Mythri:SGLT2i are the initial therapy for T2DM (FALSE)SGLT2i are beneficial in heart failure with reduced ejection fraction as it reduces both preload and afterload (TRUE)SGLT2i are analogs of Phlorizin (TRUE)Explanation for 1. SGLT2i are not the initial therapy. Initial therapy consists of lifestyle modifications, diet and exercise (American diabetes association guidelines 2021).Explanation for 2. SGLT2 inhibitors promote osmotic diuresis and natriuresis in patients with and without diabetes, and thus may reduce preload. SGLT2 inhibitors may also have vascular effects (including improving endothelial function) that promote vasodilation and thus may also reduce afterload. It has also been postulated that SGLT2 inhibitors may improve myocardial metabolism and thus improve cardiac efficiency. SGLT2 inhibitors promote osmotic diuresis and natriuresis in patients with and without diabetes, and thus may reduce preload (Joshi et al, 2021).Explanation for 3:A natural compound, phlorizin, was isolated from apple trees in the early 1800s and for decades played an important role in diabetes and renal physiology research. The compound is poorly absorbed from the gastrointestinal tract and inhibits both SGLT1 (primarily found in the gastrointestinal tract) and SGLT2. Analogs of phlorizin have been developed that circumvent these two problems. These are the current SGLT2i (Atanasov et al, 2016).Susan: That was great Dr. Mythri, thank you, I feel like I learned so much! Moving on to Dr. Dana, can you give us your 2 truths and a lie?Dana:Awesome, thank you Susan! Alright, please identify the lie from among these statements all concerning potential SGLT2 side effects:SGLT2 inhibitors definitively increase the risk of vulvovaginal candidiasis and may increase the risk of urinary tract infections. (TRUE)SGLT2 inhibitors do not definitively increase risk of bladder cancers. (TRUE)SGLT2 inhibitors definitively increase risk for limb amputations. (FALSE)Do you think you have the answer!?! Let's take a closer look…My first statement, SGLT2 inhibitors definitely increase the risk of urinary tract infections and vulvovaginal candidiasis is TRUE. Multiple studies on SGLT2 inhibitors including a 2018 canagliflozin RCT and a 2013 dapagliflozin RCT have shown 2-4 fold increase in vulvovaginal candidiasis in 10-15% of patients on SGLT2 inhibitors compared with placebo (Neal et al, 2017). A 2019 meta-analysis of over 100 RCTs with SGLT2s compared with other anti-diabetic agents or placebo did NOT show an increase in risk of UTIs for SGLT2s as a group, though there was a signal for increased risk of UTIs specifically for dapagliflozin, mechanistically it is unclear why this would be the case (Donnan et al, 2019). At this time, where there is definitive increased risk of vulvovaginal candidiasis, increased risk of UTI is likely not something you need to counsel your patients on.Alright, moving on, our second statement, SGLT2 inhibitors do not definitely increase risk of bladder cancers is also TRUE. While few cases of bladder cancers have been diagnosed in patients taking dapagliflozin, half of these occurred within the first 6 months, which is thought to be too soon for tumorigenesis promotion by dapagliflozin itself. EMPA-REG trial did not find increased incidence of bladder cancer once event rates that occured within the first 6mo of drug therapy were removed (Kohler et al, 2017). Currently, the FDA recommends ongoing postmarketing surveillance And finally, moving on to our final statement which must be FALSE given the name of the game, the statement says SGLT2 inhibitors definitively increase risk for limb amputations. While the CANVAS program found that in the over 10,000 combined patients from their two major trials there was an increased risk of amputations 6.3 vs 3.4 per 1000 participants with hazard ratio 1.97, these amputations were primarily at the level of the toe or metatarsal, not the limb (Neal et al, 2017). Furthermore, there is ongoing discussion over true risk of amputation attributed to SGLT2 inhibitors as post hoc analysis of empa-reg and CREDENCE, the renal outcomes trial for canagliflozin, no association for increased risk of lower extremity amputation was found (Perkovic et al, 2019). While further investigation into the topic is warranted, we can rest assured that this is our FALSE statement on side effects of SGLT2-inhibitors. Susan: Wow Dana, thanks so much for those very important lessons on SGLT2i side effects, I certainly have a lot of take home points from your discussion! Perfect, now we'll move on to Dr. Sandhya. Please join me in welcoming her to give us our final set of 2 truths and a lie today.Sandhya:Thank you Susan. So here, I will be focussing my 2 truths and a lie on the cardioprotective effects of SGLT2 inhibitors. Without further ado, here are my 3 statements:Statement 1: Increased ketone body production is postulated as one of the mechanisms for the cardioprotective effects of SGLT2 inhibitors (TRUE)Statement 2: Glucose lowering effect and cardiovascular benefits both decline at lower GFRs (FALSE)Statement 3: Sotagliflozin in a combined SGLT2 and SGLT1 inhibitor which has demonstrated cardioprotective benefits (TRUE)Explanations for the above statements: Let me go through the explanation for each statement one by one.Statement 1 is true. The cardioprotective effects of SGLT2 inhibitors may be multifactorial. While they target the traditional cardiovascular risk factors through their glycosuric and natriuretic effects, it is also postulated that SGLT2 inhibitors improve the cardiac metabolism and bioenergetics. 90-95% of cardiac energy is derived from mitochondrial oxidative metabolism for which the predominant fuel is free fatty acids. In a diabetic heart, the metabolic flexibility in terms of substrate utilization is impaired and the myocardium becomes more dependent on free fatty acids as fuel leading to build up of free fatty acid intermediates which lead to lipotoxicity and myocardial dysfunction. SGLT2 inhibitors produce a starvation simulation with reduced insulin and higher glucagon levels which promotes lipolysis and ketogenesis. They also reduce the excretion of ketone bodies by reducing the GFR. These ketone bodies like beta hydroxybutyrate serve as an alternate super fuel for myocardial cells producing ATP more efficiently and help to preserve the mitochondrial integrity and these factors lead to improved cardiac efficiency (Joshi et al, 2021).Now coming to statement 2. The glucose lowering effect of SGLT2 inhibitors does decrease with declining GFRs because the magnitude of glucose excretion and consequently the HbA1c reduction is dependent on the filtered glucose load. This filtered glucose load is high in diabetic patients with normal GFR and reduced in patients with renal impairment thereby leading to reduction in the glucose lowering effect of SGLT2 inhibitors (Kelly et al, 2018). Conversely, the cardioprotective effects of this class of drugs seems to be remarkably preserved at lower GFRs as has been demonstrated in several trials. For example, in the EMPAREG OUTCOME trial, analysis of a subgroup of patients with prevalent kidney disease was done which included type 2 diabetic patients with established cardiovascular disease and an estimated GFR between 30-60 . There was significant reduction in the cardiovascular and all-cause mortality as well as hospitalization for heart failure in this subgroup and this effect was consistent across different categories of GFR (Wanner et al, 2017). So statement 2 is false.So by that logic statement 3 has to be a truth. We often talk about the 4 traditional flozins so I just wanted to throw in a statement about this new subclass within this class of agents. Sotagliflozin is an SGLT2 inhibitor which also inhibits the intestinal SGLT1 transporters. It was originally targeted for use in patients with type 1 diabetes mellitus with the hope that SGLT1 inhibition in the intestine could reduce postprandial hyperglycemia and improve overall glycemic control in these patients. Studies have also shown excellent efficacy for this purpose. However they also showed a higher incidence of Diabetic ketoacidosis episodes. 2 cardiovascular trials were conducted, both of which unfortunately, ended early as they lost funding sometime during the COVID pandemic. The SCORED trial included CKD patients and the SOLOIST-WHF trial included patients who had recently recovered from an episode of decompensated heart failure. I won't go into the strengths and limitations of these trials but they did show benefit in terms of cardiovascular endpoints in the sotagliflozin group compared to placebo (Bhatt et al, 2021; Bhat et al, 2021). The drug isn't commercially available as of now and is not FDA approved yet but it remains as a novel agent within the SGLT2i landscape.Susan (Conclusion by host):Amazing, thank you so much Dr. Sandhya! That was an enlightening discussion on cardioprotection with SGLT2i use. And this has been so much fun! I hope you've all found our conversation really helpful and informative - I certainly know that I have learned a lot from my colleagues today. I can't thank them enough for sharing their time and expertise with us. Be sure to tune in next time for more FOAMed nephrology education.

Today we had Dr. Patricia Liu to talk about a new study from Journal of Hospital Medicine on the management of opioid use disorder in the hospital. And then we got a little carried away covering way too many articles!  Inpatient Management of Opioid Use DisorderHepatitis C Care for People Who Inject DrugsFinal SOLIDARITY trial results for RemdesivirTAVI for Moderate Risk Severe Aortic StenosisMediterranean Diet vs Low Fat Diet for Secondary Prevention of CVDSteroids for IgA NephropathyGLP-1 Agonists and Gallbladder DiseasePig to Human Kidney XenotransplantationAspirin for Primary Prevention of CVDMusic from Uppbeat (free for Creators!):https://uppbeat.io/t/soundroll/dopeLicense code: NP8HLP5WKGKXFW2R

Editor's Summary by Linda Brubaker, MD, Associate Editor of JAMA, the Journal of the American Medical Association, for the May 17, 2022 issue.

Go online to PeerView.com/GPD860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. In this activity, an expert in nephrology discusses the prevention and management of nephropathy in patients with Fabry disease. Upon completion of this activity, participants should be better able to: Employ evidence-based tools and strategies to identify patients with FD and prevent nephropathy in a timely manner, Assess safety and efficacy of current and emerging treatments for patients with FD, Apply individualized treatment for patients with FD with an emphasis on preventing nephropathy.

Go online to PeerView.com/GPD860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. In this activity, an expert in nephrology discusses the prevention and management of nephropathy in patients with Fabry disease. Upon completion of this activity, participants should be better able to: Employ evidence-based tools and strategies to identify patients with FD and prevent nephropathy in a timely manner, Assess safety and efficacy of current and emerging treatments for patients with FD, Apply individualized treatment for patients with FD with an emphasis on preventing nephropathy.

Go online to PeerView.com/GPD860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. In this activity, an expert in nephrology discusses the prevention and management of nephropathy in patients with Fabry disease. Upon completion of this activity, participants should be better able to: Employ evidence-based tools and strategies to identify patients with FD and prevent nephropathy in a timely manner, Assess safety and efficacy of current and emerging treatments for patients with FD, Apply individualized treatment for patients with FD with an emphasis on preventing nephropathy.

Go online to PeerView.com/GPD860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. In this activity, an expert in nephrology discusses the prevention and management of nephropathy in patients with Fabry disease. Upon completion of this activity, participants should be better able to: Employ evidence-based tools and strategies to identify patients with FD and prevent nephropathy in a timely manner, Assess safety and efficacy of current and emerging treatments for patients with FD, Apply individualized treatment for patients with FD with an emphasis on preventing nephropathy.

Go online to PeerView.com/GPD860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. In this activity, an expert in nephrology discusses the prevention and management of nephropathy in patients with Fabry disease. Upon completion of this activity, participants should be better able to: Employ evidence-based tools and strategies to identify patients with FD and prevent nephropathy in a timely manner, Assess safety and efficacy of current and emerging treatments for patients with FD, Apply individualized treatment for patients with FD with an emphasis on preventing nephropathy.

Go online to PeerView.com/GPD860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. In this activity, an expert in nephrology discusses the prevention and management of nephropathy in patients with Fabry disease. Upon completion of this activity, participants should be better able to: Employ evidence-based tools and strategies to identify patients with FD and prevent nephropathy in a timely manner, Assess safety and efficacy of current and emerging treatments for patients with FD, Apply individualized treatment for patients with FD with an emphasis on preventing nephropathy.

References Dr Guerra lecture notes Front. Endocrinol., 14 October 2014. Sci Rep. 2020; 10: 21628. --- Send in a voice message: https://anchor.fm/dr-daniel-j-guerra/message Support this podcast: https://anchor.fm/dr-daniel-j-guerra/support

Join 3 experts in discussion about how to best identify patients at high-risk of progression and the role of proteinuria in IgA nephropathy management. Credit available for this activity expires: 4/4/2023 Earn Credit / Learning Objectives & Disclosures: https://www.medscape.org/viewarticle/971060?src=mkm_podcast_addon_971060

References Journal of Biological Chemistry.2013. 288 Issue 52 Pages 37355-37364. Prostaglandins & Other Lipid Mediators. 2022(April) . Volume 159, 106621 --- Send in a voice message: https://anchor.fm/dr-daniel-j-guerra/message Support this podcast: https://anchor.fm/dr-daniel-j-guerra/support

References Dr. Guerra's lecture notes Prostaglandins & Other Lipid Mediators 2022.April. 159. 106621 Reviews in Endocrine and Metabolic Disorders. 2020. 21: 631–643 --- Send in a voice message: https://anchor.fm/dr-daniel-j-guerra/message Support this podcast: https://anchor.fm/dr-daniel-j-guerra/support

The findings of CREDENCE Trial

IgA nephropathy is a cause of glomerulonephritis and is the most common chronic glomerular disease in children. Like the name suggests, it is characterised by kidney damage due to IgA (an immunoglobulin) which deposits in complexes in the kidney. The classic presentation is recurrent episodes of macroscopic haematuria a couple of days after the onset of an URTI. About 25% of children will eventually develop end stage renal failure.  In this episode, we discuss IgA nephropathy and its pathophysiology, presentation, management and more!   Links and resources: Follow us on Instagram @yourekiddingrightdoctors Facebook: https://www.facebook.com/yourekiddingrightpod-107273607638323/ Our email is yourekiddingrightpod@gmail.com Make sure you hit SUBSCRIBE/FOLLOW so you don't miss out on any pearls of wisdom and RATE if you can to help other people find us! (This isn't individual medical advice, please use your own clinical judgement and local guidelines when caring for your patients)

In this episode, Kidney Essentials hosts Drs. Sophia Ambruso and Judy Blaine along with guest-host Dr. Jake Hershey discuss the diagnosis and treatment of diabetic nephropathy and some of the nuances of our favorite RAAS inhibition medications.

In a companion interview to his June 7 talk with Stanford's Michael Snyder, Harry speaks this week with Noosheen Hashemi, who—with Snyder—co-founded the personalized health startup January.ai in 2017. The company focuses on helping users understand how their bodies respond to different foods and activities, so they can make diet and exercise choices that help them avoid unhealthy spikes in blood glucose levels.January's smartphone app collects blood glucose levels from disposable devices called continuous glucose monitors (CGMs), as well as heart rate data from patients' Fitbits or Apple Watches. The app also makes it easier for users to log the food they eat, and see what impact each food has on their glucose levels. Once the app has enough data, January's machine learning algorithms can start predicting the effects of different foods and activities on blood glucose. It can then recommend meals and exercise that'll help users keep their blood glucose in a healthy target range. The goal isn't to prevent glucose spikes completely, but rather to prevent diabetes from emerging over the long term in people at risk for a cluster of serious conditions known metabolic syndrome. That could help individuals live longer, healthier lives. And at a population level it could save billions in healthcare costs.Please rate and review MoneyBall Medicine on Apple Podcasts! Here's how to do that from an iPhone, iPad, or iPod touch:• Launch the “Podcasts” app on your device. If you can't find this app, swipe all the way to the left on your home screen until you're on the Search page. Tap the search field at the top and type in “Podcasts.” Apple's Podcasts app should show up in the search results.• Tap the Podcasts app icon, and after it opens, tap the Search field at the top, or the little magnifying glass icon in the lower right corner.• Type MoneyBall Medicine into the search field and press the Search button.• In the search results, click on the MoneyBall Medicine logo.• On the next page, scroll down until you see the Ratings & Reviews section. Below that, you'll see five purple stars.• Tap the stars to rate the show.• Scroll down a little farther. You'll see a purple link saying “Write a Review.”• On the next screen, you'll see the stars again. You can tap them to leave a rating if you haven't already.• In the Title field, type a summary for your review.• In the Review field, type your review.• When you're finished, click Send.• That's it, you're done. Thanks!Full TranscriptHarry Glorikian: I'm Harry Glorikian, and this is MoneyBall Medicine, the interview podcast where we meet researchers, entrepreneurs, and physicians who are using the power of data to improve patient health and make healthcare delivery more efficient. You can think of each episode as a new chapter in the never-ending audio version of my 2017 book, “MoneyBall Medicine: Thriving in the New Data-Driven Healthcare Market.” If you like the show, please do us a favor and leave a rating and review at Apple Podcasts.Harry Glorikian: I've been making the show long enough that you can see a kind of family tree emerging, with branches that connect many of our episodes.That's definitely the case with today's interview with Noosheen Hashemi, the co-founder and CEO of the precision health company January AI.The branch leading to Hashemi started back in June of 2021 when I interviewed Professor Michael Snyder, the chair of Stanford's Department of Genetics.Snyder is a huge proponent of using wearable devices to help people make better decisions about their own health. In fact, the day we spoke he was wearing seven separate devices, including one called a continuous glucose monitor or CGM.A CGM is standard equipment these days for about 3.5 million diabetics in the U.S. who need to know when their blood sugar is too high and when it's time to take more insulin. But Snyder believes that blood glucose data could also help tens of millions of other people who don't yet take insulin but may be on their way to developing full-blown diabetes.Back in 2016 Snyder got a visit from Hashemi. She's a longtime Silicon Valley tech executive and philanthropist who'd been searching for a way to use AI, wearable devices, and big data to get more people involved in medical research. Hashemi told me it took just two meetings for her and Snyder to decide to join forces to co-found January. The company makes a smartphone app that collects blood glucose data from disposable CGMs, as well as heart rate data from patients' existing wearable devices such as their Fitbit or Apple Watch. The app also makes it easier for users to log the food they eat, and see what impact each food has on their glucose levels. Once the app has enough data, January's machine learning algorithms can start predicting the effects of different foods and activities on blood glucose. It can then recommend meals and exercise that'll help users keep their blood glucose in a healthy target range. The goal isn't to prevent glucose spikes completely, but rather to prevent diabetes from emerging over the long term in people at risk for a cluster of serious conditions known metabolic syndrome. That could help individuals live longer, healthier lives. And at a population level it could save billions in healthcare costs.As you're about to hear, Hashemi and I talked about why glucose monitoring is so important and what companies like January can do in the future to make the predictive power of AI available to more people.Harry Glorikian: Noosheen, welcome to the show. Noosheen Hashemi: Thank you, Harry. Harry Glorikian: So, it's great to have you on the show. It was interesting that, you know, the minute Dr. Snyder mentioned the company, I was immediately Googling it. And I was like, oh, I have to talk to this company. I have to understand what they're doing and, and what's going on.And to be quite honest, I've been doing my homework for the past couple of weeks. And I'm like: I think I have to call my doctor and get a ‘script to actually use the product. Just to help everybody get up to speed on this, can you bring people up to speed on where we are with glucose monitoring and health in general? Whether they have diabetes or whether they're just, you know, what, I, maybe someone like me who I hope is a generally a healthy person.Noosheen Hashemi: Sure, absolutely.  Yeah. So from Mike Snyder's four-year multi-omic IPOP research,  we learned that people who are so-called healthy and have healthy A1C levels could actually have huge glycemic variability. He sometimes calls these people with pre pre-diabetes.  I think eight people developed diabetes during his four-year study.There haven't been enough longitudinal studies in healthy people with glycemic variability to suggest that they will necessarily develop diabetes. So to date, there's really no conclusive evidence that healthy people can benefit from balancing their blood sugar. Also, not all sugar spikes are bad and a two-hour bike ride might produce a big spike, but that's fine. It's not the spike by itself that we worry about. It's really  how high the spike is against our baseline, against the population, whether the spike comes down quickly, the shape of the curve, the area under the curve. These are the things that are illuminating in terms of our state of metabolic health.So  at January we really view metabolic health as a spectrum. So we want to support people to figure out kind of where they are on that spectrum. And to try to really help them move up to healthier points on that spectrum. So we don't see it as a moment in time where you are something or you are not something. You are kind of on a spectrum of metabolic health, and we continuously want you to be self-aware and, and really improve your location on that spectrum. Now, something to keep in mind,  and why I think it's important for people to take action on this, is that 84% of the 88 million people believed to have pre-diabetes today, and 22% of the 34 million people that are believed to have diabetes today, are not diagnosed. They are undiagnosed. That's 75 million people walking around with pre-diabetes and don't even know. So, if we don't measure people's health, that doesn't mean they're healthy.  So we really encourage people to be  you know, vigilant with their health learn so that they can, they can act, you know, self-advocate. Be able to self-manage.So we do think that wearables are an easy, useful way to kind of see where things are, but then you need companies like January to make sense of it all. Harry Glorikian: Yeah. I mean  you know, it's interesting because you know, I'll go to my doctor and they'll do that one time measurement. It's like taking your car in and you're like, it was making a noise. It's not making the noise right now, but, you know, try and diagnose when that event is not happening. Whereas with the wearables, I can, I can actually see, you know, my, my heart rate variability change depending on my exercise process. I can see my sleep change if I had one too many glasses of wine. I have to tell you, I hate it because I would like to have more wine than my monitor allows me to have, but you know, you see the immediate feedback, which would let you sort of course-adjust accordingly. And you know, when I, there was a paper, I believe that was published in Israel where there, I think it was 500 people that they looked at and where you could see that every person, they could eat the same foods, but their spikes would be different or how long that spike would be based on genetics, based on their microbiome. And so if you're not monitoring, how will you know that your quote, healthy diet is actually healthy for you? Noosheen Hashemi: You don't.  You definitely don't. And yes, that's study shows variability between people, but also we've shown glycemic variability for the same person. So we had somebody at the office have the same good sleep nine days in a row, and they had a different glycemic response to that. Mostly every single day, nine days in a row, depending on how much they had slept, how stressed they were, how much workout they had done. And most importantly, how much fiber was in there.  So we are radically different person to person, and this is why we encourage people.  No one is going to know you as well as you do. And no one's going to be as interested in your health as you are  as you should be, as you might be. So we really encourage people to learn, learn, be self-aware self-advocate, self-educate. Harry Glorikian: So, help people understand this term metabolic syndrome, you know, and, and talk about how many people, maybe who are pre-diabetic go to full-blown diabetes, you know? Noosheen Hashemi: Okay. Yeah. So  I mentioned that 122 million people have either diabetes or pre-diabetes in America.  88 million plus 34 [million]. And then a larger number of people, if you believe Mike Snyder's pre-diabetes number, that's even a larger number. But metabolic syndrome is a cluster of conditions that leads to type 2 diabetes, heart disease, and stroke. These conditions are basically high blood sugar—which has been historically measured by A1C  blood tests called hemoglobin A1C, but increasingly it's measured by time and range using a CGM—high cholesterol and triglyceride levels, high blood pressure, high BMI, and high waist to hip ratio. So this kind of fat right in the middle.So the 2002 diabetes prevention study showed that unless there's an intervention, 58% of the people that have pre-diabetes could end up with diabetes. And usually they think of this prevention as weight loss.That's what the DPP programs, diabetes prevention programs, are about.So if you have pre-diabetes the cells in your body don't respond normally to insulin. And insulin is a hormone that facilitates your cells taking up glucose, which is a source of energy for your body. Your pancreas basically makes more insulin to try to get the cells to take up glucose. You sort of get into this terrible vicious circle. So eventually your pancreas can't keep up and then you have this sort of excess sugar sitting in your bloodstream, which is really a problem. And it can really lead to microvascular complications like retinopathy or neuropathy or diabetic nephropathy.So as you know, diabetic retinopathy is the most common cause of blindness in working adults in the developed world. And in diabetic neuropathy, essentially high blood sugar can injure nerves throughout the body. And usually damages nerves in the feet, in the legs and feet, which hear about foot ulcers and amputations coming from this.And of course  diabetic kidney disease. Nephropathy is something that  is the number one cause of kidney failure, actually. Almost a third of people with diabetes develop kidney disease. So you add this with the high blood pressure we can increase the force of blood through your arteries and damage arteries. And then you have excess blood pressure, you knowblood pressure and diabetes together, basically increase your risk for heart disease. So it's really a terrible cluster of conditions to have. And so if you have three of these conditions, three of these five, you essentially have metabolic syndrome. And if you have metabolic syndrome, you're at a higher risk of developing these different diseases. You really don't want to go down this path. The path itself is not great. And then the comorbidities from this path are just worse and complications of course are very painful, costly, and potentially, deadly.Harry Glorikian: And so that's one end of the spectrum, but in reality, even someone like me who tries to watch he eats, who goes running regularly, or tries to go running regularly. I mean, you know, I have sleep apnea because they tell me my BMI is too high. Right. So  but this sort of technology, you know, I could be spiking and keeping a high glucose level, which would inhibit my ability to lose weight, et cetera. So how can more data about blood glucose, and its relationship to diet, help people avoid diabetes?Noosheen Hashemi: Yeah. So for so long, we've been able, we've been told just to avoid refined sugar, refined flour, eat a lot of vegetables, walk 10,000 steps. You'll be fine. Or, you know, weight loss is given as the end goal to cure all diseases. You know, why don't you, Harry, drop 25 pounds? Or how about drop 5 to 10% of your weight? Harry Glorikian: Just like that!Noosheen Hashemi: It's true, weight loss really improves biomarkers. But how many people who get this advice can actually do that? And at the timeframe that they need to. So we feel like that's just not a practical approach to solving a problem.A more practical approach is to really figure out what works for each individual. You know, you mentioned you've dialed your own wine drinking based on its impact. I've done the same. I was, you know, enjoying two, three sips of wine. And then I learned that it would wake me up in the middle of the night. So I stopped having even the two, three sips of wine. So don't feel bad that you can't have your second and third and fourth glass. But basically we offer a multitude of levers that you can dial for your lifestyle. For example, intermittent fasting and calorie restriction together have shown benefits in clinical studies for improving insulin sensitivity, if you do them together. So you can't just fast and then gorge yourself. But if you fast and you restrict your calories together, you can really improve insulin sensitivity. So we let you, we help you using the January program to learn to experiment with fasting and calorie restriction and figure out what works for you. How much of it you can make. You know, slowly  help you essentially build it into your habits and your daily routines to fast. You know, we increase your fasting period 15 minutes at a time. So you may start with January you're eating 16 hours a day and you're fasting eight hours. You may end the program having reversed that.And other thing is we, we really pro promote fiber consumption. So increased fiber intake has been associated with higher levels of bacteria-derived short chain fatty acids, which is a regulator of GLP-1 production. As you know, GLP-1 is an incretin and a recognized regulator of glycemic homeostasis and satiety. So we help you track how much fiber you're eating. We encourage you to eat more, knowing what foods spike you, spike your blood sugar, helps you basically eliminate or reduce consumption of those foods. It tells you how much, how much of those things to eat  or alternatives that kind of honor your food preferences  and food tastes, but have lower glycemic index. If you can't walk 10,000 steps a day, okay. January tells you how much you need to walk, when you need to walk to keep your blood sugar in a healthy range. So you really need data  to, to dial your lifestyle. There are many levers and there are no silver bullets and there's too much to keep in your head. Which is why it's nice to have AI sort of help you kind of make, you know, take it all in to a platform and then synthesize it and give you insights.Harry Glorikian: Yeah. I mean, like,  I've got my, my Apple Watch. I've got my, you know, Whoop band. Right.I don't have as many as he [Mike Snyder] does, but  I know, I think my wife would kill me if I, if I was wearing eight things, but, but it's, you know, it's true. Like it's, you know, each one of these, because they're not holistically designed, give me a different piece of data that then I can then react to. You know, one is probably more of a coach that causes me to push a little bit farther, you know, et cetera. So  I mean, I hope one day we evolve to something that's a little bit more holistic so that the average person can sort of, it becomes more digestible and more actionable. But you know, I do believe, based on my conversation with him and even all the work that I do multi-factorial biomarkers or multi biomarkers are going to be how you manage, you know, yourself much better.But you know, tell me how January started. What is the thing that excited you about what you saw and what attracted you to this role? Noosheen Hashemi: Yes, absolutely. So January's origin story started with me deciding in 2016 to start my own company, essentially, after many years of running a family office, investing in, serving on boards of companies and nonprofits.  I had early success at Oracle  where I rose basically from the bottom of the organization in 1985 to vice-president by age 27. Along [with] Mark Benioff, who at the time was 26. It was quite the time, taking the company from $25 million to $3 billion in revenue. So  you know  a really, really amazing tenure there. In 2016, I started this massive research in, into theses that were getting a lot of attention, you know, big trends over the next decade. And most importantly, what I really knew. You know, the classic kind of [inaudible].  I happened to attend a conference, a White House Stanford University conference on societal benefits of AI and how to integrate sort of ever-changing AI into everyday life and into the real world. It was a healthcare panel that took my breath away. So Faith A. Lee who had organized the conference with Russ Goldman. They suggested that interested parties run off to this machine learning and healthcare conference in LA two weeks. I immediately booked my ticket. And there I met Larry Smarr. I don't know if you've come across him or not, but he was the first quantified self, maniacal quantified self person I had come across. And he had diagnosed his own Crohn's disease way before symptoms had manifested. And so, and then the common theme of this conference, between all of these presentations was that machine learning could essentially fill in for missing variables in research, not just going forward, but going backwards. So I was just hooked and I never looked back.But it was a hard problem. My own husband had been investing in healthcare and warned of like an opaque sector. He was like, “Honey, this is heavily regulated incentives are aligned with acute disease, not with chronic disease, not to mention even anything or prevention. It's just not a market economy.” And he knew how interested I am in market economies. My first love before medicine was economics. So that's a whole different podcast. So he warned that I'd be sort of fighting this uphill battle, but I was not discouraged. I basically kept on researching.I came across the MIT economist Andrew Lo. I don't know if you've come across him, but you should definitely talk to him. He's brilliant. His work showed that so little research had been done compared to what we really need to do in terms of medical research. And he comes up with ways of funding, medical research, he has a lot of innovative ways that we could really change  the whole model of medical and scientific research, but it kind of became obvious to me that the answer was that we needed to get everyone involved in research.So just, just putting things in perspective. After Nixon declared a war on cancer 50 years ago, we now have some therapeutics and some solutions to cancer. We have really nothing for neurological diseases. We're spending over $300 billion just on symptoms of Alzheimer's— don't talk about even the cure or anything like that. We have nothing for aging, which is the ultimate killer. So it was, to me, the answer was obvious, which was, we have to get everyone contributing to research. Everyone should be looking at themselves. And then with the data, we can also learn across populations. And so deep phenotyping of the population sort of in a multi-omic way was the answer.And that's what led me to Mike Snyder. I actually looked for multi-omics. I went to Stanford medical school and I met with the CEO. He said, what are you interested in? I said I'm interested in multi-omics. He said, you have to talk to Mike Snyder. And so  basically what Larry Smarr had done at the [San Diego Supercomputer Center] was to measure everything by himself. But Mike had essentially extended this kind of research to others, not just to himself. So not only sort of diagnosed himself with diabetes before the doctors, but he'd also run the Human Microbiome Project, the IPOP study, innumerable other research using metabolomics, proteomics, transcriptomics, wearables, and so on.So he had spent a lifetime studying how people went from healthy to disease essentially. And he had taken a whole person approach, which is what I was interested in.  And so in his role as chairman of genetics at Stanford and head of precision medicine at Stanford, he was kind of already living in the future. And that's kind of where I thought, you know, all of us needed to go. So our first meeting was supposed to take 45 minutes. It took 90 minutes. And in our second meeting, we agreed to join forces. It was like, it was instant.  It was just instant chemistry. Like the universe just brought us together.And then all of a sudden sort of everything fell into place for me. Looking back at my life, I been getting ready for this actually all along. Caring for my dad who had been diagnosed with cancer too late to actually give him  a surviving chance. My mom  had been misdiagnosed with asthma when she had heart failure. So I had to leave my family, you know, everyone get together and really intervene. Really changed her, her lifestyle in order to save her life. She is thankfully now 91 years old and living fine, but it has absolutely no salt in her life and a completely different, different life. My own health, my own health journey sitting in front of a computer for three decades, more than three decades, as we know that now they call it called sitting, you know, Harry Glorikian: Right, the new smoking. Noosheen Hashemi: The new smoking. My experience running a couple of hardware companies, my love of food, and my skills of kind of scaling companies. You know, all of this came together. I just basically became obsessed with prevention and I felt that, you know, food could play an outsized role.So wearables, you know, give you signals from the body continuously, which is incredible.  But you also need to understand what people are eating and, you know, we can talk about that a little bit later, but we can basically now imagine predicting chronic conditions, much like Larry and Mike had. And then, you know, postponing and potentially preventing them. And if they've already started, prevent them. Harry Glorikian: Yeah, I was lucky enough to be there and help when Evidation Health was getting off the ground and, you know, once we started to see the data coming in, I remember looking at the data. Is that real, like, is that actually happening? And I was like, the first thing I was thinking of was like, how do we design a clinical trial? Like if you're going to actually say that's happening, that trial is not going to be trivial to set up, to make that claim, but you could see it in the data.And, you know  I actually think some of the shifts that you're talking about, if it wasn't for things like the Affordable Care Act, if it wasn't for putting EMRs in place, if it wasn't for some of these shifts that have happened, you and I would still be, you know, battling this system that pays you no matter what. Right? And I think now is technology is a way that that can empower the average person to manage their own health. I'm not going to say optimally, but boy, a hell of a lot better than no information. I mean, at least some information can maybe give you an early warning light of something that you might be able to intervene in.And I don't know anybody that likes being sick. I mean, I don't do well when this thing starts to age a little bit and not function the way that I want it to. So I've tried to try and keep it in as good of a running condition as I can. So it lasts as long as possible. I mean, I'm one of those people that would listen if I just drop dead at 95, like just boom gone. I would be so happy. Right. As opposed to this sort of chronic  dynamic. [musical transition]Harry Glorikian: I want to pause the conversation for a minute to make a quick request. If you're a fan of MoneyBall Medicine, you know that we've published dozens of interviews with leading scientists and entrepreneurs exploring the boundaries of data-driven healthcare and research. And you can listen to all of those episodes for free at Apple Podcasts, or at my website glorikian.com, or wherever you get your podcasts.There's one small thing you can do in return, and that's to leave a rating and a review of the show on Apple Podcasts. It's one of the best ways to help other listeners find and follow the show.If you've never posted a review or a rating, it's easy. All you have to do is open the Apple Podcasts app on your smartphone, search for MoneyBall Medicine, and scroll down to the Ratings & Reviews section. Tap the stars to rate the show, and then tap the link that says Write a Review to leave your comments. It'll only take a minute, but it'll help us out immensely. Thank you! And now back to the show.[musical transition]So you mentioned AI, you mentioned machine learning. Where do machine learning and other forms of AI fit into January's service and you know, what do you do on consumer data? What kind of predictions can you make that wouldn't otherwise be possible?Noosheen Hashemi: Okay. I can first talk about exactly that. What did we do that hadn't been done before. What is really unique? What are we filling? So essentially in one word, it is prediction. You said it. So  as you know, there've been, there have been glycemic prediction models for type 1 diabetes, but type 1, as, you know, is a serious condition, which, you know, precision really matters for type one. It's life and death.But there hasn't been much done with type 2 diabetes. And so we set out to do predictions, for type 2 diabetes. And  the type 1 diabetes models are pretty simple. They basically are an insulin-carb calculus, essentially. But as we dug in, we realized that  you know, carbs are not all the same and that there are so many other factors besides carbs that affect glycemic response, including things like fiber fat and protein, water, and foods. We wanted to understand glycemic index and glycemic load of foods. So our major  machine learning  research projects, we basically did research for two and a half years before we sold anything.  One of the first things that we did was to try to understand the foods themselves. So we essentially built the largest database. Essentially we licensed all the, these curated food databases, and then we labeled the foods that didn't have food labels, because right now the only food labeling you really have is like grocery foods and chain restaurants.So we labeled foods and then, recognizing that glycemic response was better associated with glycemic index than carbs alone, we set out to create glycemic index and glycemic load for all these foods. Then we ran a clinical trial and associated people's glycemic response to the glycemic load of foods they were eating. And then we turned that into a prediction. So, the prediction model.  Why is it so cool? Well, why should you use your body to figure out how many glasses of wine is going to spike you? Why not have the AI tell you that? Why not do that in silico?  It's this weekend, you want to cook for your wife. You want to get her the right fried chicken recipe. Well, check those out in January, check out those recipes in January. If you know what the glycemic response of, of each one of those recipes could be, it really helps you compare foods. For kind of recipes you can comparefood items in your local cafe. You want to figure out what to eat. You don't have to put them through your body to figure out how you're going to respond, put them through the AI to figure out how you're going to respond.And then in terms of, you know, how we're different. I mean, we essentially live in the future. We, we don't  we don't live in blood pricks and strips and blood glucose meters. We kind of live in the CGM, HRM (heart rate monitor) precision foodworld. We've turned food into actionable health data, which is a necessary ingredient you need if you want to understand people's glycemic response. And if you want to be able to predict it, and that is our huge innovation that nobody has. And we have quite a bit of IP around it. There are a number of things that we're using. We're using meta-learning.  We're using  neural networks. I don't know how much I should say about what we're using. Yeah. We have one paper that we've put out, which is really, really, really simple.  But we, we always talk about, what kind of papers we want to put out and how much we should put out and how much should we not put out, but essentially you can look at the people that advise the company and you can see that, you know, we have a lot of expertise around  essentially… Harry Glorikian: But Noosheen, when you're doing this right, you need to, at some point, I think you need a baseline on say me for a certain period of time before the algorithm can then respond appropriately to that. And then doesn't that potentially change over time, time you mentioned the yogurt, the meusli, right.  And how that affects. So it's constantly gotta be in a feedback learning loop.Noosheen Hashemi: Yes. Yes. And the beauty of January is that essentially you don't have to wear a CGM 365 days out of the year. We think that with AI, we allow you to wear a CGM intermittently. So maybe you want to wear it every quarter  to update our models  just to see how things are going, but you don't need to wear it all the time. You can wear it for a period of training and then basically run your simulations in silico rather than through your body. Let the AI do the work. So you definitely should wear it intermittently so we can update our, our models because people do age. People do have inflection points in their health. They get pregnant, they travel, a lot of things change, but we don't think it's necessary for healthy people to wear CGMs all year long necessarily. Harry Glorikian: So now we're talking about consumer behavior, right, for a, for a tech product like this. And if, you know, if you look at some of the data that I've read in some of these papers, you know, the potential market is significant. It's, you know, it's quite large. I mean, if I just said, you know, 15% of the people have pre-diabetic levels of glucose after eating, that would translate to like 50 million people in the United States alone. But the service depends on the CGM, the app, the external heart monitor. It's, you know, users have to be diligent about monitoring and logging food intake and activities during the introductory month. So for a quantified self junkie, I get it. They're all over this.  What's the plan for getting everybody else on to this? Noosheen Hashemi: Well, I think it's all about the user experience. And I think we have a, we have a long way to go as an industry and for us as well.As a company we have, what we imagine to be the user experience is nowhere near where we are today.I'm old enough to remember world before Starbucks. So you would see ads on TV for MJB coffee, which is something you made at home. You know, I don't know if you remember that but Starbucks created a new experience, really a place between home and work where you would stop by for coffee.And so the outrage around the, you know, $3, $4 latteat the time, do you remember that?Well, Starbucks continue to improve the experience. They added wi-fi, they had ethical coffee, they had kind of a diverse employee population. People's initial wonder and worry gave way to this, you know, gigantic global brand. And I think all of that is because of the experience that people had. I think we need to make health a positive experience. We need to—we, including January—need to make health something that people….it's going to be a little clunky in the beginning, just like the old, you know, cell phones used to be. But while we're going through this process, the companies need to work on to improve the experience and people need to be patient with the clunkiness of everything  to get us to a place where these things become much, much more pleasant to use and easier to use, and essentially AI starts reading your mind about what you were eating and what you were doing. That is going to happen. You know, I've gotten so used to my Apple Watch now that I actually love it. It actually is doing a very good job training me. Just at the right time, you know, “Come on, you still have a chance. Let's go.” You know, all the things that it's doing  I'm actually liking it. It's it's enjoyable. Because it Is coaching. And I feel like the answer for mass adoption lives in experience. We need to improve the experience dramatically. Harry Glorikian: It's interesting though, because I I'm play with a lot of these different things and I noticed that depending on how they're designed, how they're put together, it nudges me to do that much more or et cetera. I don't always listen. Human beings don't always do what they're supposed to do for their better good. But  you can see how, when the app is designed in a way to nudge someone the right in through the right mechanisms. And that's the problem, right, is trying to—not the same mechanism works on everybody. So you may have to have multiple approaches that the system tries like AB testing for a website to, to get them to do that.But so, if the average person like me wants to do something like this, obviously I have to get a ‘script from my doctor, which just drives me crazy that I can't just—because I can buy a finger-prick, right, over the counter and poke myself a thousand times and then write down these numbers to see what happens. Which seems a little clunky in my opinion. But I can't buy the CGM that does it automatically. There's gotta be some medical person saying like, we're gonna make more money off this if we do this or do that, or, or it just doesn't make any sense to me.  How do you, how does January come at the expense reimbursement or the insured part of it, or is this just out of pocket for everybody? Noosheen Hashemi: Sure. So right now  government insurance, companies, and private insurance companies cover CGMs for people that are intense insulin users. So people that prick themselves four times a day. And so that's three and a half million out of 122 million people that have pre-diabetes or diabetes. So it's a very small population. And the rest is all cash paid. And it it's really out of pocket. So we have an early access price of $288. And we, you know, we include the CGM, but you can also buy CGMs only from January. You can just, if you just want a CGM, you don't want to do anything else. You're just curious. You want an introduction to this world? You can order a CGM from January for $80 if you want to do that. So if you're one of the 12 million people that are insured by Kaiser—and Kaiser doctors will not write you a prescription, you can go to your doctor and ask them, they won't write you a prescription—come to January. We will give you a CGM. You can be introduced to the program and then, you know, take, take up January from there and experience the magic of CGMs alone. I really do think they are a magical product because they they're showing you for the first time you kind of can see inside your body, which is really phenomenal. Unfortunately by themselves, they're not that effective and they're not that effective by themselves longitudinally. So if you really want to keep track of how you've been doing, what food spiked you, how you can, you know, what kind of exercise, things like that. They don't really have that additional intelligence, but they are magical, they are really magical tools. But, you know, you want an insightful experience on top of that. With the AI that can essentially synthesize this kind of data from your heart rate, monitor from your food, from your glucose monitor and sort of let you know how much to eat, what to eat, how to hack your food, how much to walk, how much, how much to fast, when to fast, how much fiber you're having, not having. That's where we come in. Harry Glorikian: I feel like at some point I'm going to need a big monitor in my house that just tells me these things as I'm walking by. But you know, it, it's interesting. I mean, we are entering the era of real wearables and apps and big data and, and, you know, but here's the question though. Soyou know, Apple just announced what's going to be the update to their iOS and, you know, pretty soon I'm going to be able to push a button and share data with my physician.  Which is funny because I go in his office and I pull up my phone and I'm like, here's my longitudinal. And here's my longitudinal. And I'm like, look, you can take the measurement because you're supposed to, but here's how it looks over the last three months as opposed to the one time when I'm here. Can January's customers export and share the data with their doctor? Noosheen Hashemi: We have a report  midstream at 14 days that you can share  with, with your doctor. But of course we intend to, you know, we have features planned that are going to make things way more easily done, much more easily in the future. We really strongly believe that people should own their own health data. We are huge advocates for people owning their own health data, because there are a lot of people hanging onto your health data and they don't want to give it to you. I'm talking about device makers and others. You're paying for the device, which comes with the data, but they don't want you to have the data. So they're like, “You can have the data and study it yourself, but you can't give that data to other people.” But that doesn't work.We are living in a multi-omics world. Single 'omics by themselves, the single side node biomarkers, you know, “Harry, you just manage your cholesterol. Noosheen, you can't keep two things in your head. Why don't you just manage your A1C? And Mike, you should watch your blood pressure.” That just doesn't work. There are many, many markers that you've just, as you just said, that we need to keep in our heads. We can't keep them in our heads, but that's where AI comes in. We need to feed them into something and people must have the right to own their data and share their data with whoever they want. If it's their coach, it's their doctor, it's their wife or spouse or significant other, their dog. They should be able to share the data that they own.As long as they provision it properly to whoever they want to give it to because you know, someone doesn't want their employer to know X, Y, and Z. Somebody else wants their coach to know that is people's rights. And coming from kind of a libertarian point of view, I really think people, you know, people should own their own data and they should be able to mix it with other data  for synthesis, if they want to. Harry Glorikian: Yeah, it's interesting. I mean, I totally believe in that. I always, I also understand that people may not understand the implications of sharing sometimes.  And that's not clear, but I do believe that the next iteration of where we're going to see this technology go is multifactorial software programs that can take a number of different inputs to give a much more holistic view of what's going on with me, so I can manage myself better share that information. My biggest worry is most physicians I know are—it's not totally like, it's not their fault, right….Noosheen Hashemi: They're so busy, so they're spending 15 minutes a year with you. And during that 15 minutes, you know, they're taking a point in time, you know, to see a snapshot of your health. And your health is way more complicated than that. We're talking about reverse engineering, 5 billion, years of evolution. And you know, they're going to get, see if such an infinite small part of that. We need to be way more self-aware.Harry Glorikian: Well, it's funny because I do have, some of my physician friends will be like, you want me to understand that genomic marker that whatever, like, I can't, I can't get my patient to manage their insulin level!Noosheen Hashemi: I have a lot of empathy for that. They just don't have the time.  I completely fully understand. Which is why I think we should carry more of the, we should have more agency over our health and we should carry the burden a little bit more.Harry Glorikian: So what is wild success for January? Noosheen Hashemi: Well, we want to keep on this path of developing our multi-omic platform. We want to essentially  help people understand themselves deeply and figure out how to dial their lifestyles and sort of tweak and tune their health. This is non-trivial obviously because there's not enough research in food science or enough research on prevention. You know, out of the $3.8 trillion that we spend on healthcare, 2.9% goes to prevention and 10% goes to acute care end of life care. Just think about that. More than three times as much goes to end of life acute care than goes to prevention. And I'm talking about healthcare costs, I'm not talking about research costs in terms of what NIH and USAID and all of those people spend. So there's not enough research that's happening. You know, people's health data is not organized today. I'm sure there are companies who are trying to organize the world's data. You know, the company that tries to organize the world's data is trying to organize your health data. So I think that's pretty smart.  I think today it's still very opaque and it lives in silos, but I think in the future is going to be mixed.  I think today people just aren't fully empowered yet, you know, with the knowledge and with the agency and with the tools they need to really manage their health.Wild success for us means that people, that we're part of this revolution of consumerized healthcare. We're part of the food-as-medicine revolution, the precision nutrition revolution. So we see ourselves coming up with tools that can essentially get amazing experiences in the hands of millions of people.If you can think about a company like Livongo going public with 192,000 patients. Or if you think about everyone that's playing in the metabolic health today, if you put 12 or 13 companies together, maybe they have a million users, or maybe a million and a half users. Where is that compared to 122 million people that have pre-diabetes diabetes and another a hundred million people that are optimizers? They're either wearing a wearable, they belong to a gym, they're on a diet. You have the entire population as your market. And we have very little that has really made a major foray into health. So wild success means having a product that becomes mainstream. Harry Glorikian: So I think what you're saying is January is moving beyond just CGMs and metabolic syndrome, right?Noosheen Hashemi: Absolutely. Yeah, we, we imagine ourselves, we have built an expandable platform. Our goal is to keep doing deep phenotyping. So we will add 'omics  you will see us adding 'omics beyond what we have today. You will see us  get to other cardio-metabolic disease, you know, cardiometabolic disease, essentially going beyond metabolic disease to the rest ofmetabolic syndrome. You'll see us be ahardware-agnostic company. We want to essentially let people wear whatever they want.  Whatever works for them and, and still try to bring that data, synthesize it and make sense of it and feed it back to them so they can take action. Harry Glorikian: Excellent. Well, that's, that's a great way to end the program with. We have so much more to see from the company and what it's going to be able to do with the data and, and, and help  you know, people live a healthier life. Or like I said, with me I'm constantly trying to measure what's going on. It's just distilling it to make it easily consumable to do what I need to do rather than have me learn statistics so that I can figure it out. Noosheen Hashemi: We have to get, all of us need to get better than that. I remember when I first put on my Oura ring, you know, there's, you know, most people  first when they wear their Fitbits, you know, first it was like, how much did I sleep? And then they kind of learned about REM and sort of deep sleep and then slowly. And then Oura came and then it was like, oh, and Whoop had already had heart rate variability, but then, you know, Oura came in with their other markers, you know, restfulness. And efficiency, sleep efficiency and timing, et cetera. And so people are slowly wrapping their heads around this. It takes a little whil. And yes, January gives you a lot of levers. You know, there's fasting, there's fiber, there's calorie management. There's you know, the spikers. There is the activity counterfactuals—I ate this, but had I eaten this other thing, this would have been my glycemic response. Or had I walked X number of minutes after that, this would have been my glycemic response. At the beginning it's a lot, but that's where it goes back to the experience. We must make the experience enjoyable and better, and we must, companies like us should strive to make the experience enjoyable, make them fantastic consumer experiences like Apple products. But remember Apple's 45 years old and we're just getting going with this, But [Apple is] a great role model. Harry Glorikian: Wellyou know, my doctor may not like it, but I may have to get one of these. He's listening to this podcast. I know that he will, because he always comments on them. Noosheen Hashemi: We're definitely doing that. And you know what? You can have Mike Snyder, you can chat with Mike  about your numbers after. That would be a lot of fun.Harry Glorikian: Excellent. Oh, I look forward to it. So thank you so much for participating. Noosheen Hashemi: Thank you, Harry. It was pleasure.Harry Glorikian: That's it for this week's show. You can find past episodes of MoneyBall Medicine at my website, glorikian.com, under the tab “Podcast.” And you can follow me on Twitter at hglorikian.  Thanks for listening, and we'll be back soon with our next interview.

A study in the Western Journal of Emergency Medicine finds a low incidence of clinically significant outcomes in chronic kidney disease patients who undergo emergent contrast CT. Acute Kidney Injury After CT in Emergency Patients with Chronic Kidney Disease: A Propensity Score-matched Analysis | Hospital Medicine Virtual Journal Club

Renee Agular-Lucander is CEO of Calliditas Therapeutics a Sweden-based clinical-stage biopharmaceutical company focused on the rare kidney disease IgA nephropathy. While there is a genetic predisposition for this autoimmune disease, it is still not clear what triggers the condition and there is no current cure. Renee talks about: Lead drug candidate Nefecon which starts at the top of the disease cascade in the ileum part of the small intestine. Delivering this disease-modifying agent directly interrupts and disrupts the beginning of the disease How clinical trial data is showing the value of addressing the gut-renal axis and treating this indication in an organ-specific way Other orphan indications that might benefit from this approach What the FDA priority review of Nefecon potentially means for the 1 in every 4 adults with IgAN who will eventually succumb to kidney failure. @Calliditas1 #IgANephropathy #IgAN #Kidney #KidneyDisease #EndStageRenalDisease #AutoimmuneDisease #Nefecon #RareDisease Calliditas.se/en Listen to the podcast here

Renee Agular-Lucander is CEO of Calliditas Therapeutics a Sweden-based clinical-stage biopharmaceutical company focused on the rare kidney disease IgA nephropathy. While there is a genetic predisposition for this autoimmune disease, it is still not clear what triggers the condition and there is no current cure. Renee talks about: Lead drug candidate Nefecon which starts at the top of the disease cascade in the ileum part of the small intestine. Delivering this disease-modifying agent directly interrupts and disrupts the beginning of the disease How clinical trial data is showing the value of addressing the gut-renal axis and treating this indication in an organ-specific way Other orphan indications that might benefit from this approach What the FDA priority review of Nefecon potentially means for the 1 in every 4 adults with IgAN who will eventually succumb to kidney failure. @Calliditas1 #IgANephropathy #IgAN #Kidney #KidneyDisease #EndStageRenalDisease #AutoimmuneDisease #Nefecon #RareDisease Calliditas.se/en Download the transcript here

It's the JournalFeed Podcast for the week of May 24-28, 2021. We cover management of low velocity GSWs, another look at contrast nephropathy, CT with contrast for kidney stones, safety of steroid bursts for children, and ketamine and hypotension risk once again.

Dr. Chantal Lewis is a board-certified endocrinologist at Hamilton Diabetes and Endocrinology Center. She specializes in diabetes and thyroid treatment and practices in both Dalton and Ringgold, Georgia. For more information about Hamilton Diabetes and Endocrinology Center call 706-278-1622 or visit HamiltonHealth.com/diabetes.  This program in no way seeks to diagnose or treat illness or to replace professional medical care. Please see your healthcare provider if you have a health problem.

Diabetes complications is a concern for everyone living with diabetes. This week Tracy Herbert shares the importance of having the right mindset to help with lowering blood sugar levels while reducing the risk of developing diabetes complications.

A macrovascular complication of diabetes, diabetic nephropathy is progressive, chronic kidney disease seen in patients with both type 1 and type 2 diabetes mellitus, usually after at least 10 years of hyperglycemia (high blood glucose levels). The three main lesions that are seen in the kidney in patients with diabetes are glomerular lesions, vascular lesions, and pyelonephritis. This brick will focus primarily on the first two of these three lesions; diabetic pyelonephritis is covered in a separate brick. After listening to this AudioBrick, you should be able to: Define diabetic nephropathy. Outline the timeline of progression of diabetic nephropathy (DN) by urine, serum, and histologic criteria. Describe the diagnosis of diabetic nephropathy. Outline the prevention of diabetic nephropathy and, once it is established, how to slow its progression. Describe the management of diabetic nephropathy. You can also check out the original brick from our Renal collection, which is available for free. Learn more about Rx Bricks by signing up for a free USMLE-Rx account: www.usmle-rx.com You will get 5 days of full access to our Rx360+ program, including nearly 800 Rx Bricks.  After the 5-day period, you will still be able to access over 150 free bricks, including the entire collections for General Microbiology and Cellular and Molecular Biology. *** If you enjoyed this episode, we'd love for you to leave a review on Apple Podcasts.  It helps with our visibility, and the more med students (or future med students) listen to the podcast, the more we can provide to the future physicians of the world. Follow USMLE-Rx at: Facebook: www.facebook.com/usmlerx Blog: www.firstaidteam.com Twitter: https://twitter.com/firstaidteam Instagram: https://www.instagram.com/firstaidteam/ YouTube: www.youtube.com/USMLERX Learn how you can access over 150 of our bricks for FREE: https://usmlerx.wpengine.com/free-bricks/

Dr. Robert Odell and Dr. Michael Moses from the Nephropathy and Pain Center in Las Vegas stop by for their weekly visit. Three and Out explores why Eric Bieniemy is not a top candidate for head coaching jobs. And as always Vinny takes calls from Raider Nation. See omnystudio.com/listener for privacy information.

This episode covers contrast nephropathy!

Effect of a Single Apolipoprotein L1 Gene Nephropathy Variant on the Risk of Advanced Lupus Nephritis in Brazilians Gisele Vajgel, Suelen Cristina Lima, Diego Jeronimo S. Santana, Camila B.L. Oliveira, Denise Maria N. Costa, Pamela J. Hicks, Maria Alina G.M. Cavalcante, Carl D. Langefeld, Lucila Maria Valente, Sergio Crovella, Gianna Mastroianni Kirsztajn, Barry I. Freedman and Paula Sandrin-Garcia The Journal of Rheumatology August 2020, 47 (8) 1209-1217; DOI: https://doi.org/10.3899/jrheum.190684

Dr. Tracy Palmer Our world is made up of dualities. It always has been. Tall or short. Black or white. Fast or slow. Up or down. Good or bad. Similarly, every human has some semblance of duality in both masculine and feminine energies, and while they can't always be seen, both are equally important to our inner harmony and well-being. And, there is definitely something magical about feminine energy that is so often overlooked, underrated or downright neglected in modern society. Throughout history, womanhood has been associated with weakness, sacrifice, co-dependency, over-sensitivity, and emotionality. And even in modern society, whether you identify as male, female or non binary, we continue to live in a world where feminine energy is suppressed, and masculine energy is glorified. I mean, I think we can all agree that in today's world, we tend to be more dialed into a “get-more-done” mentality, constantly on a mission to achieve more, do more, get more, assert more, be more. Masculine energy translates into qualities like drive, determination, independence, aggression, competitiveness, and confidence, which I think we can all recognize as pretty essential traits for succeeding in today's world. And, don’t get me wrong, these are not bad traits, we need them. In fact, these qualities have probably allowed the amazing women that you can think of to become CEOs, business owners, public figures and leaders. But feminine energy embodies something a little less revered: feminine energy depicts the nurturer, the healer, the creative, one of feelings, morality, passivity and peacemaking. So while the masculine energy is focused on doing, the feminine energy revels in being. And according to today's guest, Dr Tracy Palmer, the value we put on masculine energy has led us to lose touch with our real power – our divine feminine energy and because of this we are often left feeling frazzled and depleted without truly understanding why. Tracy believes that because we tend to prioritize masculine over feminine energy, the key is in finding balance and achieving our own unique harmony between these two types of energies. Fatigue, perpetual hustle and energy depletion don't have to be part of your story. In fact, there are many ways to embrace and prioritize your divine feminine energy so that you arent left feeling drained and unfulfilled, and today Dr. Tracy is sharing tangible techniques for managing your life and divine energies so you can start taking back your life, your divine self and most importantly your energy. So, are you ready for a wee spiritual awakening? Ok, Grab yourself a cup of something delicious and let's dig in. In this episode, we talk about: Giving yourself permission to have hobbies and do FUN things (and not feel guilty about it).Cultural pressure being the reason that women tend to put their own fun time on the back burner.The negative “positive” feedback loop of receiving praise for being selfless and judgement when not.REST! And why women are less likely to do it (STOP glorifying the hustle).Why we seem to have the image of rest being unproductive when it, in fact, INCREASES our productivity.Snacking like a pro – Eating for energy and how to prevent energy crashes (hangry).Changing the narrative – being busy is NOT a badge of honour.The Wild Collective initiative and why you need to sign up TODAY!How you still need fun outside your job – even if you have a job you love! Put yourself in the mix – pick one thing that you can do with just yourself with no guilt and, ideally, has no purpose attached.Dr. Tracy Palmer Wow. I can definitely relate to the suppression of my own divine feminine energy to make way for my more esteemed masculine side, for sure. So as you carry on your own journey of dual masculine and feminine energies, whether you identify as male, female, or non binary I want you to remember that taking time to embrace your feminine energy in order to seek your unique balance isn't selfish; it’s a necessary act of self care. In the words of author Elizabeth Gilbert, “You are a unique event in the history of the universe. There has never been a you—not your particular soul, living at this particular moment, faced with your particular challenges. Your existence is a mystery, a miracle, and an experiment of creation, and you are allowed to examine that mystery to the fullest.” Once you accept that, you allow your real spiritual journey to begin and I can't wait to hear all about it. Thank you again so much for tuning in to another episode of the workshop weekly podcast. I am truly honoured, as always, to be a part of your day. Bye for now. Connect with Tracy https://www.facebook.com/Tracy-Palmer-Naturopathic-Doctor-476132735754739 RootsToBranchesNB.com Check Out Today’s Sponsors Save 10% on Sheertex pantyhose with code KELLYSLAWSON10: https://kellylawson.ca/sheertex Save $40 on your first box with HelloFresh: https://kellylawson.ca/hellofresh Save 15% on your new TONIC site with code KELLYLAWSON https://kellylawson.ca/tonicsite Learn what's in Kelly's capsule this season: https://kellylawson.ca/mystyle

PSGN vs IgA nephropathy how to tell them apart in an exam

With Dr. Ashley Margeson, Cornerstone Naturopathic Inc. Ok. Is this you? Some days, you are totally in the zone. You are grooving so hard that you knock all the things off your lengthy to-do list and then slay half way through tomorrow's list too. You are on fire, and you are so impressed with yourself that you want to replace your work attire for a superhero suit, place your fists firmly on your hips, stand on a mildly windy mountaintop with your chin raised. There is nothing you cant conquer. Then, other days, you find yourself slumping, spinning your wheels, wasting time, mindlessly scrolling social media, distracted by everything and not really getting anything done. Frustrated with yourself you close your eyes and picture your bed, stretchy pants and a giant bowl of doritos. You doodle or scroll social media and on these days you're probably meantalking yourself and your lazy ways. Some days you feel unafraid and like a confident social networking rockstar, while other days you are so irritable and anxious that you can't get out of your own way long enough to even decide what clothes to put on your body that day. And these strange swings in your mood, appetite, and cognition, you can't seem to find a reason for any of it. Well, what if I told you there was a reason for it? And not only a reason, but a predictable pattern for it, a mood schedule, of sorts. What if you could align your life schedule with cycles of high energy, creativity, intuition and the need for reflection, in order to calibrate your expectations for yourself? What if I told you that for a long time now, women have been conditioned to adjust to a man's workplace, environment, schedule and approach to productivity and you are about to learn how this impacts our ability to be our best productive selves every day of life. What if I told you that many of us are never taught how to unlock the potential in our cycles? Well, my guest Dr Ashley Margeson is here today to change all of this for you. Ashley wants you to know that not only do Female hormonal cycles have natural and predictable fluctuations, but that they also affect your mood, energy and cognition in really predictable ways. And if you're like me, you've been conditioned to ignore all of these cues from your body. Ashley teaches women how to live in sync with their menstrual cycle and she explains how you can better understand the various phases of your cycle and how they impact your mood, your energy levels, your creativity and even how you'll perform on your first date, or maybe your job interview or client pitch. Today Ashley is breaking down our cycle for us so that we can begin to understand exactly why we feel the way we feel and what tasks we are optimized for at any given stage in our hormone cycle. You guys, my mind was blown many times over during my conversation with Dr. Ashley. I think after hearing today's episode we will all agree that it's time to look at syncing our work and socialization schedules up with our menstrual schedules, or in the very least, to understand our body's needs on a deeper level. Your mind is about to be blown. Your life is about to change. I'm serious. Are you ready? In this episode, Ashley talks to us about: How understanding your hormones and owning your cycle can optimize your LIFE.How your reproductive cycle isn’t just about fertility.The Superwomen Code (I KNOW you want to know more about this).How our periods are trying to communicate what is happening in our body – your period is a vital sign.What the perfect period looks likeHow each phase of your cycle gives you a new superpower and what they are.How to know when in your cycle to ask for a raise ;).Why we get cravings before our period.What part of your cycle is best for creative work.The apps you can use for tracking your cycle and how being armed with this data can help you plan and optimize your day to day life and be more forgiving of yourself.How birth control actually works and how to plan around this modified cycle.The ONE THING you need to do today to get closer to working with your hormone cycle instead of against it. Check out These Apps and Resources: Clue (tracking app) Me V PMDD (symptom tracker) The Superwoman Code (podcast) Connect with Ashley facebook.com/CornerstoneNaturopathic/ cornerstonenaturopathic.ca pinterest.ca/cornerstonenat/ instagram.com/cornerstonenaturopathic/ When asked if there was one thought she would like listeners to take away from this conversation: Track. Your. Cycles.Dr. Ashley Margeson Is your life different now? Has your mind been blown? Do you suddenly have the explanation you've been looking for as to why some days you are on your game while others you are not? Well, me too you guys. I dont know how I have lived to 40 without listening to my body on a deeper, more empathetic level. I am pretty confident that in just 12 short weeks from now we will all learn how to better manage our energy, how to work smarter instead of against the grain, and how to optimize our schedules according to our internal needs. Let's go on this discovery journey together. And, Was it just me or did this episode go by way too fast? Thank you so much from the bottom of my heart for tuning in to yet another episode of the workshop weekly podcast. I'll catch you again next week, workshop warrior. Check Out Today’s Sponsors Save 10% on Sheertex pantyhose with code KELLYSLAWSON10: https://kellylawson.ca/sheertex Save $40 on your first box with HelloFresh: https://kellylawson.ca/hellofresh Save 15% on your new TONIC site with code KELLYLAWSON https://kellylawson.ca/tonicsite Learn what's in Kelly's capsule this season: https://kellylawson.ca/mystyle

Join Yvonne Brandenburg, RVT, VTS SAIM and Jordan Porter RVT, LVT, VTS SAIM as we talk about: Protein loss coming from within the kidneys from, typically, glomerular damage as well as discussing other potential causes for protein loss aside from renal damage.    Question of the Week What personal experience do you have with PLN? Leave a comment at https://imfpp.org/episode41   Resources We Mentioned in the Show  Eclin Path,Urinalysis » Chemical constituents https://eclinpath.com/urinalysis/chemical-constituents/ Harley, L., & Langston, C. (2012). Proteinuria in dogs and cats. The Canadian veterinary journal = La revue veterinaire canadienne, 53(6), 631–638. Protein Losing Nephropathy- breed predispositions chart https://www.vetsmall.theclinics.com/article/S0195-5616(10)00143-9/pdf Cathy E. Langston, DVM, DACVIM.Protein losing nephropathy. https://www.dvm360.com/view/protein-losing-nephropathy-proceedings. April 1, 2008.      Thanks so much for tuning in. Join us again next week for another episode!  Get Access to the Waitlist Sign up at www.imfvt.com  Get Access to the Technician Treasure Trove  Sign up at https://imfpp.org/treasuretrove    Thanks for listening!  – Yvonne and Jordan 

Here is the JournalFeed Podcast for the week of June 22-26, 2020. We cover vitamin K for INR >10, DOSE VF dual sequential defibrillation pilot RCT, aortic dissection risk score, NTG for food impaction, and the ACR/NKF statement on IV contrast nephropathy.

Cast:Joel TopfSwapnil HiremathSamira FaroukJennie LinMatt SparksAnd special guest Joshua WaitzMartin Pollak: http://www.nasonline.org/member-directory/members/20033579.htmlJosh Waitz @jwaitz100 Days of COVID-19: https://www.voanews.com/episode/100-days-covid-19-4236811MinTac: http://www.nephjc.com/news/mintacMy magical experience with minimal change disease. This is not the actual tweet, but a dramatization: http://pbfluids.com/2020/04/the-magic-of-treating-minimal-change-disease/Non-inferiority, NephJC: http://www.nephjc.com/news/2019/7/8/understanding-the-vortex-of-non-inferiority-trialsNon-inferiority, through the looking glass: https://pubmed.ncbi.nlm.nih.gov/21539749/Kevin Fowler on Tacrolimus side effects: https://twitter.com/gratefull080504/status/1247697780736512000?s=20Mt Sinai is converting some transplant patients from tacrolimus to belatecept: https://www.nejm.org/doi/full/10.1056/nejmoa1506027CAPSULOLOGY: Open the “Images” tab https://www.webmd.com/drugs/2/drug-10097-6108/tacrolimus-oral/tacrolimus-oral/detailsTacrolimus for your cat and dog dry eye needs: https://vcahospitals.com/know-your-pet/tacrolimus-ophthalmic-in-dogsWHO, NSAIDs, and double negatives: https://twitter.com/kidney_boy/status/1240452941187821570?s=20CJASN stands for the Clinical Journal of the American Society of Nephrology. The C does not stand for Canada. Sorry Swap.Conversion calculator from old world (SI) units, mg/mole Cr, to freedom units (gram protein / gram creatinine): http://www.scymed.com/en/smnxps/psdjf223.htmMichelle Rheault about starting the clock to relapse tweet: https://twitter.com/rheault_m/status/1247703322200596483?s=20Marvin Gonzalez calls for larger studies: https://twitter.com/MarvinGonzlez16/status/1247701186972733442?s=20Acute PD for COVID-19 is discussed in this article from CJASN: https://cjasn.asnjournals.org/content/early/2020/04/03/CJN.03750320PD for AKI, the experience from Brazil https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3525422/The lead author, Daniela Ponce is really the world authority on PD and AKI: https://www.ncbi.nlm.nih.gov/pubmed/?term=Ponce%20D%5BAuthor%5D&cauthor=true&cauthor_uid=22641732Nursing home outbreaks in Durham: https://www.newsobserver.com/news/coronavirus/article241975401.htmlPrison outbreak: https://www.npr.org/2020/04/06/827922287/inmates-staff-on-edge-as-covid-19-spreads-through-federal-prisonsOttawa COVID-19: https://ottawacitizen.com/news/local-news/covid-19-long-term-care-outbreaks-continue-devastating-spread-across-ontario/West Coast herd immunity: https://www.ksbw.com/article/new-study-investigates-californias-possible-herd-immunity-to-covid-19/32073873#The History of HIV associated Nephropathy: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3494840/Racial breakdown of NYC coronavirus deaths reveals ‘disparities,’ de Blasio says https://nypost.com/2020/04/08/de-blasio-releases-racial-breakdown-data-of-coronavirus-deaths/Michelle Rheault is tired: https://twitter.com/rheault_m/status/1248371721356402689?s=20KidneyCon Lite! Saturday April 18 from 9-11. Kidney Pathology workshop.Lunch Doodles with Mo Willems: https://youtu.be/7KBkUyE6MOwDr Glaucomflecken and Telehealth: https://twitter.com/DGlaucomflecken/status/1247709538322657282?s=20NephSim for kindergartner’s https://nephsim.comNephSim live: https://twitter.com/Neph_SIM/status/1247637727048327170?s=20

Talk to a Dr. Berg Keto Consultant today and get the help you need on your journey (free consultation). Call 1-540-299-1557 with your questions about Keto, Intermittent Fasting or the use of Dr. Berg products. Consultants are available Monday through Friday from 8:30 am to 9 pm EST. Saturday & Sunday 9 am to 5 pm EST. USA Only. Join my FREE 30-Day Low-Carb, No-Cheat Challenge Here! http://bit.ly/30-DayKetoChallenge Take the Free Keto Mini-Course: https://bit.ly/2Cpb03l Download Keto Essentials https://m.me/drericberg?ref=w2128577 Take Dr. Berg's Advanced Evaluation Quiz: http://bit.ly/EvalQuiz Your report will then be sent via email analyzing 104 potential symptoms giving you a much deeper insight into your body issues. It's free and very enlightening. DATA: https://bit.ly/33MOyOB Fasting insulin is between 3–8 uIU/mL (18–48 pmol/L) https://bit.ly/33JLQcR https://bit.ly/2JdhuGn https://bit.ly/3bqVqE9 https://bit.ly/2WLZOJJ In this podcast, we're going to talk about type 2 diabetes. Type 2 diabetes is more a disease of insulin than glucose. When you're diagnosed with type 2 diabetes, they usually use a blood test to measure how much glucose is in your blood. But, the problem is that serious issues occur before you get high blood sugar. This is because these serious issues occur with high insulin. Issues that occur with high levels of insulin: • Retinopathy - retina • Neuropathy - nerves • Nephropathy - kidney • Hypertension • Memory loss • Visceral fat Dr. Eric Berg DC Bio: Dr. Berg, 51 years of age is a chiropractor who specializes in weight loss through nutritional & natural methods. His private practice is located in Alexandria, Virginia. His clients include senior officials in the U.S. government & the Justice Department, ambassadors, medical doctors, high-level executives of prominent corporations, scientists, engineers, professors, and other clients from all walks of life. He is the author of The 7 Principles of Fat Burning. FACEBOOK: fb.me/DrEricBerg?utm_source=Podcast TWITTER: http://twitter.com/DrBergDC?utm_source=Podcast YOUTUBE: http://www.youtube.com/user/drericberg123?utm_source=Podcast DR. BERG'S SHOP: https://shop.drberg.com/?utm_source=Podcast MESSENGER: https://www.messenger.com/t/drericberg?utm_source=Podcast DR. BERG'S VIDEO BLOG: https://www.drberg.com/blog?utm_source=Podcast

It’s Around Ocean County with Lisa Anderson and guest Bonnie Scneider.  Bonnie and her husband Ed founded the IGA Nephropathy Foundation of America.   In 2004, their son was diagnosed with IGA Nephropathy. This is a disease which causes kidney failure, when an antibody called immunoglobulin A (IgA) builds up in your kidneys. The result is a local inflammation that can over hamper your kidneys' ability to filter waste from your blood. IgA Nephropathy usually progresses slowly over years, but the course of the disease varies from person to person.

We’re back with guest Bonnie Scneider.  Bonnie along with her husband founded the IGA Nephropathy Foundation of America.   Did you know some people leak blood in their urine without developing problems?  Some eventually achieve complete remission and others develop end stage kidney failure.   No cure exists, but certain medications can slow its course. Keeping your blood pressure under control and reducing your cholesterol levels also slows the disease.   For more information, visit igan.org. 

Check out the second episode in unzipping the confusion of imaging studies where we explore contrast. How contrast works, the types of contrast, when to use contrast and when not to are just some of the topics discussed in this episode. We also tackle contrast allergies and contrast nephropathy with a bonus on incidental findings.  Imaging PDF: https://www.medmechanix.com/wp-content/uploads/2020/02/imagingdoc1.pdf Our Website: https://www.MedMechanix.com

Diagnosed with IgA nephropathy at a young age of 19. Scott Hobbs was determined to fight. Having had a transplant from his brother on September 2019, here's a story of a kidney fighter who went 12 rounds and is now sharing his story to stay positive and keep fighting. --- This episode is sponsored by · Anchor: The easiest way to make a podcast. https://anchor.fm/app

Are you struggling with pain in your foot? Do you need a healing touch from God? Then this episode is for you! Listen to this testimony by Pastor Linda Budd of RiverGate Church in Tulsa Oklahoma. 

In this episode I cover diabetic nephropathy.If you want to follow along with written notes on diabetic nephropathy go to https://zerotofinals.com/medicine/renal/diabeticnephropathy/ or the renal section in the Zero to Finals medicine book.This episode covers the definition, diagnosis and management of diabetic nephropathy.The audio in the episode was expertly edited by Harry Watchman.

This is a podcast article summary of "IgA Nephropathy in Elderly Patients" by Angel M. Sevillano and Manuel Praga on behalf of themselves and their coauthors.

This is a podcast article summary of "IgA Nephropathy in Elderly Patients" by Angel M. Sevillano and Manuel Praga on behalf of themselves and their coauthors.

Andrew Frankel, Consultant Physician and Nephrologist at Imperial College Healthcare NHS Trust, tells medwireNews about the rationale and key findings of the CREDENCE trial, and discusses the potential benefits of SGLT2 inhibitors beyond type 2 diabetes. Find more on Medicine Matters diabetes This content was originally published on Medicine Matters diabetes (https://diabetes.medicinematters.com) on April 17, 2019.

Joel TopfJennie LinMatt SparksSwapnil HiremathShow Notes: IgA Nephropathy ScoreLevi Strauss: https://www.biography.com/fashion-designer/levi-straussLevey MDRD study: https://www.ncbi.nlm.nih.gov/pubmed/10075613ADPKD Total Kidney Volume: https://www.nejm.org/doi/10.1056/NEJMoa054341Halt PKD: https://www.nejm.org/doi/full/10.1056/nejmoa1402685Tempo 3:4 Trial: https://www.nejm.org/doi/full/10.1056/NEJMoa1205511Description description of IgA nephropathy by Berger and Hiunglais: https://www.ncbi.nlm.nih.gov/pubmed/4180586The reprint in JASN in 2000 with commentary as part of the Milestones in Nephrology series: https://jasn.asnjournals.org/content/jnephrol/11/10/1957.full.pdf JASN supplies an English translation from the original French.Nice reference from JASN backing up Matt’s assertion that preeclampsia and not IgA nephropathy is the most common glomerular disease in the world: https://jasn.asnjournals.org/content/18/8/2281Description of the Singapore Army screening recruits from the Oxford Textbook of Clinical Nephrology: https://books.google.com/books?id=fVItBQAAQBAJ&lpg=PA485&ots=JRoOnUnleT&dq=singapore%20kidney%20biopsy%20army&pg=PA485#v=onepage&q&f=falseDescription of the Japanese glomerulonephritis screening program: https://cjasn.asnjournals.org/content/2/6/1360Swapnil’s studies on autopsy studies:Finland: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC501386/Japan: https://www.ncbi.nlm.nih.gov/pubmed/12753320/Nephrology Secrets, either one of the best or the best nephrology textbooks ever: https://www.amazon.com/Nephrology-Secrets-Book-Edgar-Lerma-ebook/dp/B079TSYNQW/ref=sr_1_1TESTING Trial on NephJC: http://www.nephjc.com/news/2017/8/28/testingStop-Iga Trial on NephJC: http://www.nephjc.com/iga-nephropathyTesting Trial two: Therapeutic Evaluation of Steroids in IgA Nephropathy Global Study Low Dose Study: https://clinicaltrials.gov/ct2/show/NCT01560052MEST Score versus MEST-C in NephJC: http://www.nephjc.com/news/2016/10/16/do-crescents-matter-for-iga-nephropathyNice discussion of the statistical tests during the Tweet Chat by people who know their stats (I.e. not Joel): https://twitter.com/NephJC/status/1133546750814367746Tweet-length description of IDI: https://twitter.com/kiwiskiNZ/status/1133595698929098752Assessing the performance of prediction models: a framework for traditional and novel measures. https://www.ncbi.nlm.nih.gov/pubmed/20010215/Net Reclassification Indices for Evaluating Risk-Prediction Instruments: A Critical Review https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3918180/Predicting Progression in CKD: Perspectives and Precautions https://www.ajkd.org/article/S0272-6386(15)01413-4/abstractThe Article by Nancy Cook in Circulation that Jennie was talking about: Use and misuse of the receiver operating characteristic curve in risk prediction. https://www.ncbi.nlm.nih.gov/pubmed/17309939Discovery of new risk loci for IgA nephropathy implicates genes involved in immunity against intestinal pathogens https://www.nature.com/articles/ng.3118Genome-wide polygenic risk predictors for kidney disease https://www.nature.com/articles/s41581-018-0067-6Where does Matt find minutia like the grams of IgA produced a day? Here: https://www.annualreviews.org/doi/abs/10.1146/annurev-pathol-011110-130216Animal models of IgA nephropathy: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4337240/Matt’s Book Originals: https://www.amazon.com/gp/product/014312885X/ref=dbs_a_def_rwt_bibl_vppi_i1Eric Neilson, Dean of Northwestern University https://www.feinberg.northwestern.edu/faculty-profiles/az/profile.html?xid=23239Brussels sprout Insta-famous dog and future dean of the medical school: https://www.instagram.com/brussels.sprout/?hl=enJosh Farkas Rantorial about Contrast Nephropathy: https://twitter.com/PulmCrit/status/1134922050794139648Swapnil’s Tweetorial about Contrast Nephropathy: https://twitter.com/hswapnil/status/1133906398096609280Tukaram’s pic of NEJM’s progression from Contrast Induced Nephropathy to Contrast Associated Nephropathy: https://twitter.com/tukaramj/status/1135214980985266178Zero sodium dialysate for heart failure? https://twitter.com/i/moments/1134811009217155072

Ref: Canagliflozin and Renal Outcomes in Type 2 Diabetes and Nephropathy. N Engl J Med. 2019 Apr 14.

Contrast induced nephropathy is the "white walker" of critical care and emergency medicine. Come take a listen as we discuss the potential error in creating a clinically non-meaningful entity, and how we should address this in our daily clinical work.

Lead investigator Vlado Perkovic talks about the main findings from the CREDENCE trial – demonstrating that canagliflozin is associated with a reduced risk for kidney failure and cardiovascular events in people with type 2 diabetes and chronic kidney disease – and discusses how these results will impact clinical practice. Find more on Medicine Matters diabetes This content was originally published on Medicine Matters diabetes (https://diabetes.medicinematters.com) on April 15, 2019.

Kevin Fernando, GP Partner at the North Berwick Health Centre near Edinburgh, UK, talks to medwireNews about the importance of the CREDENCE trial from a primary care perspective. Find more on Medicine Matters diabetes This content was originally published on Medicine Matters diabetes (https://diabetes.medicinematters.com) on April 17, 2019.

The TWiVidae review universal influenza vaccines that are in clinical trials, and discovery of an atypical parvovirus that causes chronic kidney disease in middle aged, immunocompromised laboratory mice. Hosts: Vincent Racaniello, Dickson Despommier, Alan Dove, Rich Condit,  Kathy Spindler, and Brianne Barker Subscribe (free): iTunes, Google Podcasts, RSS, email Become a patron of TWiV! Links for this episode PhD and postdoctoral programs at Dept of Microbiology, Icahn School of Medicine at Mount Sinai MSc program Molecular Biology and Pathology of Viruses, Univ College London Virology Comics on sale (Amazon) Outbreak at the Smithsonian NIAID strategic plan for universal influenza vaccine Fauci article on universal influenza vaccine (J Inf Dis) Severe 2017-18 flu season (CDC) Progress on universal influenza vaccine (The Scientist) Influenza vaccine is safe for those with egg allergies Atypical parvovirusdrives mouse kidney disease (Cell) Contagious Thinking: Visible Viruses AR app Letters read on TWiV 520 Timestamps by Jolene. Thanks! Weekly Science Picks 1:17:24 Brianne - Nebula Genomics: a new start-up offering free genome sequencing (with a catch) Alan- GRE scores are poor predictorof degree completion Rich- The Science Mill(video) Dickson- The 12 cranial nerves (mnemonic) Kathy- NAS report on Sexual Harassment of Women (free pdf) Iceberg figure Vincent - The Tangled Tree by David Quammen and TWiEVO #37 Listener Pick Mark- Weekly US Map: Influenza Summary Intro music is by Ronald Jenkees. Send your virology questions and comments to twiv@microbe.tv

NAC + Contrast Nephropathy (May 2007) by Oregon 1-800-222-1222

 This week Dr. Silva discusses the history of diabetes mellitus and the seminal discoveries that led to our current understanding of diabetes and kidney disease.

On this podcast we explore two very recent papers on the topic of cardiac catheterization. The first is a large study reviewing the impact of NaHC03 + /- acetylcysteine on prevention of contrast nephropathy and the second is a comparison of endocarditis rates in surgical versus transcatheter pulmonary valve replacement. Dr. Gentian Lluri, the first author of the PVR paper joins us to discuss this work from UCLA and the "take away" points. As last week, we end with a wonderful piece from an operatic legend. Please leave a review or comment in iTunes! See you next week and I hope you enjoy....

On this podcast we explore two very recent papers on the topic of cardiac catheterization. The first is a large study reviewing the impact of NaHC03 + /- acetylcysteine on prevention of contrast nephropathy and the second is a comparison of endocarditis rates in surgical versus transcatheter pulmonary valve replacement. Dr. Gentian Lluri, the first author of the PVR paper joins us to discuss this work from UCLA and the "take away" points. As last week, we end with a wonderful piece from an operatic legend. Please leave a review or comment in iTunes! See you next week and I hope you enjoy....

Editor's Summary by Howard Bauchner, MD, Editor in Chief of JAMA, the Journal of the American Medical Association, for the December 05, 2017 issue

Editor's Summary by Howard Bauchner, MD, Editor in Chief of JAMA, the Journal of the American Medical Association, for the August 01, 2017 issue

Membranous Nephropathy is a typical type of Nephrotic Syndrome. We all know diet plays an important role in the treatment of kidney disease. Well then, what is the diet for membranous nephropathy patients?

Editor's Audio Summary by Edward Livingston, MD, Deputy Editor, the Journal of the American Medical Association, for the September 1, 2015 issue

Medical Grand Rounds with Stephen Coca, DO, MS

Fri, 17 Jan 2014 12:00:00 +0100 https://edoc.ub.uni-muenchen.de/16581/ https://edoc.ub.uni-muenchen.de/16581/1/Ribeiro_Andrea.pdf Ribeiro, Andrea ddc:610,

The pathomechanisms of the progression of chronic kidney diseases involve progressive glomerulosclerosis with renal parenchymal cell loss by proapoptotic factors. Tumor necrosis factor-alpha (TNF-α) is a proapoptotic cytokine that is produced by macrophages as well as by a variety of cell types. TNF-α signaling regulates cell survival and death. Like in other inflammatory renal diseases, the increased intrarenal TNF-α expression contributes to the disease progression of Alport nephropathy, “a non-inflammatory” murine CKD model. I show that TNF-α expressed by podocytes as well as by infiltrating leukocytes progressively activates renal parenchymal cells, inducing apoptotic pathways that can trigger glomerulosclerosis in Alport disease. The blockade of TNF-α by etanercept prolonged mean survival of Col4a3-deficient mice. The beneficial effect on life span was associated with a significant improvement of the glomerulosclerosis, proteinuria, and the glomerular filtration rate (GFR). In particular, etanercept treatment significantly increased the number of glomerular podocytes (WT-1 and nephrin co-staining) and the renal mRNA expression of nephrin and podocin without affecting markers of renal inflammation. The increased number of podocytes was consistent with less TUNEL-positive podocytes that undergo apoptosis. Importantly, exogenous signals, e.g. infections or toxins, have the potential to regulate the influx of immune cells including dendritic cells, macrophages, neutrophils, and T cells. Here I report a large influx of leukocyte subsets that are mostly dendritic cells and macrophages in Col4a3-deficient mice as compared to wildtype mice. While bacterial endotoxin treatment had no effect on the renal disease progression, bacterial cytosine-guanine (CpG)-DNA exacerbated all aspects of Alport nephropathy and reduced the overall life span of Col4a3-deficient mice. This effect of CpG-DNA was associated with a significant increase of renal CD11b+/Ly6Chigh macrophages, intrarenal production of TNF-α, iNOS, IL-12, and CXCL10. CpG-DNA switched intrarenal macrophages from non-activated phenotype (M2) towards the classically activated form (M1). These M1 macrophages increased the secretion of TNF-α, which accelerated the disease progression of Alport nephropathy by inducing podocyte loss. Taken together, I demonstrated that TNF-α is a crucial cytokine which induces podocyte loss in the natural course of the progression of Alport nephropathy. Moreover, the expression of TNF-α is enhanced by selective exogenous factors, e.g. TLR9 activation, which alter the phenotype of renal macrophages towards the M1 phenotype. TNF-α blockade might therefore represent a novel therapeutical option to delay the progression of Alport nephropathy and potentially of other forms of glomerulosclerosis in non-inflammatory and inflammatory conditions.

Celia Bradford gives a brief and superb summary of contrast induced nephropathy. The Prezi presentation she refers to can be found here: http://prezi.com/t79w4fwm1i_u/renal-protection-should-i-care/ Thanks for all the following for the podcasts - please subscribe on iTunes and leave feedback!

Background: Oxalosis is a metabolic disorder characterized by deposition of oxalate crystals in various organs including the kidney. Whereas primary forms result from genetic defects in oxalate metabolism, secondary forms of oxalosis can result from excessive intestinal oxalate absorption or increased endogenous production, e.g. after intoxication with ethylene glycol. Case presentation: Here, we describe a case of acute crystal-induced renal failure associated with excessive ingestion of rhubarb in a type 1 diabetic with previously normal excretory renal function. Renal biopsy revealed mild mesangial sclerosis, but prominent tubular deposition of oxalate crystals in the kidney. Oxalate serum levels were increased. Conclusion: Acute secondary oxalate nephropathy due to excessive dietary intake of oxalate may lead to acute renal failure in patients with preexisting renal disease like mild diabetic nephropathy. Attention should be payed to special food behaviors when reasons for acute renal failure are explored.

In this episode: Intro: Intodown will be helping create a better sounding Alternefit Podcast as well as doing the music! Information and Education and Questions and Comments: Acne: There are a number of acne sufferers who could benefit from these natural and easily done remedies! Anyone can also prevent acne by some of these methods: Cut out dairy Use distilled or purified water Keep hands away from face Use clean bed linens Tea Tree Oil Calendula Willow Bark Omega-3s Anti-inflammatory diets and more! Thanks to my sister-in-law for this topic and question! Recipe Section: To go along with the recipe from last week, I thought I'd teach you how to make a mashed potato substitute out of cauliflower! Yummmmm! It's soooo good! Tidbits: Dr. Charles V. Mobbs of Mt. Sinai School of Medicine finds that diabetic nephropathy might be reversed by a ketogenic diet. Learn more about this exciting development! Also, articles have surfaced about how certain nutrition can assist with relief of bi-polar! Closing: Intodown will be helping soon! Here are the links for this show: Bi-polar article: http://www.medicalnewstoday.com/articles/224447.php Dr. Charles V. Mobbs' Research into Diabetic Nephropathy and the Ketogenic Diet: http://www.plosone.org/article/info:doi/10.1371/journal.pone.0018604 Acne information: http://www.marksdailyapple.com/primal-advice-for-acne-sufferers/ and Primal Toad: http://www.primaltoad.com/ Bruce Fife on Underground Wellness about Coconut: http://www.blogtalkradio.com/undergroundwellness/2011/04/29/the-coconut-oil-miracle-with-bruce-fife What is Nephropathy: http://www.medterms.com/script/main/art.asp?articlekey=7225 Jimmy Moore's Livin' La Vida Low Carb: http://livinlavidalowcarb.com/ Thanks and Have a Healthy Day!

Summary and hypothesis Role of pro-inflammatory chemokines in diabetic nephropathy Beyond hemodynamic and metabolic abnormalities associated with diabetes, the role of inflammation in development and progression of diabetic nephropathy is well accepted. Recruitment and activation of macrophages in different renal compartment is considered to be hallmark of all inflammation in diabetic nephropathy. Although recruitment of macrophages to the renal compartment has been extensively studied, the exact mechanisms involved are still to be explored. The chemokine-chemokine receptor interactions are implicated to be mainly responsible for trafficking and infiltration of different monocytes and macrophages. Contribution of macrophages to the development of DN can be addressed in either by inhibiting chemokines or chemokine receptor associated with diabetes. We hypothesized that inhibition of CCL2 may inhibit macrophages infiltrating into different compartments in kidney and inhibition started at earlier stage of disease progression may show more beneficial effects than CCL2 blockade at late stage of DN. To address the involvement of additional chemokine receptors we hypothesized that blocking CCR5 and CCR2 simultaneously might have some additive or synergistic effects. Role of homeostatic chemokines in diabetic nephropathy Homeostatic chemokies are mainly involved in hematopoeisis, immune cell survival and adaptive immune responses. CXCL12 attracted our attention as it is being extensively studied and reported to be responsible for different functions like stem cell survival and homing and trafficking to different compartments. The role of CXCL12 in diabetic nephropathy has not been explored yet. CXCL12 is constitutively expressed by different renal cells. It may contribute to tissue repair and inhibit disease progression by stem cell recruitment or may cause increased tissue fibrosis and aggravate the disease. We hypothesized that CXCL12 plays role in development and progression of diabetic nephropathy. In order to address this question we used CXCL12 blocker in a mouse model of diabetic nephropathy.

Fri, 8 Feb 2008 12:00:00 +0100 https://edoc.ub.uni-muenchen.de/9058/ https://edoc.ub.uni-muenchen.de/9058/1/Block_Carolin.pdf Block, Carolin

Fri, 8 Feb 2008 12:00:00 +0100 https://edoc.ub.uni-muenchen.de/9057/ https://edoc.ub.uni-muenchen.de/9057/1/Blutke_Andreas_Falko.pdf Blutke, Andreas Falko ddc:500,

Diabetic nephropathy (DN) is a complex and chronic metabolic disease that evolves into a progressive fibrosing renal disorder. Effective transcriptomic profiling of slowly evolving disease processes such as DN can be problematic. The changes that occur are often subtle and can escape detection by conventional oligonucleotide DNA array analyses. We examined microdissected human renal tissue with or without DN using Affymetrix oligonucleotide microarrays (HG-U133A) by standard Robust Multi-array Analysis (RMA). Subsequent gene ontology analysis by Database for Annotation, Visualization and Integrated Discovery (DAVID) showed limited detection of biological processes previously identified as central mechanisms in the development of DN (e.g. inflammation and angiogenesis). This apparent lack of sensitivity may be associated with the gene-oriented averaging of oligonucleotide probe signals, as this includes signals from cross-hybridizing probes and gene annotation that is based on out of date genomic data. We then examined the same CEL file data using a different methodology to determine how well it could correlate transcriptomic data with observed biology. ChipInspector (CI) is based on single probe analysis and de novo gene annotation that bypasses probe set definitions. Both methods, RMA and CI, used at default settings yielded comparable numbers of differentially regulated genes. However, when verified by RT-PCR, the single probe based analysis demonstrated reduced background noise with enhanced sensitivity and fewer false positives. Using a single probe based analysis approach with de novo gene annotation allowed an improved representation of the biological processes linked to the development and progression of DN. The improved analysis was exemplified by the detection of Wnt signaling pathway activation in DN, a process not previously reported to be involved in this disease.

Background/Aim: Phenotype-driven screening of a great pool of randomly mutant mice and subsequent selection of animals showing symptoms equivalent to human kidney diseases may result in the generation of novel suitable models for the study of the pathomechanisms and the identification of genes involved in kidney dysfunction. Methods: We carried out a large-scale analysis of ethylnitrosourea (ENU)-induced mouse mutants for albuminuria by using qualitative SDS-polyacrylamide gel electrophoresis. Results: The primary albuminuria screen preceded the comprehensive phenotypic mutation analysis in a part of the mice of the Munich ENU project to avoid loss of mutant animals as a consequence of prolonged suffering from severe nephropathy. The primary screen detected six confirmed phenotypic variants in 2,011 G1 animals screened for dominant mutations and no variant in 48 G3 pedigrees screened for recessive mutations. Further breeding experiments resulted in two lines showing a low phenotypic penetrance of albuminuria. The secondary albuminuria screen was carried out in mutant lines which were established in the Munich ENU project without preceding primary albuminuria analysis. Two lines showing increased plasma urea levels were chosen to clarify if severe kidney lesions are involved in the abnormal phenotype. This analysis revealed severe albuminuria in mice which are affected by a recessive mutation leading to increased plasma urea and cholesterol levels. Conclusion: Thus, the phenotypic selection of ENU-induced mutants according to the parameter proteinuria in principle demonstrates the feasibility to identify nephropathy phenotypes in ENU-mutagenized mice. Copyright (C) 2005 S. Karger AG, Basel.

N-acetylcysteine (NAC) has been suggested to prevent radiocontrast-induced nephropathy (RCIN) in patients with a reduced renal function. However, clinical studies have not been demonstrating this effect consistently. Also, reviews and meta-analyses dealing with the question of prevention of RCIN by NAC have been controversial. Nearly all investigators used serum creatinine as surrogate end point of their trials, and changes in serum creatinine concentrations are thought to reflect the extent of renal injury as primary outcome. In a recent study, an effect of NAC on creatinine values and estimated glomerular filtration rate without any effect on cystatin C levels has been shown in volunteers with a normal renal function. Therefore, before renal protective effects of NAC in RCIN are proposed, any direct effects of NAC on creatinine, urea, and estimated glomerular filtration rate should be addressed. In future trials, the glomerular filtration rate should preferentially be measured directly, or at least additional markers of the renal function ( e. g., serum cystatin C) have to be assessed. Furthermore, additional `hard' end points, i.e., hospital morbidity, mortality, or dialysis dependency, should be considered in the design of future studies of RCIN. Copyright (C) 2004 S. Karger AG, Basel.