Podcasts about Alport

What does feeling truly seen and supported mean in your health care? For many LGBTQIA+ people with kidney disease, the answer isn't simple. Jess Walters is a mixed-media artist, Board Certified Patient Advocate, and independent scholar living with a kidney transplant. Marissa is the Patient Programs Director at the National Kidney Foundation (NKF) and a social worker working to make kidney care more inclusive. Together, they share what supportive care and community look like and why they matter. In today's episode we heard from: Jess Walters (they/them) is a mixed-media artist, Board Certified Patient Advocate (BCPA), and independent scholar from Charlottesville, Virginia. They are a multiply-neurodivergent, queer, nonbinary person with Alport syndrome, a rare genetic disorder which caused late-onset deafness and kidney failure at age 29. In 2018, after undergoing two months of peritoneal dialysis, Walters received a kidney transplant from a living donor at the University of Virginia, where they currently serve as an inaugural FusionLab Arts Research Fellow at the Center for Health Humanities and Ethics in the School of Medicine. Their research focuses on the intersections of art and health, navigating accommodations in cultural arts spaces to promote individual and community wellbeing by including disabled, neurodivergent, and chronically ill participation and perspectives. They regularly participate in Kidney Patient Summits with the National Kidney Foundation and have served as a member of their Diversity & Health Equity Advisory Committee for 4 years. Marissa Argentina, LMSW is a licensed social worker who has been in the field of nephrology since 2010. She has worked for the National Kidney Foundation since 2015 and has been working on the NKF Peers program 2017. She is currently the Patient Programs Director at the National Kidney Foundation. She had previously worked as a dialysis center social worker in the Bronx, NY.   Additional Resources: The Impact of Unequal Care for LGBTQ+ Kidney Patients NKF Online Community: LGBTQIA NKF Peers Jess Walters Art Rivanna Area Queer Center New City Arts Initiative   Do you have comments, questions, or suggestions? Email us at NKFpodcast@kidney.org. Also, make sure to rate and review us wherever you listen to podcasts.  

O que você faria por um amigo? Neste episódio do Podcast da Semana, Gama traz a história de uma amizade extraordinária, um amigo que deu a possibilidade da vida ao outro. O ator Thiago Amaral doou um rim para o dramaturgo e músico Vinicius Calderoni.Calderoni havia sido diagnosticado com uma doença genética que afeta os rins, a síndrome de Alport, que evoluiu para a necessidade de um transplante. Enquanto estava na fila da doação, a doença avançava rápido e dois amigos se dispuseram a doar. Um deles era Amaral, que foi confirmado como doador após todos os testes. O transplante ocorreu há três meses e foi bem sucedido.Ao Podcast da Semana, eles contam os detalhes dessa história e dizem como passaram a ver as amizades depois desse evento. Antes amigos, os dois, que são filhos únicos, agora se consideram irmãos.“A noção da amizade como um cultivo deixou de ser uma frase feita e virou uma coisa muito urgente e presente para mim desde então. Olho cada mensagem recebida, cada conversa, cada encontro com o tamanho que isso tem”, afirma Calderoni.“Os nossos grupos de amizade se juntaram e teve um momento em que cresceram para além da gente — virou uma coisa coletiva, uma sensação muito fortificante”, afirma Amaral.Agora, o ator e o dramaturgo trabalham juntos em um projeto que conta a história da doação no teatro. Os dois dizem que se tornaram ativistas pela doação de órgãos. “Doar é uma maneira de viver feliz num mundo em desencanto. É uma coisa meio contraintuitiva, porque as pessoas acham que o mundo está em dívida com elas. Ao doar, parece que você está subtraindo uma coisa de você, mas você está se preenchendo”, diz Calderoni.Roteiro e apresentação: Isabelle Moreira Lima

We explore Alport syndrome, a genetic kidney disease that goes beyond the kidneys. From the role of  genetics test, involved in making diagnosis, to the clinical features, and management, we cover it all. 

Send us a textWe're BACK with our very special Midwinter Monday series! We love having the opportunity to reflect on all the wonderful conversations we get to have with friends at the Chicago Midwinter Meeting each year. Clinician's Choice believes in teaching better dentistry. They develop products & solutions that can assist clinicians in reducing treatment times, improve efficiency, and - most importantly - better clinical outcomes for patients. Join us as he walks us through some of the best product lines that can benefit your practice. 

It's the quarter-final stage of both the FA Trophy and the FA Vase. We turn to the ever faithful, the never inexact, master of the stats Mr Phil Annets. He wears three hats this week @FATrophyFacts @FAVaseFactffile and @FACupFactfile inspiring us all with records, patterns, and with connections that would leave Victoria Coren Mitchell swooning if Non League was ever a category on Only Connect. Our managerial insight this week comes from the manager of Midland Premier side Whitchurch Alport. Not only does he know the quirky history of his wonderful club, but Adam Shillcock is also at the heart of the revolution that will see a second FA Vase quarter-final within a handful of years and is bringing the town and the community together across the ages. Matt Badcock is our man from the Non League Paper this week. He has his own Trophy and Vase insights, ground grading foresight and managerial movement background knowledge that he brings to the table along with another packed Non League Paper this weekend.

On this ASN Kidney Translation episode, Dr. Matthew Sparks hosts discussions on nephrology research in genetics. Topics include genetic testing in CKD, ADTKD screening, and digenic Alport syndrome insights.

The Friends of NPACE podcast is back for Season 2! In this episode we are joined by Alport Syndrome Foundation's Patient Engagement Coordinator, Maddison Martin! Maddie is 25 years old and received a kidney transplant from a living donor when she was 19.  In volunteering for, and now working with ASF, she has also come to know the stories and experiences of many other Alport syndrome patients.  She is also a nurse, having worked on the same transplant floor where she received her own kidney transplant. Listen to her amazing story and how ASF is able to assist other Alport syndrome patients. Tune in every other Wednesday for new episodes of the Friends of NPACE Podcast on your favorite streaming platform (Spotify, Apple Music, YouTube, and Amazon Music).

In this first episode, I sit down with Nic Wetton, the Headteacher at Malpas Alport Primary School in Cheshire. With over six years of experience using myHappymind in multiple schools, Nic is one of our longest-standing myHappymind Headteachers and a truly inspiring leader. Having worked in both inner-city and rural schools, Nic has witnessed the significant impact myHappymind has had on her school communities in both settings.

Listen as Dr. London Smith (.com) and his producer Cameron discuss Hereditary Nephritis (Alport Syndrome) with Tony the Wonder Llama (Hunter Altman). Not so boring! https://www.patreon.com/join/jockdocpodcast Hosts: London Smith, Cameron Clark. Guest: Hunter Altman. Produced by: Dylan Walker Created by: London Smith

Dylan lives in Tennessee. He's a magazine editor. He has a wife. He has a young daughter. And he has Alport syndrome, a hereditary kidney disease. In this episode of Lifespan, Dylan describes his years on kidney dialysis, how a kidney transplant recently transformed his life, and the uniqueness of being part of an extended family with so many members affected by an inherited illness.

*SOLIDARITY EPISODE* This month in partnership with ⁠Alport Syndrome Foundation⁠! Our Carrier Connections program features a different X-linked condition each month with the goal to increase awareness of X-linked conditions and how they impact the lives of women and girls. Some of these X-linked conditions are part of a larger disease umbrella with other types of inheritance patterns. This month, we are featuring Alport syndrome. Alport syndrome is an inherited disorder caused by mutations, or changes, in the genes COL4A3, COL4A4, and COL4A5 that inhibit their ability to produce a protein called collagen IV. There are four main types of Alport syndrome characterized by their mode of inheritance; the X-linked version of this syndrome, X-linked Alport syndrome (XLAS), is the most commonly reported and brought on specifically by a defective COL4A5 gene. Other inheritance forms include autosomal recessive, autosomal dominant, and digenic. Alport syndrome is most frequently associated with symptoms of progressive kidney disease as well as bilateral sensorineural hearing loss and eye abnormalities. Today, we are bringing on Rachel. Rachel is a 24 year old with X-linked Alport syndrome who lives in Boston and is an aspiring genetic counselor. She is passionate about raising awareness for the carrier community and advocating for women's healthcare rights. She loves to play soccer, ski, and read. Carrier Connections is sponsored by Kyowa Kirin, Amgen, and Sanofi. For more information about our organization, check out ⁠⁠⁠⁠⁠⁠⁠rememberthegirls.org⁠⁠⁠⁠⁠⁠⁠.

This month in partnership with ⁠Alport Syndrome Foundation⁠! Our Carrier Connections program features a different X-linked condition each month with the goal to increase awareness of X-linked conditions and how they impact the lives of women and girls. Some of these X-linked conditions are part of a larger disease umbrella with other types of inheritance patterns. This month, we are featuring Alport syndrome. Alport syndrome is an inherited disorder caused by mutations, or changes, in the genes COL4A3, COL4A4, and COL4A5 that inhibit their ability to produce a protein called collagen IV. There are four main types of Alport syndrome characterized by their mode of inheritance; the X-linked version of this syndrome, X-linked Alport syndrome (XLAS), is the most commonly reported and brought on specifically by a defective COL4A5 gene. Other inheritance forms include autosomal recessive, autosomal dominant, and digenic. Alport syndrome is most frequently associated with symptoms of progressive kidney disease as well as bilateral sensorineural hearing loss and eye abnormalities. Today, we are bringing on Jennie Feiger. Although she has no accent to reveal her origins, Jennie grew up in Brooklyn, New York.  She attended Wesleyan University for her undergraduate degree, and then earned two masters degrees from the University of California at Berkeley, in Biochemistry and Genetic Counseling. She has worked in genetic research, genetic counseling, and teaching at the college and graduate level.   As a genetic counselor, she focused on adult onset conditions, including cancer and dementia.  She has presented her findings at national meetings, as well as founded support groups for families impacted by adult-onset conditions and is active in training graduate students in genetic counseling.   As a physician assistant program, she has worked in internal medicine, geriatrics and gastroenterology, and now nephrology.  Jennie enjoys getting to know her patients deeply and takes pride in providing comprehensive care, including genetic counseling.  She lives in Boulder with her husband and is recently an “empty nester” with her two young sons in college.  She loves to garden, cycle and cross country ski. Carrier Connections is sponsored by Kyowa Kirin, Amgen, and Sanofi. For more information about our organization, check out ⁠⁠⁠⁠⁠⁠⁠rememberthegirls.org⁠⁠⁠⁠⁠⁠⁠. Novel therapies for Alport syndrome: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9081811/

*SOLIDARITY EPISODE* This month in partnership with Alport Syndrome Foundation! Our Carrier Connections program features a different X-linked condition each month with the goal to increase awareness of X-linked conditions and how they impact the lives of women and girls. Some of these X-linked conditions are part of a larger disease umbrella with other types of inheritance patterns. This month, we are featuring Alport syndrome. Alport syndrome is an inherited disorder caused by mutations, or changes, in the genes COL4A3, COL4A4, and COL4A5 that inhibit their ability to produce a protein called collagen IV. There are four main types of Alport syndrome characterized by their mode of inheritance; the X-linked version of this syndrome, X-linked Alport syndrome (XLAS), is the most commonly reported and brought on specifically by a defective COL4A5 gene. Other inheritance forms include autosomal recessive, autosomal dominant, and digenic. Alport syndrome is most frequently associated with symptoms of progressive kidney disease as well as bilateral sensorineural hearing loss and eye abnormalities. Today, we are bringing on December West. December has been married to Tarik West for 19 years. They have five children Alexis, Obed, Xyia, Nhalani, and Othniel. They reside in Akron, Ohio. Nhalani, who is 12-year-old now, was diagnosed with autosomal recessive Alport syndrome at the age of 6. Nhalani was misdiagnosed several times. Several years later, after a failed hearing screening and diagnosed with bilateral sensorineural hearing loss, Nhalani was referred to a geneticist who properly diagnosed her with autosomal recessive Alport syndrome. Carrier Connections is sponsored by Kyowa Kirin, Amgen, and Sanofi. For more information about our organization, check out ⁠⁠⁠⁠⁠⁠rememberthegirls.org⁠⁠⁠⁠⁠⁠.

A small patch of land and the buildings located on it contain radiological contamination, posing a cancer risk for workers on the site and nearby neighbors. Work is ongoing to get rid of the threat — but it hasn't been easy to get there. Samantha Maldonado, senior reporter at THE CITY,  and independent journalist Jordan Gass-Pooré dig in on episode three of Hazard NYC, a four-part FAQ NYC Presents limited series exploring the city's Superfund sites.

Thank you for joining us for our 2nd Cabral HouseCall of the weekend! I'm looking forward to sharing with you some of our community's questions that have come in over the past few weeks…   Julia: Hi Dr Cabral, I looked into past podcast episodes and couldn't find the information I was looking for. What is your opinion on IV iron infusions using Ferric carboxymaltose? My iron and ferritin levels have been low for years and my doctor recommended it to me. Thank you   Lara: Hi, dr. Cabral :) I hope you and your family are doing well.. My question is about seasoning the cast iron pan.. we found lots of videos on HOW to do it (they differ but all in all I guess you need to bake the oil into it many times in the oven) but which oil to use? Some say flaxseed, because of its polymerisation properties, others say of course not flax because it becomes toxic when heated.. some say olive oil, others are strongly against it.. so we need your help! ;) You are our favourite source of information! How would you do it? And please don't say lard, because I'm plant-based.. If you could explain the whole procedure that you think is best, that would be a bonus :) Thank you so much, and a great day to everyone !   Anonymous: Hello I have a question about EMFs in the bedroom… We live in a house with different flats… the main wifi router in in the staircase, underneath our bedroom and it's for all tenants… we also have a built in fridge on the other side of the bedroom wall… how can we protect our bedroom from these EMFs? Also, there's a cupboard for food storage touching the fridge from the side… is that also bad for the food that's inside that cupboard? Thank you   Kelsi: hi dr. cabral, thanks for all you do! i get colonics monthly and just wanted to get your opinion on the frequency. is that okay/safe to do?   Autumn: Hi, Dr. Cabral. I hope you can help. Is time restricted feeding beneficial in slowing progression of chronic kidney disease? I & two of my 3 children have just recently tested positive for the non-sex linked Alport syndrome. I already practice the IF 16:8 protocol, but wonder if a weekly 24-hour fast might be beneficial. I've listened to your podcasts on kidney health. Good stuff! My most recent labs (UA and blood) have come back clean for the first time since I was 12. (no protein, blood, leukocytes). For the last 2 years I've been practicing whole food nutrition, intermittent fasting, 3 days of strength training & 2 days of HIIT. My body's responding well. I'm curious how IF factors in. *FYI 137 pound female. 5' 7". Macro intake @ 2200 cal/day with a 45/25/30 (carbs/protein/fat) split   Thank you for tuning into this weekend's Cabral HouseCalls and be sure to check back tomorrow for our Mindset & Motivation Monday show to get your week started off right! - - - Show Notes and Resources: StephenCabral.com/2858 - - - Get a FREE Copy of Dr. Cabral's Book: The Rain Barrel Effect - - - Join the Community & Get Your Questions Answered: CabralSupportGroup.com - - - Dr. Cabral's Most Popular At-Home Lab Tests: > Complete Minerals & Metals Test (Test for mineral imbalances & heavy metal toxicity) - - - > Complete Candida, Metabolic & Vitamins Test (Test for 75 biomarkers including yeast & bacterial gut overgrowth, as well as vitamin levels) - - - > Complete Stress, Mood & Metabolism Test (Discover your complete thyroid, adrenal, hormone, vitamin D & insulin levels) - - - > Complete Food Sensitivity Test (Find out your hidden food sensitivities) - - - > Complete Omega-3 & Inflammation Test (Discover your levels of inflammation related to your omega-6 to omega-3 levels) - - - Get Your Question Answered On An Upcoming HouseCall: StephenCabral.com/askcabral - - - Would You Take 30 Seconds To Rate & Review The Cabral Concept? The best way to help me spread our mission of true natural health is to pass on the good word, and I read and appreciate every review!  

The Lexington couple put up poster ads on MBTA trains and buses to try and find someone willing to donate a kidney. Deborah Savuto has Alport's Syndrome, a rare genetic disease that caused her to lose liver function. WBZ's Shari Small reports:

Steve Glover, Co-founder and CEO of ZyVersa Therapeutics, focuses on rare kidney diseases and diseases with an inflammation component. Inflammasomes, the first response in the innate immune system, create an inflammation cascade.  The ZyVersa approach targets multiple inflammasomes to address diseases caused by the malfunction of this response. Steve explains, "Inflammation drives a lot of different diseases. And as we get into this a little bit more today, it's everything from kidney disease such as rare diseases such as FSGS and Alport syndrome and diabetic kidney disease all have an inflammation component. And in addition to that, when you look at diseases like Alzheimer's or MS, or Parkinson's, they're inflammation driven as well. So there is a connection between the two disease classes." "I've been in the industry a long time, and every so often the industry finds a new interesting discovery, and inflammasomes are clearly one of those new discoveries. In fact, one of the things I talk about quite a bit is that ten years ago, there were about two or so publications that were available on inflammasomes. Now there are over 20,000 publications available on inflammasomes. And this whole concept of inflammation driving certain diseases has become an area of an immense amount of research and development of products that can inhibit the inflammation you don't want in the human body." "When inflammasomes go into overdrive and are left uninhibited, they can cause a lot of damage to organs and cells in the body. And so, for example, they drive a lot of different diseases, everything from cancers to diseases such as Parkinson's and Alzheimer's disease, and a whole host of CNS diseases, as well as non-CNS diseases, that are driven by this inflammasome activation. So it's really important to find a way to inhibit those cytokines by inhibiting the inflammasome." #ZyVersa $ZVSA #RareDisease #InflammatoryDiseases #KidneyDisease #RenalDisease #FSGS #FocalSegmentalGlomerulosclerosis #AlportSyndrome #DiabeticKidneyDisease #Inflammasomes   ZyVersa.com Download the transcript here

Steve Glover, Co-founder and CEO of ZyVersa Therapeutics, focuses on rare kidney diseases and diseases with an inflammation component. Inflammasomes, the first response in the innate immune system, create an inflammation cascade.  The ZyVersa approach targets multiple inflammasomes to address diseases caused by the malfunction of this response. Steve explains, "Inflammation drives a lot of different diseases. And as we get into this a little bit more today, it's everything from kidney disease such as rare diseases such as FSGS and Alport syndrome and diabetic kidney disease all have an inflammation component. And in addition to that, when you look at diseases like Alzheimer's or MS, or Parkinson's, they're inflammation driven as well. So there is a connection between the two disease classes." "I've been in the industry a long time, and every so often the industry finds a new interesting discovery, and inflammasomes are clearly one of those new discoveries. In fact, one of the things I talk about quite a bit is that ten years ago, there were about two or so publications that were available on inflammasomes. Now there are over 20,000 publications available on inflammasomes. And this whole concept of inflammation driving certain diseases has become an area of an immense amount of research and development of products that can inhibit the inflammation you don't want in the human body." "When inflammasomes go into overdrive and are left uninhibited, they can cause a lot of damage to organs and cells in the body. And so, for example, they drive a lot of different diseases, everything from cancers to diseases such as Parkinson's and Alzheimer's disease, and a whole host of CNS diseases, as well as non-CNS diseases, that are driven by this inflammasome activation. So it's really important to find a way to inhibit those cytokines by inhibiting the inflammasome." #ZyVersa $ZVSA #RareDisease #InflammatoryDiseases #KidneyDisease #RenalDisease #FSGS #FocalSegmentalGlomerulosclerosis #AlportSyndrome #DiabeticKidneyDisease #Inflammasomes   ZyVersa.com Listen to the podcast here

Dr. Charlotte Jones-Burton is the Senior Vice President of Product Development and Strategy at Chinook Therapeutics, which is on a mission to change the course of kidney care by discovering and developing precision therapies to maintain kidney function in people who have rare, severe chronic kidney diseases. Charlotte explains, "Our lead clinical program is atrasentan, a highly potent and selective endothelin receptor inhibitor. We believe that it's going to be a best-in-class molecule that's going to target the endothelin pathway. And the condition for which we are developing it is IgA nephropathy. Now, IgA nephropathy is an autoimmune disease that attacks the kidneys, and it affects how our blood is filtered in the small blood vessels of the kidneys that I spoke about. And what happens with IgA nephropathy is that immune complexes can deposit in the kidney and really damage those filtering units inside the kidneys. And when this happens, individuals can have symptoms such as protein spilling into their kidneys. And we know that proteinuria, as we call that, is a strong risk factor for those who will then develop end-stage kidney disease, which means that they may need dialysis or a kidney transplantation to survive." "Now, we know that there are few treatments that are available, and that's why it's really important for patients to also ask the question if there are any clinical trials. And we at Chinook Therapeutics are enrolling patients into clinical trials who have IgA nephropathy. We also are enrolling patients into our AFFINITY clinical trial if they have FSGS, which is also a type of kidney disease, Alport syndrome, or diabetic kidney disease." #ChinookTherapeutics #KidneyDisease #ChronicKidneyDisease #Atrasentan #BIO1301 #PrecisionMedicine #Nephrology #ClinicalTrials #IGAN #RareDisease chinooktx.com Download the transcript here

Dr. Charlotte Jones-Burton is the Senior Vice President of Product Development and Strategy at Chinook Therapeutics, which is on a mission to change the course of kidney care by discovering and developing precision therapies to maintain kidney function in people who have rare, severe chronic kidney diseases. Charlotte explains, "Our lead clinical program is atrasentan, a highly potent and selective endothelin receptor inhibitor. We believe that it's going to be a best-in-class molecule that's going to target the endothelin pathway. And the condition for which we are developing it is IgA nephropathy. Now, IgA nephropathy is an autoimmune disease that attacks the kidneys, and it affects how our blood is filtered in the small blood vessels of the kidneys that I spoke about. And what happens with IgA nephropathy is that immune complexes can deposit in the kidney and really damage those filtering units inside the kidneys. And when this happens, individuals can have symptoms such as protein spilling into their kidneys. And we know that proteinuria, as we call that, is a strong risk factor for those who will then develop end-stage kidney disease, which means that they may need dialysis or a kidney transplantation to survive." "Now, we know that there are few treatments that are available, and that's why it's really important for patients to also ask the question if there are any clinical trials. And we at Chinook Therapeutics are enrolling patients into clinical trials who have IgA nephropathy. We also are enrolling patients into our AFFINITY clinical trial if they have FSGS, which is also a type of kidney disease, Alport syndrome, or diabetic kidney disease." #ChinookTherapeutics #KidneyDisease #ChronicKidneyDisease #Atrasentan #BIO1301 #PrecisionMedicine #Nephrology #ClinicalTrials #IGAN #RareDisease chinooktx.com Listen to the podcast here

On episode 28, I'm joined by longtime central Oregonian Pete Alport.  An award-winning photographer, videographer and producer, Pete has called Central Oregon home since  moving in 1994 after a traumatizing childhood growing up in Portland Oregon.  Pete has, and continues to influence and  shape the growth of Central Oregon through the quality and creativity of the content he captures.  With subjects ranging  from many of the world's best outdoor athletes to some of the most remote landscapes in our backyard, Pete's work resonates strongly  with both those who call Central Oregon  home and those who appreciate the magic found in nature.   Known for an unrelenting work ethic driven by passion and fueled by life experience and the love of nature, Pete has the gift of seeing opportunity and possibility where others don't.   Yo Pete, Thanks for continuing to produce content that keeps your community hyped on getting outside. And a special thank you for your level of humility and vulnerability during our conversation. You're a significant human and a significant member of our community that we can all learn from. The Circling Podcast is proud to be associated with Nota. Since adding show notes to Nota, feedback from listeners has been extremely positive. Vista Nota at www.Nota.fm and experience how NOTA takes you beyond the episode and makes podcasts even better with visual show notes.The Circling Podcast is supported by Stillwater Traditional Paddle-board club.  Stillwater is committed to fostering the growth of inland prone paddle-boarding while paying homage to the history and culture of this ocean-born lifestyle.  Thanks for listening to The Circling Podcast. Our Theme song was written by Carl Perkins and performed by Erin Cole-Baker and Dr. Erin Zurflu. A big shout out to Pete Alport for allowing us to use his photography for the background cover art during the winter season. See more of Pete's work and learn how you can own his images the capture the magic of where we life at www.petealport.com. Have Ideas or art that you'd like to submit, please do. We love mail, so please send us comments, questions,  show ideas or art to thecirclingpodcast@gmail.com.  Follow us on Instagram @thecirclingpodcast to learn more about past, current and upcoming episodes. Please subscribe to the circling podcast on most major podcast platforms and leave us a review, it really does help. Follow Pete on Instagram for your daily dose of dopamine release @pete_alport. Also visit his website www.petealport.com and check out his work, it's insane. A special thank you to Dan Norkunas, Sage Cattabriga-Alosa, Jared Elston, James Nicol and Will Dennis, I appreciate your time you guys, this episode would not be what it is without your help. Lastly, if you know someone who you think would enjoy today's episode, please share it with them today. Thanks for your time Central Oregon. Get outside, we'll see you out there, and remember the health of our community relies on us.  https://nota.fm/thecircling

Kent speaks with Rachelle McCray about her journey with Alport Syndrome and her experience with Renasight, a Natera product that determines if there is a genetic cause for an individual's kidney disease or if there is an increased hereditary risk due to family history. Rachelle McCray—Rachelle is a television host, entrepreneur, and patient advocate for chronic kidney disease. Rachelle is the founder and creator of a registered 501(c)3 non-profit that gifts comfort teddy bear kits to children and families affected by kidney disease, the MinMinBear Foundation. She brings a personal perspective to her advocacy, as she and multiple generations of her family have lived with CKD. Rachelle credits Natera's Renasight genetic test for giving her the knowledge to make more informed decisions about her care. Her goal is for other CKD patients to have that same confidence and participation in their healthcare. Rachelle is also a paid consultant for Natera. If you have questions regarding items discussed during this episode or would like more information about Kidney Solutions weekly Support Group, contact Kent at kent.bressler@kidneysolutions.org For more information about Kidney Solutions, visit them at www.kidneysolutions.org Host: Kent Bressler Producer: Jason Nunez

Bridge City's David Alport talks Cannabis licensing (transportation, cultivation, retail), licensing in various states, where things are headed (interstate, rollups), shares Cannabis startup marketing advice, and more. Unique info you need on your radar is here, so tune in! --- Send in a voice message: https://anchor.fm/dopecfo/message

Remedios Zafra es un referente en la filosofía. Escritora, ensayista, científica titular en el Instituto de Filosofía del Consejo Superior de Investigaciones Científicas y ganadora de reconocimientos como el Premio Internacional de Ensayo Jovellanos con 'El bucle invisible' o el Premio Anagrama de Ensayo con 'El entusiasmo', el libro con el que se dio a conocer al gran público. En su conversación con Mara, la gataparda también ha contado cómo es vivir con el síndrome de Alport, la enfermedad degenerativa que le afecta a la visión y a la audición: "Es un regalo quitarme los audífonos, desconectar del mundo y conectar con mi pensamiento", explica.

Remedios Zafra es un referente en la filosofía. Escritora, ensayista, científica titular en el Instituto de Filosofía del Consejo Superior de Investigaciones Científicas y ganadora de reconocimientos como el Premio Internacional de Ensayo Jovellanos con 'El bucle invisible' o el Premio Anagrama de Ensayo con 'El entusiasmo', el libro con el que se dio a conocer al gran público. En su conversación con Mara, la gataparda también ha contado cómo es vivir con el síndrome de Alport, la enfermedad degenerativa que le afecta a la visión y a la audición: "Es un regalo quitarme los audífonos, desconectar del mundo y conectar con mi pensamiento", explica.

Interview with Megan Dunleavy, a female patient with {X-linked} Alport Syndrome and current medical school student with a special interest in genetics and nephrology.

Interview with Janine Reed, a female patient with {X-linked} Alport Syndrome.

Interview with Afton DeLucca, a female patient with {X-linked} Alport Syndrome.

Interview with Cassie Smith, a female patient with {X-linked} Alport Syndrome.

Remember The Girls collaboration with The Alport Syndrome Foundation.

In this episode of Look Beneath the Surface: An Expert Dive into Alport Syndrome, Dr George Bakris welcomes Dr Jochen Reiser for a close look at what COL4A genotyping can tell us about the course and impact of Alport syndrome for both patients and their families. Additional resources are available through the Alport Syndrome Foundation at alportsyndrome.org.

In the debut episode of Look Beneath the Surface: An Expert Dive into Alport Syndrome, Dr George Bakris is joined by Dr Joshua Zaritsky to discuss the link between inherited genetic defects and the inflammation and fibrosis that drive disease progression in Alport syndrome.

As we wrap up our Alport Awareness Series, I am so excited to welcome to the show, Grant Bonebrake & Maddie Martin, Volunteer Patient Advocate Alport Foundation.  About Grant: Grant Bonebrake is a high school senior in San Diego, CA. He was misdiagnosed with the wrong kidney disease until age 11 when he experienced hearing loss that led to proper diagnoses of Alport syndrome, a rare genetic kidney disease. His involvement with Alport Syndrome Foundation led him to become an active patient advocate. In December 2020, Grant received the national RareVoice Award (Teen Category) for Legislative Advocacy from the EveryLife Foundation for Rare Diseases. He also volunteers with the Young Adult Representatives of Rare Disease Legislative Advocates program, and National Kidney Foundation. Grant is currently working with other teens to document the experiences and insights of young people living with Alport syndrome. About Maddie: Maddison Martin just turned 22. She was originally misdiagnosed with Glomerulonephritis at age 2 before receiving a formal diagnosis of Alport syndrome, via kidney biopsy, at 4-years-old. At the age of 20, she received the Gift of Life in the form of a kidney transplant from her high school attendance secretary, Tammy. Inspired by her Alport journey, Maddison is currently a nursing student and enjoys spending free time with her family. Listen in as Maddie & Grant share their personal journeys, the physical & emotional aspects of being a teen with rare disease and how they have embraced their diagnosis.  #AlportAwareness   

Leslie Marie White shares her incredible story with battling Alport syndrome, causing her hearing loss & kidney disease. Please tune in to listen to this amazing journey! For more info on Leslie Marie White: kidney solutions: www.kidneysolutions.org https://www.facebook.com/Kidney-Solutions-A-Network-of-TransplantExperience-106225571112120/ https://instagram.com/kidneysolutions_org?r=nametag https://twitter.com/k_solutions_org?s=21 https://youtube.com/channel/UCaHrn7-RwEncyN221fJ-ffw Kent Bressler 830-285-2140 Kidney Solutions PO Box 294722 Kerrville, TX   78029 Email: info@kidneysolutions.org Hope with Jonathan: Hope - Our page is here to create awareness for kidney disease/dialysis/transplant patients. We also share inspiring stories of Hope. www.hopewithjonathan.com https://jetsr1177.wixsite.com/hopeforjonathan https://linktr.ee/JTHope77 https://youtube.com/channel/UCt_XicPnD0u4E0IrZz4w5Fg https://www.facebook.com/hopewithjonathan/ https://instagram.com/hope_with_jonathan?r=nametag Twitter: https://twitter.com/hope_host?s=21 https://vm.tiktok.com/ZMJvfaudK/ https://www.snapchat.com/add/jonathan_t1177 http://linkedin.com/in/jonathan-traylor77 https://www.reddit.com/u/Boogiedabear77/?utm_source=share&utm_medium=ios_app&utm_name= Come join me on MeWe! It's the only social network built on trust, control and love. https://mewe.com/i/jonathavtraylor https://hopewithjomathan.tumblr.com/ https://twitch.tv/hopejon77 WhatsApp : Jonathan Traylor Hope with Jonathan Podcast: Hope with Jonathan Podcast. We will discuss kidney disease, kidney dialysis and kidney transplant. We will also advocate for Kidney patients a living organ donation. https://anchor.fm/hope-with-jonathan https://linktr.ee/JTHope77 https://www.facebook.com/hopewithjonathanpodcast/ https://instagram.com/hope_with_jonathan_podcast?r=nametag https://twitter.com/jonathanpodcast?s=21 --- Support this podcast: https://podcasters.spotify.com/pod/show/hope-with-jonathan/support

In this episode of the Wisdom & Wanderlust Podcast, Michael and Robyn talk with David Alport, a certified personal and professional development coach who helps his clients navigate through life’s transitions and live with more intention. Before he became a coach, David spent more than 20 years in the travel industry and founded Out & About, a company that provided guidance for LGBTQ travelers through print and digital media. David talks about a trip to India that changed his life and how he approaches travel. He also talks about the similarities between the Burning Man festival and a refugee camp in Kenya. He shares why he goes back to certain destinations more than once and what it means to travel and live with intention.    "The real magic of travel is how it changes your perspective." - David Alport [47:54]   What You Will Learn: [00:01] Intro [02:44] Working with a coach [05:02] David’s strengths as a coach [08:16] Meet David Alport [10:02] What it’s like coaching during the pandemic [15:59] How his focus has shifted and where he wants to go after the pandemic [20:58] Where David’s sense of wanderlust comes from [21:08] His first international travel experience and some favorite travel experiences [24:14] David’s experiences traveling to India [33:57] What he’s learned exploring the human condition [35:28] The emotional overlap between the refugee camps in Kenya and Burning Man [41:42] Why he chooses to revisit places [44:51] The perspective circle exercise [48:08] How to bring intentional mindset to traveling [54:34] Three key tools/hacks for traveling with intention [1:02:15] Why David doesn’t have friends who don’t like to travel [1:07:54] Rapid fire questions [1:19:58] Where to contact David [1:21:02] Outro   Resources:   David Alport’s website David Alport on Twitter David Alport on LinkedIn David Alport on Facebook The Transformational Travel Council Burning Man FilmAid Kakuma refugee camp The Dadaab refugee complex The perspective circle exercise The Overstory by Richard Powers

This episode aims to raise the awareness on a rare genetic disease that affects the renal function in addition to hearing and vision loss over time. --- Send in a voice message: https://anchor.fm/magpie-concept/message

As we kick of our Alport Awareness Series & support National Kidney & Alport Syndrome Awareness Month, I am so excited to welcome to the show, Kevin Schnurr, Director of Communications, Alport Syndrome Foundation.   Kevin began volunteering for Alport Syndrome Foundation in 2012 at age 26 after experiencing unexpected renal failure. After two years on dialysis, he received a living donor transplant from a close friend. Kevin's desire to help others in the rare disease community led to his position as ASF Social Media Specialist in 2014 and part-time Patient Outreach Coordinator in 2016. He has facilitated the Teen program at ASF Family Meetings, represented ASF at patient advocacy events and conferences, and co-moderates the ASF Facebook Support Group Page. In addition to his background in graphic design and experience in college administration, Kevin's perspective and communication skills as a patient bring great value to ASF.   Listen in as Kevin shares his personal journey with Alport as well all about the Alport Syndrome Foundation and the amazing resources they offer.

As we wrap up our Alport Awareness Series & support National Kidney & Alport Syndrome Awareness Month, I am so excited to welcome to the show, Cassandra Smith ICU Nurse and Volunteer Patient Advocate, Alport Foundation.  Cassie Smith, a Kentucky native, is a registered nurse and mom to three young children. She was first diagnosed with Alport syndrome in late childhood. Two of her three children were diagnosed in early 2019. Both her professional and personal experiences make her passionate about patient advocacy. Cassie recently accepted the opportunity to Co-Chair the newly established Emerging Leadership Council for Alport Syndrome Foundation. In this role, she is volunteering with others to better address the unique needs of Alport patients in the 25-35 year old age range.  Listen in as Cassie shares her journey of rare disease from the perspective of patient, parent and nurse. 

In today's episode of R is for Rare, I'm interviewing my good friend Grant Bonebrake, who has a rare genetic kidney disease called Alport Syndrome. We talk about what his life has been like leading up to and since his diagnosis, why he loves to advocate, how great the rare disease community is, and much more! Be sure to subscribe to R is for Rare on Apple Podcasts, Spotify, or wherever you get your podcasts! Leave a review to let me know your thoughts, and share the podcast on social media! Find Grant Bonebrake on Instagram — @grant_bonebrake Support the Alport Syndrome Foundation — https://www.alportsyndrome.org YARR — https://everylifefoundation.org/young-adult-representatives/yarr-leadership-academy/#toggle-id-4 National Kidney Foundation — https://www.kidney.org Living Donor Protection Act — https://www.congress.gov/bill/116th-congress/house-bill/1224?s=1&r=1 --- This episode is sponsored by · Anchor: The easiest way to make a podcast. https://anchor.fm/app --- Send in a voice message: https://anchor.fm/annie-watson/message

In 2012, at the age of 26, Kevin Schnurr was unexpectedly diagnosed with Alport syndrome after being rushed to the hospital with high blood pressure. After two years on peritoneal dialysis, he received a living donor kidney transplant from a close friend in May 2014. Kevin's desire to help others in the rare disease community led to him volunteering at Alport Syndrome Foundation (ASF) in 2012. He later served in a position as ASF Social Media Specialist in 2014 and part-time Patient Outreach Coordinator in 2016. Kevin currently serves as the Director of Communications & Patient Engagement (since Oct. 2019). He has facilitated the Teen Program at ASF Family Meetings, represented ASF at patient advocacy events and conferences, and co-moderates the ASF Facebook Support Group Page. In his free time, Kevin loves playing guitar, attending concerts, and collecting/voraciously reading books. Website: alportsyndrome.org Socials: https://www.facebook.com/alportsyndromefoundation/ https://twitter.com/AlportSyndFndn https://www.instagram.com/alportsyndromefndn/ https://www.youtube.com/user/TheASFoundation Other links: https://www.organdonor.gov/ https://www.donatelife.net/

In 2012, at the age of 26, Kevin Schnurr was unexpectedly diagnosed with Alport syndrome after being rushed to the hospital with high blood pressure. After two years on peritoneal dialysis, he received a living donor kidney transplant from a close friend in May 2014. Kevin’s desire to help others in the rare disease community led to him volunteering at Alport Syndrome Foundation (ASF) in 2012. He later served in a position as ASF Social Media Specialist in 2014 and part-time Patient Outreach Coordinator in 2016. Kevin currently serves as the Director of Communications & Patient Engagement (since Oct. 2019). He has facilitated the Teen Program at ASF Family Meetings, represented ASF at patient advocacy events and conferences, and co-moderates the ASF Facebook Support Group Page. In his free time, Kevin loves playing guitar, attending concerts, and collecting/voraciously reading books. Website: alportsyndrome.orgSocials: https://www.facebook.com/alportsyndromefoundation/ https://twitter.com/AlportSyndFndn https://www.instagram.com/alportsyndromefndn/ https://www.youtube.com/user/TheASFoundation Other links:https://www.organdonor.gov/https://www.donatelife.net/

In this months episode we explore a spectacular shorter walk in the Peak District. We'll be passing the waters of the Derwent and Howden reservoirs, famous for The Dambusters of WW2, and taking in the stunning views from Alport Castles. As one of the gems of the Peaks, Alport is the largest land slide in the UK and when approached the direction we come from in the episode it is sure to take your breath away.It's worth mentioning that the podcast is no substitute for a map, and the ability to read it. You'll be walking at times in some pretty remote areas:Make sure you confident in your abilitiesTell someone where you're going and when you're due backTake a rucksack with a sensible set of kitWe're also publishing each route through the Ordnance Survey online map service so members can access the detailed route card.There is a high chance that you won't have phone signal for the entirety of the walk, so be sure to download the episode to your

Alport Syndrome

Academy Manager David Longwell talks to IFollow after the Shropshire Senior Cup #salop

  Episode 278 is an all inclusive guide to kidney anatomy, health, bloodwork, and MORE for physique and performance based athletes! First I dig into some basics on kidney anatomy and function before moving into some considerations for athletes looking to get bloodwork done to track kidney health, and all before ending with practical application on how to maintain kidney health while pushing for your goals! Also, theres a few references I'll provide below for those looking to take things further!   REFERENCES Adelstein RS, Sellers JR. Effects of calcium on vascular smooth muscle contraction. The American journal of cardiology. Jan 30 1987;59(3):4b-10b.   Agre P, King LS, Yasui M, Guggino WB, Ottersen OP, Fujiyoshi Y, . . . Nielsen S. Aquaporin water channels--from atomic structure to clinical medicine. The Journal of physiology. Jul 1 2002;542(Pt 1):3-16.   AHA. American Heart Association. Kidney Damage and High Blood Pressure. Available at: http://www.heart.org/HEARTORG/Conditions/HighBloodPressure/WhyBloodPressureMatters/Kidney-Damage-and-High-Blood-Pressure_UCM_301825_Article.jsp. Last updated 9/11/2014a. Accessed 8/10/2014.     Akinwusi PO, Oluyombo R, Ogunro PS, Adeniji AO, Okunola OO, Ayodele OE. Low dose aspirin therapy and renal function in elderly patients. International journal of general medicine. 2013;6:19-24.   Al-Awqati Q, Barasch J, Goldman L (ed.), SchaferAI (ed.). Goldman's Cecil Medicine, Twenty-Fourth Edition. Chapter 117: Structure and Function of the Kidneys; 716-720. Copyright 2012 Saunders, an imprint of Elsevier, Inc. Available at: www.clinicalkey.com Accessed: 6/9/2014.   Alpern RJ, Sakhaee K. The clinical spectrum of chronic metabolic acidosis: homeostatic mechanisms produce significant morbidity. American journal of kidney diseases : the official journal of the National Kidney Foundation. Feb 1997;29(2):291-302.   Amodu A, Abramowitz MK. Dietary acid, age, and serum bicarbonate levels among adults in the United States. Clinical journal of the American Society of Nephrology : CJASN. Dec 2013;8(12):2034-2042.   Anders HJ, Andersen K, Stecher B. The intestinal microbiota, a leaky gut, and abnormal immunity in kidney disease. Kidney international. Jun 2013;83(6):1010-1016.   Babaei-Jadidi R, Karachalias N, Ahmed N, Battah S, and Thornalley PJ. Prevention of incipient diabetic nephropathy by high-dose thiamine and benfotiamine. Diabetes. 2003;52(8):2110–20   Bae EH, Lee J, Ma SK, et al. alpha-Lipoic acid prevents cisplatin-induced acute kidney injury in rats. Nephrology, dialysis, transplantation: official publication of the European Dialysis and Transplant Association - European Renal Association. 2009;24(9):2692–700   Balakumar P, Bishnoi HK, Mahadevan N. Telmisartan in the management of diabetic nephropathy: a contemporary view. Current diabetes reviews. May 2012;8(3):183-190.   Balakumar P, Rohilla A, Krishan P, Solairaj P, and Thangathirupathi A. The multifaceted therapeutic potential of benfotiamine. Pharmacol. Res. 2010;61(6):482–8   Bankir L, Bouby N, Trinh-Trang-Tan MM, Ahloulay M, Promeneur D. Direct and indirect cost of urea excretion. Kidney international. Jun 1996;49(6):1598-1607.   Barbagallo M, Dominguez LJ, Galioto A, Pineo A, Belvedere M. Oral magnesium supplementation improves vascular function in elderly diabetic patients. Magnesium research : official organ of the International Society for the Development of Research on Magnesium. Sep 2010;23(3):131-137.   Bashir B, Sharma SG, Stein HD, Sirota RA, D'Agati VD. Acute kidney injury secondary to exposure to insecticides used for bedbug (Cimex lectularis) control. American journal of kidney diseases : the official journal of the National Kidney Foundation. Nov 2013;62(5):974-977.   Baynes JW, Dominiczak MH. Medical Biochemistry, Fourth Edition. 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Advanced glycation end-products and the kidney. Eur J Clin Invest. 2010;40(8):742–55   Cacciapuoti F. Lowering homocysteine levels may prevent cardiovascular impairments? Possible therapeutic behaviors. Blood coagulation & fibrinolysis : an international journal in haemostasis and thrombosis. Dec 2012;23(8):677-679.   Calhoun DA. Hyperaldosteronism as a common cause of resistant hypertension. Annu. Rev. Med. 2013;64:233–47   Ceglia L, Harris SS, Abrams SA, Rasmussen HM, Dallal GE, Dawson-Hughes B. Potassium bicarbonate attenuates the urinary nitrogen excretion that accompanies an increase in dietary protein and may promote calcium absorption. The Journal of clinical endocrinology and metabolism. Feb 2009;94(2):645-653.   Chao MC, Hu SL, Hsu HS, Davidson LE, Lin CH, Li CI, . . . Lin WY. Serum homocysteine level is positively associated with chronic kidney disease in a Taiwan Chinese population. Journal of nephrology. Jan 16 2014.   Chaudhary DP, Sharma R, Bansal DD. 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Food Funct. 2012;3(12):1251–64     Davis KE, Prasad C, Vijayagopal P, Juma S, Imrhan V. Advanced Glycation End Products, Inflammation, and Chronic Metabolic Diseases:Links in a Chain? Critical reviews in food science and nutrition. Sep 26 2014.   De la Fuente M, Hernanz A, Viniegra S, Miquel J. Sulfur-containing antioxidants increase in vitro several functions of lymphocytes from mice. International immunopharmacology. Jun 2011;11(6):661-669.   Debreceni B, Debreceni L. The role of homocysteine-lowering B-vitamins in the primary prevention of cardiovascular disease. Cardiovascular therapeutics. Jun 2014;32(3):130-138.   Dempsher J. The nerve impulse in the axon--a new theory. Acta biotheoretica. 1981;30(2):121-137.   Di Vito R, Sirolli V, Amoroso L, Bonomini M. [Nephrotoxicity induced by chemotherapy]. Giornale italiano di nefrologia : organo ufficiale della Societa italiana di nefrologia. May-Jun 2011;28(3):296-304.   Dong JY, Xun P, He K, Qin LQ. Magnesium intake and risk of type 2 diabetes: meta-analysis of prospective cohort studies. Diabetes care. Sep 2011;34(9):2116-2122.   Downie WW. Prostaglandins and NSAID in the kidney. The Journal of rheumatology. Supplement. Mar 1991;28:19-21.   Duranton F, Cohen G, De Smet R, Rodriguez M, Jankowski J, Vanholder R, Argiles A. Normal and pathologic concentrations of uremic toxins. Journal of the American Society of Nephrology : JASN. Jul 2012;23(7):1258-1270.   Eknoyan G. Obesity and chronic kidney disease. Nefrologia : publicacion oficial de la Sociedad Espanola Nefrologia. 2011;31(4):397-403.   Eknoyan G, Latos DL, Lindberg J, National Kidney Foundation Carnitine Consensus Conference. Practice recommendations for the use of L-carnitine in dialysis-related carnitine disorder. National Kidney Foundation Carnitine Consensus Conference. Am J Kidney Dis. 2003;41(4):868–76.     Faloon W. FDA Approves Deadly Drugs, Delays Lifesaving Therapies. Life Extension Magazine. http://www.lef.org//Magazine/2004/5/awsi/Page-01. May 2004. Accessed 1/26/2015.   Feng B, Yan X-F, Xue J-L, Xu L, and Wang H. The Protective Effects of α-Lipoic Acid on Kidneys in Type 2 Diabetic Goto-Kakisaki Rats via Reducing Oxidative Stress. Int J Mol Sci. 2013;14(4):6746–56   Fenton TR, Tough SC, Lyon AW, Eliasziw M, Hanley DA. Causal assessment of dietary acid load and bone disease: a systematic review & meta-analysis applying Hill's epidemiologic criteria for causality. Nutrition journal. 2011;10:41.   Ferri FF. Ferri's Clinical Advisor. Chronic Kidney Disease. Available at: www.clinicalkey.com. Copyright © 2014c. Accessed 6/12/2014.   Ferri FF. Ferri's Clinical Advisor. Acute Kidney Injury. Available at: www.clinicalkey.com. Copyright © 2014a. Accessed 6/12/2014.   Ferri FF. Ferri's Clinical Advisor. Polycystic Kidney Disease. Available at: www.clinicalkey.com. Copyright © 2014b. Accessed 6/12/2014.   Finkielstein VA, Goldfarb DS. Strategies for preventing calcium oxalate stones. CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne. May 9 2006;174(10):1407-1409.   Fjellstedt E, Denneberg T, Jeppsson JO, Tiselius HG. A comparison of the effects of potassium citrate and sodium bicarbonate in the alkalinization of urine in homozygous cystinuria. Urological research. Oct 2001;29(5):295-302.   Fliser D, Ritz E. Serum cystatin C concentration as a marker of renal dysfunction in the elderly. American journal of kidney diseases : the official journal of the National Kidney Foundation. Jan 2001;37(1):79-83.   Forbes JM, Cooper ME, Oldfield MD, Thomas MC. Role of advanced glycation end products in diabetic nephropathy. Journal of the American Society of Nephrology : JASN. Aug 2003;14(8 Suppl 3):S254-258.     Fung TT, Chiuve SE, McCullough ML, Rexrode KM, Logroscino G, Hu FB. Adherence to a DASH-style diet and risk of coronary heart disease and stroke in women. Archives of internal medicine. Apr 14 2008;168(7):713-720.   Gaedeke J, Fels LM, Bokemeyer C, Mengs U, Stolte H, Lentzen H. Cisplatin nephrotoxicity and protection by silibinin. Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association. Jan 1996;11(1):55-62.   Gazdíková K, Gvozdjáková A, Kucharská J, Spustová V, Braunová Z, and Dzúrik R. Oxidative stress and plasma concentrations of coenzyme Q10, alpha-tocopherol, and beta-carotene in patients with a mild to moderate decrease of kidney function. Nephron. 2001;88(3):285   Geleijnse JM, Giltay EJ, Grobbee DE, Donders ART, and Kok FJ. Blood pressure response to fish oil supplementation: metaregression analysis of randomized trials. J. Hypertens. 2002;20(8):1493–9   Genazzani AR, Mannella P, Simoncini T. Drospirenone and its antialdosterone properties. Climacteric : the journal of the International Menopause Society. Feb 2007;10 Suppl 1:11-18.   GHR. 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N-acetylcysteine rescue protocol for nephrotoxicity in children caused by ifosfamide. Journal of population therapeutics and clinical pharmacology = Journal de la therapeutique des populations et de la pharamcologie clinique. 2013;20(2):e132-145.   Harisa GI. Benfotiamine enhances antioxidant defenses and protects against cisplatin-induced DNA damage in nephrotoxic rats. J. Biochem. Mol. Toxicol. 2013;27(8):398–405   Hartweg J, Farmer AJ, Holman RR, and Neil HAW. Meta-analysis of the effects of n-3 polyunsaturated fatty acids on haematological and thrombogenic factors in type 2 diabetes. Diabetologia. 2007;50(2):250–8   Hataya Y, Igarashi S, Yamashita T, and Komatsu Y. Thyroid hormone replacement therapy for primary hypothyroidism leads to significant improvement of renal function in chronic kidney disease patients. Clinical and experimental nephrology. 2013;17(4):525–31   Hawley MA. The Kidney Transplant/Dialysis Association Patient Handbook. 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Community Development Manager Kevin Schaefer talks about some of the trending topics in the SMA News Today forums. SMA News Today’s Director of Multichannel Content, Michael Morale, discusses how the world’s first Alport stamp is a Macedonian mom’s latest win for rare disease patients.

Session 09 In our renal question today we are asked to identify the pattern we would see on electron microscopy. See if you can find where the question leads you! Once again, we're joined by Dr. Andrea Paul from Board Vitals. If you're getting ready to start preparing for your Step 1 or Level 1exam, check out Board Vitals and their QBank. Use the promo code BOARDROUNDS to save 15% off your QBank purchase. For more resources, be sure to check out all our other podcasts on the MedEd Media Network. [02:50] A Challenging Area Renal tends to come up in the top 3 of questions where people are going back because they answered them incorrectly or that they're saving and redoing questions in this category. This indicates a level of less confidence or knowledge gap that needs to be filled for most students. Andrea thinks renal is a challenging area being a complicated system with a lot of memorization involved in the different syndromes. It's a combination of genetics and pathophysiology and pathology. You'd have to be able to do everything from figuring out the disorder and knowing what it would look like on biopsy, looking at diagnostic studies and the physiology involved in the different renal disorders. [04:22] Question A 16-year-old boy presents. He recently immigrated from Russiam, has no major medical problems. He does mention he had an episode of light red urine three weeks ago. At the same time, he had a mild cold. He has no known allergies, no recent drug use or medications. His family has traced positive for kidney disease in his maternal uncle, but both of his parents are healthy. He also mentions that he has had lately noticed that he has mild hearing problem but he's never thought much of that. It's asking a kidney biopsy. This patient would most likely show which of the following: (A) Linear pattern of IGG with fluorescent microscopy (B) Splitting of the glomerular basement membrane (C) Mesangial cell proliferation (D) Epithelial humps or a thickened basement membrane that looks like a train track [05:50] Finding the Diagnosis The first thing to note here is the hearing loss, which is something that would lead you down a specific road. So we're given a little hint here that can be very helpful. Based on history, the hearing loss would be due to Alport syndrome, which is a collage type 4 mutation resulting in abnormal basement membrane, that includes renal involvement, ocular involvement, and sensory neural hearing loss. In this question, the answer you'd look at is the splitting of the glomerular basement membrane. The other way to describe this is the basket weave appearance, also known as the glomerular basement membrane lamellation, characterized by the layering and splitting of the membrane. The key here is the Alport syndrome and remember what the findings would be and that specific disorder. [08:30] Potential Questions One possible question could be what other symptoms the patient may be experiencing. How is this commonly inherited because Alport syndrome can be inherited in a X-linked dominant way. You can also look through everything from genetics all the way through the pathology and electron microscopy for each disorder. Or maybe they won't mention hearing loss but vision symptoms or inheritance pattern they've seen in the family, which they did when they mentioned the maternal uncle. So they've hinted this as well. [09:50] What If There Was No Hint If the question would have left the hearing loss out, they would probably mention a more extensive family history so you could see the inheritance pattern. They're also mentioning hemoturia so you're led to a nephrotic syndrome. That would also help. But they'd probably give you additional information to lead you down a more specific road for one of these different nephrotic causes. [10:32] More Things to Know About Renal Stuff You need to know the different patterns for each of the different nephrotic syndrome causes. This is part of the reason people redo these questions over and over. There's a lot of memorization involved such as APGN and RPGN and what those look like, as well as microscopy. For this question, you would think through things like Goodpasture syndrome where you'd see a different pattern then you'd see that linear pattern which is that first option. And if it's in older males then you'd have respiratory symptoms because there's lung involvement. So you have to think through all the different associated organ systems with the different disorders and memorizing what the pattern looks like on each of them. As far as symptoms, inheritance, and treatment, there are different diagnostic studies and treatments and those are the ones you can reason through based on the different disorders and what the physiologic effects of each is. Lastly, keep in mind to know the demographics are. Some of them are more common in patients with specific histories, or ages or backgrounds – anything that can help you get to the answer more quickly will be helpful. The immigration component must have been put in there too since there's not a whole lot of medical history available. So they could actually put in things that could be helpful or completely just inserted for background information to make the case more robust, but not necessarily valuable. It's important to think through each piece of information in the question to make sure they tie together and you'd be able to eliminate something that clearly doesn't help you. So you don't focus too much on every specific part of the history. [14:32] Board Vitals Going over questions is the most beneficial thing you can do as a medical student preparing for your Step 1 or Level 1 exam. Check out Board Vitals for some help. They QBanks and over 1700 questions for Step 1 and almost as many for Level1. Have a free trial and check out their system to see if it works for you. Use the promo code BOARDROUNDS to save 15% off. Links: MedEd Media Network Board Vitals (promo code BOARDROUNDS) Specialty Stories Podcast

Session 07 We often associate biochemistry with undergrad, but biochemistry is present in many specialties! Let’s dive into the types of biochem questions you may see! We're joined once again by Dr. Andrea Paul from Board Vitals as we help you prepare for your first board exam so you have what it takes to score high and match into your specialty of choice. Use the promo code BOARDROUNDS to save 15% on your QBank purchase. [03:30] Why Biochemistry? Biochemistry is more applicable to some specialties than others. But just basic genetics and metabolic diseases, for instance, are seen in many specialties. Biochemistry comes into play especially when you talk about metabolic diseases. Hence, it's a commonly tested subject on the exam, more than the other basic science components. [04:41] Question for this Week: A healthy married couple has a child who develops clinical symptoms of what you suspect to be a rare disease. Genetic testing revealed the patient's mother carries the mutated gene, but the father is not a carrier. However, the father's brother had the same disease, which has also occurred in one of his sisters' sons. This pattern is characteristic of which of the following diseases? Note from Andrea: The question is drawing you a pedigree. You can jot down a little diagram of pedigree for yourself as you're going through it. You have to figure out the pattern from the pedigree but know which diseases of the options fit that pattern of inheritance. Answer choices: (A) G6PD (B) Cystic fibrosis (C) Phenylketonuria (PKU) (D) Alpha-1 antitrypsin deficiency (E) Tay-Sachs Disease [05:50] The Thought Process Behind the Answer Once you've drawn that pedigree and determined what the inheritance pattern is, you can go through each option and cross out what doesn't fit or jot down what pattern each one has. In this case, the couple is healthy and not showing any disease. But the one child does and the father is not a carrier. This gives you another hint. So if he's not a carrier, how is that possible if the child is showing the disease? Then you're seeing that it's present in the father's brother and one of the sisters' sons. Here, you can see a distinctive pattern where this is not an autosomal recessive type pattern. This leads you to a dominant X-linked route. As you draw this out, you will start to see the pattern where the children follow up to them. The mother is a carrier, the father is not. And the child has the disease. It's likely that the child is a male because they're receiving only an X from the mom. So this would be an X-linked pattern. Now, you would only see one that follows that X-linked disease – G6PD Looking at patterns and pedigrees can really help you. Another algorithm Andrea found helpful is to ask: does the child with the disease have a parent with a disease. If no, then you're skipping a lot of things. You're left here with X-linked recessive which is 50% more common than a male child. Therefore, it's an X-linked recessive disease. [11:02] Tips and Tricks to Help You Memorize and Understand Better Most students are using mnemonics to remember all of the X-linked recessive diseases. This is most common for autosomal recessive or autosomal dominant. There's no way to think through them in a way that doesn't require memorization. The names of the disease don't really help in this case. All this being said, Andrea recommends using mnemonics. You can also use visual mnemonics you can look at or silly drawings to help you remember stuff. [12:37] Other Possible Questions Probably, if the question talked about a food that this person that this person may develop symptoms with, then you could probably remove some answer choices out. For example, G6PD is one of those diseases. If it's cystic fibrosis, they could ask what microbe commonly infects patients with this disorder. Or they could ask a treatment for that disorder. [14:00] Other Patterns Students Should Know About One pattern would be X-linked dominant. In this case, you would not see skipping of generations unlike what's in the above question. You would also see male and female as affected equally since the disease of the X chromosomes is dominant. So you think of diseases like X-linked dominant Alport syndrome or hypophosphatemic rickets. Another interesting inheritance pattern is mitochondrial where males and females are affected equally. It would skip generations but it is only transmitted from an affected female because mitochondrial diseases come from the maternal side always. And you would see a different pattern and all of the offspring would be affected – something you wouldn't see in the other types. Autosomal dominant, you would also see male and female as affected and not skipping generations. For instance, if two parents without the disease have a child with the disease, you'd think that the only way this could be autosomal dominant is there's a new mutation or there's some type of reduced penetrants or maybe the parent has the gene but just phenotypically normal. Otherwise, you would see this in every offspring because it's a dominant disease. Autosomal recessive is the opposite where you see skipping of generations. For example, if you have a couple both carrying the gene without any signs of disease, there would be 25% the child is born with two normal genes from the parents, 50% chance that they have one normal and one abnormal gene, and 25% that they would receive both. Since it's recessive that's the only case where you would see disease such as cystic fibrosis, thalassemia, sickle cell anemia, or PKU (of which some are shown in the answer choices above). Spinal muscular atrophy would be a more popular disease here, which my daughter has but me and my wife don't have, which makes us both carriers. This is going to be more popular to start talking about it on medical school and the boards because it's one of the first diseases out there that will be cured with gene therapy. [17:45] Board Vitals If you're interested in the QBank and how Board Vitals can help you prepare the best way you can for your Step 1 or Level 1, check out their site and use the promo code BOARDROUNDS to save 15% off of your QBank purchase. Links: Board Vitals (promo code: BOARDROUNDS)

Ari and Larra report back from the Alport Syndrome Foundation Family Meeting! Ari talks about what it was like to meet people outside his family who share his disease and discusses the information and emotions from the event.

In today’s episode, we sit down with David Alport as he takes us through Bridge City Collective and their unique story based in Portland, Oregon. This rock climbing enthusiast discusses the importance of adapting to the needs of the patients, as well as to the needs of the business. With his sights set on branching his dispensaries out to further areas in the future, there seems to be no obstacle Alport can’t climb.

Thu, 30 Apr 2015 12:00:00 +0100 https://edoc.ub.uni-muenchen.de/18361/ https://edoc.ub.uni-muenchen.de/18361/1/Beicht_Sonja.pdf Beicht, Sonja ddc:610, ddc:600, Medizinische Fak

Alport Syndrome is an underdiagnosed and commonly misdiagnosed disease whose symptoms often go undetected. Sharon Lagas established the Alport Syndrome Foundation after losing her 38-year-old brother to this hereditary illness and then learning that she, her mother, and her two sons and two nieces also had it. Sharon explains what is involved and shares her personal story. Listen to this interview to learn more about the disease and the ongoing research into it, and find out how to stay informed.

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.

Episode 1 – Alport Group Podcast – Is the World in Economic Turmoil? In the inaugural episode of the Alport Group Podcast we talk about: Is the world in economic turmoil? People just think everything is still bad because the economy is rebounding slower than expected but it is rebounding “One analyst said out of 35 indicators only 3 were down” The media loves to talk about the “bad” news in the economy Since Christmas the stock market has risen … Read more

Thu, 24 Feb 2011 12:00:00 +0100 https://edoc.ub.uni-muenchen.de/12757/ https://edoc.ub.uni-muenchen.de/12757/1/Jedlicka_Jan.pdf Jedlicka, Jan ddc:610, ddc:600, Medizinische Fakultät

Mit der vorliegenden Studie wurde am Beispiel der diabetischen Nephropathie und der Nephropathie beim Alport-Syndrom die Rolle des Chemokins "macrophage chemoattractant protein-1" (Mcp-1) bei der Progression der chronischen Niereninsuffizienz untersucht, da es die damit assoziierte Rekrutierung von Makrophagen in die Niere vermittelt und in Korrelation zum Erkrankungsstadium verstärkt exprimiert bzw. verstärkt im Urin ausgeschieden wird. Mcp-1-defiziente diabetische Mäuse zeigen zudem eine verlangsamte Progression. Eine therapeutische Blockade von Mcp-1 sollte daher die Infiltration von Makrophagen reduzieren und mit geringerer Nierenschädigung einhergehen. Mcp-1 wurde bei uninephrektomierten db/db-Mäusen mit fortgeschrittener diabetischer Nephropathie und bei Kollagen-IV-a3-defizienten Mäusen mit autosomal-rezessiver Alport-Nephropathie mit einem neuartigen Antagonisten, dem Spiegelmer mNOX-E36-3’PEG blockiert. Bei uninephrektomierten db/db-Mäusen führte die achtwöchige Behandlung mit dem Spiegelmer zu einer Reduktion der glomerulären Makrophagen um 40 % und der tubulointerstitiellen Makrophagen um 53 %. Dies war assoziiert mit einer signifikanten Reduktion glomerulärer und tubulointerstitieller Schäden sowie einer Verbesserung der glomerulären Filtrationsrate (GFR). Daneben konnte die Expression von Mcp-1 und Ccr2 in der Niere signifikant reduziert werden. Bei Kollagen-defizienten Mäusen führte die sechs- bzw. dreiwöchige Behandlung zu einer Reduktion der glomerulären Makrophagen um 50 % und der tubulointerstitiellen Makrophagen um 30 %. Dies war jedoch weder mit einer Reduktion der Nierenschädigung oder der Expression von Mcp-1 und Ccr2, noch mit einer Verlängerung des Überlebens assoziiert. Zusammenfassend konnte gezeigt werden, dass die spät begonnene therapeutische Blockade von Mcp-1 durch das Spiegelmer mNOX-E36-3’PEG bei der db/db-Maus einen Schutz vor Glomerulosklerose bietet, die tubulointerstitielle Schädigung reduziert und die Nierenfunktion verbessert. Die Therapie mit anti-Mcp-1-Spiegelmeren könnte demnach das derzeitige Behandlungsregime der Diabetes-assoziierten chronischen Niereninsuffizienz um einen neuen Therapieansatz ergänzen und so die Progression verlangsamen. Beim Alport-Syndrom konnte die therapeutische Blockade von Mcp-1 durch das Spiegelmer mNOX-E36-3’PEG nicht vor Glomerulosklerose schützen, die tubulointerstitielle Schädigung nicht reduzieren, die Nierenfunktion nicht verbessern und das Überleben nicht verlängern. Ein Einfluss auf die Progression des Alport-Syndroms konnte nicht nachgewiesen werden. Die Therapie mit anti-Mcp-1-Spiegelmeren bietet demnach keine zusätzliche Behandlungsoption bei der hereditären Alport-Nephropathie.

Cet enregistrement représente mon interprétation entant qu'étudiant en 2e année de Médecine. Il est fourni entant qu'aide à l'étude et n'a pas comme objectif d'être une ressource primaire. Il ne constitue pas un avis médical. Veuillez pardonner les erreurs grammaticales. Le sujet de cet épisode est les troubles de vision comme signes de maladie systémique. L’œil est un organe complexe et comme tel, il y a plusieurs conditions médicales qui se manifestent par un dérangement de la vision ou par un signe au niveau de l’organe comme tel. Il y a plus d’une façon de classifier les atteintes de l’œil. On peut classifier selon le niveau anatomique de l’atteinte, comme par exemple, l’atteinte des structures qui conduisent la lumière, comme la cornée, le cristallin ou le corps vitré, l’atteinte des structures qui sont impliqués dans l’acquisition, la transmission ou l’interprétation du signal visuel comme la rétine, le nerf optique, les radiations optiques ou le cortex occipital, ou l’atteinte des structures accessoires comme l’orbite, l’appareil lacrymal, les paupières, la conjonctive, la sclère, l’iris, la circulation de l’humeur aqueuse, la circulation sanguine ou les muscles et leur innervation. Une autre façon d’organiser les causes de l’atteinte de l’œil est selon l’étiologie : mécanique, traumatique, inflammatoire, infectieuse, néoplasique, dégénératif, congénital, vasculaire, hémorragique, toxique, métabolique, endocrinologique, nerveuse ou disruption de l’anatomie normale. Cet épisode portera sur les manifestations oculaires de maladies systémiques, mais ne discutera pas la pathogenèse, la prise en charge ou le traitement de ces conditions. • Diabète o La rétinopathie est une source de morbidité majeure chez les diabétiques et une des premières causes de cécité. Le dépistage de routine est important étant donné que la rétinopathie peut être asymptomatique jusqu’aux stades avancés de l’atteinte oculaire. o La rétinopathie diabétique peut être divisée en 3 stades. • Le premier est la rétinopathie de fond. À ce stade, on peut voir des micro anévrysmes, des hémorragies ponctuelles, des hémorragies en flammèches, des exsudats lipidiques (ou hard exsudates) et des infarcissements de la rétine (ou cotton wool spots.) • Le deuxième stade est la rétinopathie préproliférative. Elle comporte les signes de la rétinopathie de fond auxquels on a ajouté un début de néovascularisation et des veines en forme de chapelet. • Le 3e stade est la rétinopathie proliférative. La néovascularisation atteint la rétine et le vitré, et ces nouveaux vaisseaux sont l’origine d’hémorragies vitréennes. Ces hémorragies causent une prolifération de fibroblastes, et la contraction tissulaire qui s’ensuit provoque un décollement rétinien tractionnel. La néovascularisation du segment postérieur peut aussi s’accompagner d’une néovascularisation facilement visible du segment antérieur. • À n’importequel moment, on peut aussi retrouver de l’œdème maculaire causé par l’augmentation de la perméabilité des capillaires dans la zone maculaire. o De plus, les patients diabétiques développent plus rapidement des cataractes, sont plus susceptibles de développer le glaucome à angle ouvert et l’hyperglycémie peut aussi causer des changements réfractaires. o Finalement, la neuropathie diabétique ou l’atteinte microvasculaire en périphérie du nerf optique peut affecter la vision ou les organes accessoires à la vision. • La rétine est un outil pour visualiser le lit vasculaire directement, et est donc très utile dans le suivi de l’hypertension. • L’hypertension chronique peut aussi causer une forme de rétinopathie ressemblant à la rétinopathie diabétique. Les caractéristiques typiques de la rétinopathie secondaire à l’hypertension chronique sont l’encochement artérioveineux, les microhémoragies, des microanévrysmes et des infarcissements (coton wool spots). • L’hypertension maligne peut présenter avec un étoile maculaire et de l’œdème papillaire, mais ce n’est pas la seule cause d’œdème papillaire. Le différentiel pour l’œdème papillaire bilatéral inclut, entre autres : l’augmentation de la pression intracranienne (qui est une urgence médicale), les troubles congénitaux comme les drusen ou les fibres nerveuses intraoculaires myélinisées, et parfois le diabète, l’hyperviscosité, l’hypotension et l’intoxication. • AA o Graves • Les patients atteints de l’hyperthyroïdie ont un retard palpébral, leur donnant l’allure de fixer le regard. • De plus, ¼ des patients atteints d’une hyperthyroïdie de Graves manifesteront une exophtalmie, causée par une inflammation des tissus retrobulbaires, y inclus les muscles et les tissus conjonctifs. • Le retard palpébral est un facteur de risque pour les ulcères cornéens. o SEP • La névrite optique est fortement associée avec la sclérose en plaques. Environ 40% des patients atteints de la sclérose en plaques auront cette perte de vision. La perte est habituellement unilatérale et associé avec une douleur au mouvement des yeux. Une inflammation de la papille optique est observée à l’ophtalmoscopie chez seulement 1/3 des patients. On peut aussi retrouver chez ces patients une ophtalmoplégie internucléaire. o Lupus • Les symptômes universels associés au lupus n’épargnent pas les yeux. La peau des paupières peuvent être atteintes de l’érythème discoïde, ces patients peuvent avoir les yeux secs (syndrome de Sjogren), et, infréquemment, ces patients peuvent aussi avoir une uvéite, une kératite, ou une épisclérite. L’atteinte vasculaire implique souvent la rétine, formant des exsudats ou des microinfarcissements. o Vasculites • Plusieurs vasculites ont une atteinte oculaire. • Un des symptômes de la vasculite de Horton, ou artérite temporale, est une perte de vision transitoire monoculaire (ou amaurose fugace). Ces patients sont à 15 à 20% de risque de cécité permanente suite à un infarcissement du nerf optique, d’une occlusion de l’artère rétinienne ou d’une de ses branches ou d’un infarcissement de la choroïde. L’atteinte ischémique des nerfs oculomoteurs ou du nerf optique à tout point dans son trajet peut causer une diplopie ou des hémianopsies. • Une constellation de signes et symptômes ophtalmologiques accompagnent la granulomatose de Wegener, comme la conjonctivite, l’ulcération cornéenne, l’épisclérite, la sclérite, l’exophtalmie et autres. • Tout clinicien se doit d’avoir un index de suspicion élevé de la maladie de Kawasaki quand un enfant de moins de 5 ans se présente avec la majorité des symptômes suivants : une fièvre de plus de 5 jours, une injection bilatérale des conjonctives, les lèvres gercées, l’érythème et une lymphadénopathie cervicale. o Arthrite • 15 à 20% des patients arthritiques auront les yeux secs suite au syndrome de Sjogren secondaire. À l’examen par lampe à fente, les patients auront une injection de la conjonctive et un épithélium cornéen dévitalisé. • 5% des patients atteints de l’arthrite rhumatoïde auront une sclérite ou une épisclérite. • Comme pour beaucoup d’autres atteintes auto-immunitaires, on peut aussi observer chez les patients arthritiques une kératite ulcérative périphérique de la cornée. o MG • La fatigabilité musculaire de la myasthénie gravis atteint aussi les muscles extraoculaires. Il y a même un sous-type de myasthénie gravis qui est limité aux muscles oculaires. Le signe le plus fréquent et le plus évident est une ptose qui s’empire progressivement au cours de la journée. Les muscles extraoculaires peuvent aussi être atteints. Cependant, la pupille est toujours épargnée dans la myasthénie. o Behcet • La maladie de Behcet est une condition inflammatoire chronique qui se manifeste principalement par des petits ulcères sur la muqueuse orale, mais aussi par plusieurs autres manifestations y inclus une atteinte oculaire. L’uvéite bilatérale sporadique est le signe prédominant, mais il est aussi possible d’avoir un hypopyon (qui est une accumulation de cellules inflammatoires dans le segment antérieur, formant un niveau blanc derrière la cornée), ou presque tout autre atteinte occulaire – comme les occlusions vasculaires, une vasculite rétinienne, une néovascularisation, des cataractes et une ulcération conjonctivale. o Crohn’s • La maladie de Crohn’s, une inflammation inappropriée de l’appareil digestif, peut aussi comporter des manifestations occulaires comme l’uvéite, l’épisclérite et la sclérite. o Sarcoïdose • ¼ des patients atteints de la sarcoïdose auront des manifestations oculaires. Ils sont à risque d’uvéite, de glaucome, des thromboses veineuses rétiniennes et autres. • Génétique o Marfan • La manifestation oculaire cardinale de la maladie de Marfan est l’ectopie lenticulaire. Le cristallin est habituellement délogé vers le haut. Les personnes atteintes du syndrome de Marfan sont aussi plus fréquemment myopes et subissent plus fréquemment des décollements rétiniens. • Insuffisance rénale o Les manifestations ophtalmologiques sont très utiles dans la maladie rénale pour indiquer l’efficacité et le besoin pour le traitement. L’urémie peut s’accompagner d’érythème conjonctival, d’une calcification des structures et d’une cécité corticale transitoire. Les cataractes peuvent être le premier signe d’insuffisance rénale. o Le syndrome d’Alport est un syndrome génétique regroupant défaillance rénale et surdité avant l’âge de 20 ans. Ces patients ont aussi diverses atteintes oculaires, comme une rétinopathie et un cristallin en forme de cône. o L’anémie falciforme peut provoquer une prolifération vasculaire sur la rétine et des stries angioïdes qui ressemblent à des vergetures sur la rétine. Les stries angioïdes peuvent aussi être trouvées dans la maladie de Paget, le syndrome de Marfan et le syndrome Ehlers-Danlos. • Atopie o La conjonctivite la plus fréquente dans la population générale est la conjonctivite allergique, qui est relativement bénigne. • Syndrome du bébé secoué o Un examen ophtalmologique doit être effectué à chaque visite sur tous les bébés. Chez un bébé sans antécédents clairs qui pourraient expliquer les signes, des trouvailles d’hémorragies rétiniennes, sous rétiniennes ou du vitré, ou des plis dans la rétine ou un œdème papillaire, augmente fortement la suspicion d’abus. Un examen complet doit ensuite être effectué et bien documenté pour poser le diagnostique du syndrome du bébé secoué. • Infectieuse o VIH • 75% des patients atteints du VIH ont des signes et symptômes oculaires. • Le VIH comme tel peut causer une rétinopathie caractérisée par des cotton wool spots, des hémoragies rétiniennes. • L’état immunodéprimé rend le patient susceptible aux infections opportunistes, comme les kératopathies, les rétinities ou les choroïdites qui peuvent être causées par un virus herpétique, le CMV, pneumocystis carinii, Candida albicans ou le toxoplasmose. • Suite à un traitement efficace aux antirétroviraux, le système immunitaire peut combattre une rétinite aux CMV, et l’inflammation peut causer une atteinte de la vision. • Le sarcome de Kaposi, un néoplasme vasculaire fortement associé à l’infection au VIH, peut s’exprimer sur la conjonctive palpébrale ou bulbaire.

The global burden of chronic kidney diseases remains an ongoing medical challenge. Therapies that can halt or reverse advanced renal injury are not yet available. Increasing numbers of patients progress to the end-stage renal failure and require renal replacement therapy, the latter being associated with significant mortality, a lower quality of life, and high costs for national health systems. Thus, new treatment strategies that slow down, halt or even revert progressive renal damage are requested. Chemokines and their receptors are involved in the pathogenesis of renal diseases. They mediate leukocytes and macrophages recruitment and activation during initiation as well as progression of renal inflammation. Infiltrating leukocytes are the major source for proinflammatory and profibrotic cytokines and are therefore critical for mediating fibroblast proliferation, differentiation into myofibroblasts, matrix production, and tubular atrophy. Recent advances in the understanding of the molecular mechanisms that regulate renal leukocyte recruitment suggest chemokines and chemokine receptors as novel targets for specific pharmacological intervention. The aim of the present thesis was to investigate the role of chemokine receptor CCR1 for the progression of chronic kidney diseases, e.g. Alport disease and diabetic nephropathy. Two different animal models were used: Col4A3-deficient mice and type 2 diabetic db/db mice with advanced diabetic nephropathy. We blocked CCR1 in Col4A3-deficient mice with BX417, a small molecule CCR1 antagonist, and BL5923, a novel orally available antagonist with a high specificity for human and murine CCR1 in uninephrectomized type 2 diabetic db/db mice, respectively. Treatment with BX471 (25mg/kg) from weeks 6 to 10 of life improved survival of COL4A3- deficient mice, characterized by glomerulosclerosis and subsequent progressive tubulointerstitial injury, leading to fatal end-stage renal disease (ESRD). Improvement was associated with less interstitial macrophages, apoptotic tubular epithelial cells, tubular atrophy, interstitial fibrosis, and less globally sclerotic glomeruli. BX471 reduced total renal Ccl5 mRNA expression by reducing the number of interstitial CCL5-positive cells in inflammatory cell infiltrates. Intravital microscopy of the cremaster muscle in male mice identified that BX471 or lack of CCR1 impaired leukocyte adhesion to activated vascular endothelium and transendothelial leukocyte migration, whereas leukocyte rolling and interstitial migration were not affected. Furthermore, in activated murine macrophages, BX471 completely blocked CCL3-induced CCL5 production. When CCR1 was blocked with BL5923 (60mg/kg, b.i.d), the interstitial recruitment of ex vivo labeled macrophages was markedly decreased in uninephrectomized male db/db mice with type 2 diabetes. Similarly, BL5923 orally administered from month 5 to 6 of life reduced the numbers of interstitial macrophages in uninephrectomized db/db mice. This was associated with reduced numbers of Ki-67 proliferating tubular epithelial and interstitial cells, tubular atrophy, and interstitial fibrosis in uninephrectomized db/db mice. Glomerular pathology and proteinuria were not affected by the CCR1 antagonist. BL5923 reduced renal mRNA expression of Ccl2, Ccr1, Ccr2, Ccr5, Tgf-β1, and collagen I-α1 when compared to untreated uninephrectomized male db/db mice of the same age. Thus, we identified a previously unrecognized role for CCR1-dependent recruitment of interstitial macrophages for the progression of chronic kidney disease in Alport disease and diabetic nephropathy. These data identify CCR1 as a potential therapeutic target for Alport disease and late stage diabetic nephropathy or other progressive nephropathies associated with interstitial macrophage infiltrates.