POPULARITY
10 episodes with Nephron
2 episodes with Nephron
4 episodes with Nephron
4 episodes with Nephron
2 episodes with Nephron
4 episodes with Nephron
2 episodes with Nephron
2 episodes with Nephron
2 episodes with Nephron
In this episode, we review the high-yield topic of The Nephron from the Renal section.FollowMedbullets on social media:Facebook: www.facebook.com/medbulletsInstagram: www.instagram.com/medbulletsofficialTwitter: www.twitter.com/medbullets
Welcome to the Sterile Technique Podcast! It's the podcast about Surgical Technology. Whether you are a CST or CSFA, this podcast helps you earn CE credits and improve your surgery skills in the OR. This episode discusses an article in the February 2025 issue of The Surgical Technologist, the official journal of the Association of Surgical Technologists (AST). The article is titled, "Nephron-Sparing Surgery for Wilms Tumor". "Scrub in" at steriletpodcast.com and on Twitter, @SterileTPodcast (twitter.com/SterileTPodcast). This podcast is a Dybas Media production. Sound effects adapted from GarageBand and sindhu.tms at https://freesound.org/people/sindhu.tms/sounds/169065/ and licensed courtesy of https://creativecommons.org/licenses/by-nc/3.0/.
Massenresorption der Propheten - Die Reise durch die Niere geht weiter! Nun wollen wir den in der letzten Folge filtrierten Primärharn wieder resorbieren - zumindest Teile davon. Wieso das denn nun? Naja es sollen nun doch nicht alle der wertvollen Salze in der Schüssel langen. Wie wir nun die Massen der Propheten zurückgewinnen... Hört rein! Euer Duy, Tim und Leo Anzeige: Hier der Link zu Meditricks: https://www.meditricks.de Rabattcode: SitusInversus15 Instagram: https://www.instagram.com/der_vorklinikpodcast/ Website: Situs Inversus (dervorklinikpodcast.de) Kapitel: (00:00) - Überblick und Einteilung des Nephrons (07:17) - proximales Nephron (21:19) - Henleschleife (24:34) - distales Nephron (30:37) - einzelne Substanzen Für die Inhalte in diesem Podcast übernehmen wir keine Gewähr. Der Podcast kann den Besuch von Vorlesungen nicht ersetzen. Wir empfehlen das Studium von einschlägiger Fachliteratur über den Inhalt des Podcasts hinaus.
Kaue, Ingrid e Luísa conversam sobre os riscos da hipocalemia e como fazer reposição de potássio: classificação da hipocalemia, quais os riscos, reposição enteral, reposição venosa e quando usar diuréticos poupadores de potássio, tudo neste episódio. Referências: Ferreira JP, Butler J, Rossignol P, et al. Abnormalities of Potassium in Heart Failure: JACC State-of-the-Art Review. J Am Coll Cardiol. 2020;75(22):2836-2850. doi:10.1016/j.jacc.2020.04.021 Kim GH, Han JS. Therapeutic approach to hypokalemia. Nephron. 2002;92 Suppl 1:28-32. doi:10.1159/000065374 Cohn JN, Kowey PR, Whelton PK, Prisant LM. New guidelines for potassium replacement in clinical practice: a contemporary review by the National Council on Potassium in Clinical Practice. Arch Intern Med. 2000;160(16):2429-2436. doi:10.1001/archinte.160.16.2429 Kim MJ, Valerio C, Knobloch GK. Potassium Disorders: Hypokalemia and Hyperkalemia. Am Fam Physician. 2023;107(1):59-70. Asmar A, Mohandas R, Wingo CS. A physiologic-based approach to the treatment of a patient with hypokalemia. Am J Kidney Dis. 2012;60(3):492-497. doi:10.1053/j.ajkd.2012.01.031 Grobbee DE, Hoes AW. Non-potassium-sparing diuretics and risk of sudden cardiac death. J Hypertens. 1995;13(12 Pt 2):1539-1545. Ferreira JP, Butler J, Rossignol P, et al. Abnormalities of Potassium in Heart Failure: JACC State-of-the-Art Review. J Am Coll Cardiol. 2020;75(22):2836-2850. doi:10.1016/j.jacc.2020.04.021 Goyal A, Spertus JA, Gosch K, et al. Serum Potassium Levels and Mortality in Acute Myocardial Infarction. JAMA. 2012;307(2):157–164. doi:10.1001/jama.2011.1967 Macdonald JE, Struthers AD. What is the optimal serum potassium level in cardiovascular patients?. J Am Coll Cardiol. 2004;43(2):155-161. doi:10.1016/j.jacc.2003.06.021
Guest: Mark Haas, MD Kidney biopsy is the gold standard for the diagnosis of immunoglobin A (IgA) nephropathy and complement 3 glomerulopathy (C3G),1,2 and the accurate interpretation of kidney biopsy findings is important not only for diagnosis but also guiding clinical management of these conditions. Learn more about what the diagnostic process and findings for IgA nephropathy and C3G look like with Dr Mark Haas, a renal pathologist at Cedars-Sinai Medical Center in Los Angeles. References: Mehdi A, Taliercio JJ. Cleve Clin J Med. 2023;90(6)(suppl 1):e1-e4. doi:10.3949/ccjm.90.e-s1.02 Caravaca-Fontán F, Lucientes L, Cavero T, Praga M. Nephron. 2020;144(6):272-280. doi:10.1159/000507254 319698 12/23
Guest: Mark Haas, MD Kidney biopsy is the gold standard for the diagnosis of immunoglobin A (IgA) nephropathy and complement 3 glomerulopathy (C3G),1,2 and the accurate interpretation of kidney biopsy findings is important not only for diagnosis but also guiding clinical management of these conditions. Learn more about what the diagnostic process and findings for IgA nephropathy and C3G look like with Dr Mark Haas, a renal pathologist at Cedars-Sinai Medical Center in Los Angeles. References: Mehdi A, Taliercio JJ. Cleve Clin J Med. 2023;90(6)(suppl 1):e1-e4. doi:10.3949/ccjm.90.e-s1.02 Caravaca-Fontán F, Lucientes L, Cavero T, Praga M. Nephron. 2020;144(6):272-280. doi:10.1159/000507254 319698 12/23
Welcome to the Instant Trivia podcast episode 1048, where we ask the best trivia on the Internet. Round 1. Category: The Company Line 1: In 1963, live on "The Art Linkletter Show", this company served its billionth burger. McDonald's. 2: This housewares store was named for the packaging its merchandise came in and was first displayed on. Crate and Barrel. 3: This company's Accutron watch, introduced in 1960, had a guarantee of accuracy to within one minute a month. Bulova. 4: Edward Teller and this man partnered in 1898 to sell high fashions to women. (Paul) Bonwit. 5: The Kirschner brothers, Don and Bill, named this ski company for themselves and the second-highest mountain. K2. Round 2. Category: Name That Body Part 1: Dentine,Pulp,Crown. Tooth. 2: Calcaneus,Plantar arch, Sole. Foot. 3: Parietal lobe,Thalamus,Cerebellum. Brain. 4: Phagocytes,Alveoli,Bronchioles. Lungs. 5: Glomeruli,Nephron,Renal cortex. Kidney. Round 3. Category: Sports Halls Of Fame 1: A museum and hall of fame for this sport in Huntington Beach, Calif. includes a shrine to Duke Kahanamoku. surfing. 2: The Basketball Hall of Fame in Springfield, Massachusetts bears the name of this inventor of the game. (James) Naismith. 3: The original of this trophy, a silver bowl, is on permanent display at the Hockey Hall of Fame in Toronto. the Stanley Cup. 4: 1960s inductees into this hall of fame include Don Budge, Alice Marble and Brooke Shields' grandfather Frank Shields. the Tennis Hall of Fame. 5: Start your engines please and head to this Alabama city to visit the Motorsports Hall of Fame. Talladega. Round 4. Category: The 2011 Emmys 1: Emmy has spoken: he won his fourth straight award as Best Reality Host and we can tell you for sure that he knows how to rock and roll. (Jeff) Probst. 2: Guy Pearce won an acting Emmy for playing Monty in this HBO miniseries. Mildred Pierce. 3: With clear eyes and a full heart, Kyle Chandler couldn't lose Lead Actor in a Drama for this show. Friday Night Lights. 4: After joining her fellow nominees onstage, Melissa McCarthy won for this double "M" sitcom. Mike and Molly. 5: This best director was a raging bull in an Emmy shop for his work on "Boardwalk Empire". Martin Scorsese. Round 5. Category: Oscar 1: This film about a family of superheroes beat out "Shrek 2" and "Shark Tale" as 2004's Best Animated Feature. The Incredibles. 2: (Al Gore delivers the clue.) This film about my campaign to recognize climate change as a worldwide problem won the Oscar in 2006 for Best Documentary Feature. An Inconvenient Truth. 3: Michael Douglas won for producing this 1975 film that swept all 5 major Oscar categories. One Flew Over the Cuckoo's Nest. 4: 1980's Best Picture nominees included 2 black and white films: "The Elephant Man" and this boxing film. Raging Bull. 5: She received 2 1982 acting Oscar nominations, both for playing actresses--a soap star and a '40s film star. Jessica Lange. Thanks for listening! Come back tomorrow for more exciting trivia!Special thanks to https://blog.feedspot.com/trivia_podcasts/ AI Voices used
Because studies predict one in nine Americans will face some level of disease of the kidney, understanding kidney development and nephron function is key. buy furosemide online buy furosemide over the counter online pharmacy Professor Lori O'Brien discusses her research into kidney processes, describing How kidney development progresses in utero and what are the two main type of progenitor cells, What are the stages of kidney disease and how effective are dialysis and kidney transplantation, and What are challenges to kidney organoid development such as how to rid the organoid of filtrate. Lori O'Brien is a principal investigator and assistant professor in the Department of Cell Biology and Physiology at the University of North Carolina Kidney Center. buy amoxil online online pharmacy In this podcast, she discusses the focus of her work, namely to understand the development of a kidney to better understand what goes wrong in kidney disease. This work informs efforts to eventually manufacture a renal replacement, and she explains that scientists need to understand its basic biology as much as possible to do so. She also explains the damage of kidney disease as well as the mistaken notion that dialysis treatment is somehow a cure. Rather, on average, most dialysis patients will only survive about five years because dialysis treatment only mimics about 10% of what a kidney actually does for the body. She then describes her work more specifically around pluripotent stem cells that lead to the two different cell populations in the kidney: cells that eventually make nephrons and those that make up the connecting duct system. buy wellbutrin online buy wellbutrin over the counter online pharmacy She describes challenges to each cell type, the complex specialization of the cell types, and how they work in the body along with the vascular and nerve network in a way that's hard to reproduce with organoids. She describes some advances therein and various ways they hope to problem solve. For more, see her UNC website at med.unc.edu/cellbiophysio/directory/lori-obrien-phd/, and her lab's website at obrienlab.web.unc.edu. Available on Apple Podcasts: apple.co/2Os0myK
Welcome to the Instant Trivia podcast episode 895, where we ask the best trivia on the Internet. Round 1. Category: the 4th 1: The 4th Gospel of the New Testament. John. 2: The 4th dimension according to the theory of relativity. time. 3: The 4th letter of the Greek alphabet. delta. 4: The 4th oldest college in the United States, it's found in New Jersey. Princeton. 5: The 4th most populous country in the world, it follows China, India and the U.S.. Indonesia. Round 2. Category: at the "y" 1: When this song title American stuck a feather in his hat, he called it Macaroni. Yankee Doodle. 2: This type of boat's name is from a word meaning "hunting ship" and will take up your whole driveway if you park it there. yacht. 3: The jumble sale held in an English garden would be called one of these in an American suburb. yard sale. 4: The 1945 conference in this Crimean city determined that a defeated Germany would be divided into 4 zones. Yalta. 5: Incorporated as a city in 1970, this city is the capital of Canada's vast Northwest Territories. Yellowknife. Round 3. Category: classic ads and slogans 1: "Look Ma, No Cavities". Crest. 2: "I Can't Believe I Ate the Whole Thing". Alka-Seltzer. 3: It's "Two--Two--Two Mints in One". Certs. 4: "They Plump When You Cook 'Em". Ball Park Franks. 5: "We'll Leave the Light on for You". Motel 6. Round 4. Category: famous halls 1: Founding brothers Joyce, Rollie and William Hall put their stamp on this greeting card company. Hallmark. 2: Time was on Jerry Hall's side in 1990 as she married this singer after a long romance. Mick Jagger. 3: In 1987 she testified to altering and shredding documents for her boss Oliver North. Fawn Hall. 4: As head of the National Theatre, Peter Hall oversaw its 1976 move out of this "old" home. the Old Vic. 5: The 1995 movie "Kids" was written by the grandson of Huntz Hall, one of these tough movie kids. the Bowery Boys (or the Dead End Kids or the East Side Kids). Round 5. Category: name that body part 1: Dentine,Pulp,Crown. Tooth. 2: Calcaneus,Plantar arch, Sole. Foot. 3: Parietal lobe,Thalamus,Cerebellum. Brain. 4: Phagocytes,Alveoli,Bronchioles. Lungs. 5: Glomeruli,Nephron,Renal cortex. Kidney. Thanks for listening! Come back tomorrow for more exciting trivia! Special thanks to https://blog.feedspot.com/trivia_podcasts/
"...chronic kidney disease or chronic renal failure is a progressive irreversible condition characterized by either a reduction in kidney function or kidney damage as a result of any cause that a present for more than 3 months it is divided into stages based on the glomerular filtration rate which is a measure of how well the kidneys are functioning it shows the flow rate of filtrate through the glomerulus of the Nephron into the Bowman's capsule and ultimately through the renal tubules the stages are labeled 1 to 5 with 2 groups in stage 3 the definition of a reduced GFR is below 60 milliliters per minute but in groups 1 and 2 the GFR may actually be above 60 but there is evidence of kidney damage end-stage renal disease is classed as a GF are below 15 or the need for renal replacement therapy like dialysis or renal transplant kidney damage can be defined as signs of damage seen on Imaging or on testing such as a high albumin to creatinine ratio which is a measurement of the amount of protein lost in the urine in fact in combination with GFR these patients are divided into three food groups based on the albumin creatinine ratio with higher values indicating more damage and an increased likelihood of progression initially chronic kidney disease may not cause many problems and it is often asymptomatic however as it progresses it brings with it several significant complications these can include an elevated cardiovascular risk with patients are 5 to 10 times more likely to die from cardiovascular disease than end-stage renal disease the risk of stroke has been found to increase as the GFR lowers around seven percent for every 10 ml per minute lost this may also be the result of CKD contributing to hypertension as well as being caused by it this can be due to activation of the renin-angiotensin-aldosterone system and can also be because as the disease progresses the kidney is less able to excrete leading to retention and subsequent fluid overload signs of fluid overload could be dismissed near due to pulmonary edema or a fusion and peripheral edema or ascites anemia is also common which contributes to disappear and can come from a reduction in erythropoietin from the..." Learn more about your ad choices. Visit megaphone.fm/adchoices
Nephrotic syndrome is a collection of signs and symptoms that result from damage to the kidneys and is often confused with nephritic syndrome in fatigue syndrome there is a substantial amount of protein being lost through the kidneys in the urine defined as more than 3.5 grams per day this leads to hypoalbuminemia a low level of albumin in the blood as albumin is the most abundant protein normally in the blood these two are defining features in nephrotic syndrome nephritic syndrome is different in that there is less proteinuria but also the presence of hematuria and red blood cell or white blood cell casts in the urine hypertension and oliguria which is a reduced urine output typically between 80 and 400 ml per day the unit of the kidney is the nephron and normally in the glomerulus of the Nephron there is a specialized membrane that forms the filter made up of a fenestrated endothelium the Maryland basement membrane and the foot processes of podocytes which are cells that wrap around the capillary giving this additional filtration layer all together these structures normally act as a filter and prevent large molecules from passing through into the Bowman's capsule and renal tubules they have a net negative charge which may mean that they can repel other negatively charged molecules albumin is negatively charged in the fatigue syndrome there is sufficient injury to these structures to change the permeability and allow albumin and other molecules to pass into the urine leading to hypoalbuminemia the signs and symptoms linked to hypoalbuminemia which includes peripheral edema and fluid overload particularly in children this can be evident as facial swelling but can also occur in adults particularly around the eyes fluid overload can mean weight gain peripheral edema and even the development of ascites or pleural effusion which can manifest as shortness of breath known as this near the reduction in the blood levels of albumin causes the oncotic pressure of the blood 24 meaning fluid will more readily leak into the surrounding tissues causing edema this is sensed as hypovolemia because less fluid is in the vessels which then triggers the renin-angiotensin-aldosterone system causing retention of salt and water this is known as the underfill hypothesis while another is the Learn more about your ad choices. Visit megaphone.fm/adchoices
a sudden deterioration in the function of the kidneys is known as an acute kidney injury sometimes also called acute renal failure to measure this reduction in kidney function glomerular filtration rate or GFR is normally used which is a measurement of how well the kidneys are filtering the blood the functional unit of the kidney that actually does this is the Nephron made up of the glomerulus which is a modified capillary and as blood passes through it the waste is filtered into the Bowman's capsule GFR is the volume filtered through the glomerulus into the Bowman's capsule and through the Nephron in a given unit of time the filtrate passes along through the proximal convoluted tubule Loop of henle distal convoluted tubule and the distal collecting duct undergoing secretion and reabsorptionas it travels ultimately it forms urine and collects into the renal pelvis and passes into the bladder through the ureter to directly measure this process is difficult we instead use creatinine clearance to estimate the GFR creatinine is a normal breakdown product of creatine released from muscle tissue and this is freely filtered by the glomerulus and is not reabsorbed so fits the kind of substance we need however creatinine is secreted into the filtrate by the peritubular capillaries so it does tend to overestimate the GFR slightly the cockcroft and Gault formula is a famous formula used to estimate the creatinine clearance and therefore GF are taking into account age Mass gender and the serum creatinine as it travels ultimately it forms urine and collects into the renal pelvis and passes into the bladder through the ureter to directly measure this process is difficult we instead use creatinine clearance to estimate the GFR creatinine is a normal breakdown product of creatine released from muscle tissue and this is freely filtered by the glomerulus and is not reabsorbed so fits the kind of substance we need however creatinine is secreted into the filtrate by the peritubular capillaries so it does tend to overestimate the GFR slightly the cockcroft and Gault formula is a famous formula used to estimate the creatinine clearance and therefore GF are taking into account age Mass gender and the serum creatinine Learn more about your ad choices. Visit megaphone.fm/adchoices
a sudden deterioration in the function of the kidneys is known as an acute kidney injury sometimes also called acute renal failure to measure this reduction in kidney function glomerular filtration rate or GFR is normally used which is a measurement of how well the kidneys are filtering the blood the functional unit of the kidney that actually does this is the Nephron made up of the glomerulus which is a modified capillary and as blood passes through it the waste is filtered into the Bowman's capsule GFR is the volume filtered through the glomerulus into the Bowman's capsule and through the Nephron in a given unit of time the filtrate passes along through the proximal convoluted tubule Loop of henle distal convoluted tubule and the distal collecting duct undergoing secretion and reabsorptionas it travels ultimately it forms urine and collects into the renal pelvis and passes into the bladder through the ureter to directly measure this process is difficult we instead use creatinine clearance to estimate the GFR creatinine is a normal breakdown product of creatine released from muscle tissue and this is freely filtered by the glomerulus and is not reabsorbed so fits the kind of substance we need however creatinine is secreted into the filtrate by the peritubular capillaries so it does tend to overestimate the GFR slightly the cockcroft and Gault formula is a famous formula used to estimate the creatinine clearance and therefore GF are taking into account age Mass gender and the serum creatinine as it travels ultimately it forms urine and collects into the renal pelvis and passes into the bladder through the ureter to directly measure this process is difficult we instead use creatinine clearance to estimate the GFR creatinine is a normal breakdown product of creatine released from muscle tissue and this is freely filtered by the glomerulus and is not reabsorbed so fits the kind of substance we need however creatinine is secreted into the filtrate by the peritubular capillaries so it does tend to overestimate the GFR slightly the cockcroft and Gault formula is a famous formula used to estimate the creatinine clearance and therefore GF are taking into account age Mass gender and the serum creatinine Learn more about your ad choices. Visit megaphone.fm/adchoices
a sudden deterioration in the function of the kidneys is known as an acute kidney injury sometimes also called acute renal failure to measure this reduction in kidney function glomerular filtration rate or GFR is normally used which is a measurement of how well the kidneys are filtering the blood the functional unit of the kidney that actually does this is the Nephron made up of the glomerulus which is a modified capillary and as blood passes through it the waste is filtered into the Bowman's capsule GFR is the volume filtered through the glomerulus into the Bowman's capsule and through the Nephron in a given unit of time the filtrate passes along through the proximal convoluted tubule Loop of henle distal convoluted tubule and the distal collecting duct undergoing secretion and reabsorptionas it travels ultimately it forms urine and collects into the renal pelvis and passes into the bladder through the ureter to directly measure this process is difficult we instead use creatinine clearance to estimate the GFR creatinine is a normal breakdown product of creatine released from muscle tissue and this is freely filtered by the glomerulus and is not reabsorbed so fits the kind of substance we need however creatinine is secreted into the filtrate by the peritubular capillaries so it does tend to overestimate the GFR slightly the cockcroft and Gault formula is a famous formula used to estimate the creatinine clearance and therefore GF are taking into account age Mass gender and the serum creatinine as it travels ultimately it forms urine and collects into the renal pelvis and passes into the bladder through the ureter to directly measure this process is difficult we instead use creatinine clearance to estimate the GFR creatinine is a normal breakdown product of creatine released from muscle tissue and this is freely filtered by the glomerulus and is not reabsorbed so fits the kind of substance we need however creatinine is secreted into the filtrate by the peritubular capillaries so it does tend to overestimate the GFR slightly the cockcroft and Gault formula is a famous formula used to estimate the creatinine clearance and therefore GF are taking into account age Mass gender and the serum creatinine Learn more about your ad choices. Visit megaphone.fm/adchoices
Nephrotic syndrome is a collection of signs and symptoms that result from damage to the kidneys and is often confused with nephritic syndrome in fatigue syndrome there is a substantial amount of protein being lost through the kidneys in the urine defined as more than 3.5 grams per day this leads to hypoalbuminemia a low level of albumin in the blood as albumin is the most abundant protein normally in the blood these two are defining features in nephrotic syndrome nephritic syndrome is different in that there is less proteinuria but also the presence of hematuria and red blood cell or white blood cell casts in the urine hypertension and oliguria which is a reduced urine output typically between 80 and 400 ml per day the unit of the kidney is the nephron and normally in the glomerulus of the Nephron there is a specialized membrane that forms the filter made up of a fenestrated endothelium the Maryland basement membrane and the foot processes of podocytes which are cells that wrap around the capillary giving this additional filtration layer all together these structures normally act as a filter and prevent large molecules from passing through into the Bowman's capsule and renal tubules they have a net negative charge which may mean that they can repel other negatively charged molecules albumin is negatively charged in the fatigue syndrome there is sufficient injury to these structures to change the permeability and allow albumin and other molecules to pass into the urine leading to hypoalbuminemia the signs and symptoms linked to hypoalbuminemia which includes peripheral edema and fluid overload particularly in children this can be evident as facial swelling but can also occur in adults particularly around the eyes fluid overload can mean weight gain peripheral edema and even the development of ascites or pleural effusion which can manifest as shortness of breath known as this near the reduction in the blood levels of albumin causes the oncotic pressure of the blood 24 meaning fluid will more readily leak into the surrounding tissues causing edema this is sensed as hypovolemia because less fluid is in the vessels which then triggers the renin-angiotensin-aldosterone system causing retention of salt and water this is known as the underfill hypothesis while another is the Learn more about your ad choices. Visit megaphone.fm/adchoices
Nephrotic syndrome is a collection of signs and symptoms that result from damage to the kidneys and is often confused with nephritic syndrome in fatigue syndrome there is a substantial amount of protein being lost through the kidneys in the urine defined as more than 3.5 grams per day this leads to hypoalbuminemia a low level of albumin in the blood as albumin is the most abundant protein normally in the blood these two are defining features in nephrotic syndrome nephritic syndrome is different in that there is less proteinuria but also the presence of hematuria and red blood cell or white blood cell casts in the urine hypertension and oliguria which is a reduced urine output typically between 80 and 400 ml per day the unit of the kidney is the nephron and normally in the glomerulus of the Nephron there is a specialized membrane that forms the filter made up of a fenestrated endothelium the Maryland basement membrane and the foot processes of podocytes which are cells that wrap around the capillary giving this additional filtration layer all together these structures normally act as a filter and prevent large molecules from passing through into the Bowman's capsule and renal tubules they have a net negative charge which may mean that they can repel other negatively charged molecules albumin is negatively charged in the fatigue syndrome there is sufficient injury to these structures to change the permeability and allow albumin and other molecules to pass into the urine leading to hypoalbuminemia the signs and symptoms linked to hypoalbuminemia which includes peripheral edema and fluid overload particularly in children this can be evident as facial swelling but can also occur in adults particularly around the eyes fluid overload can mean weight gain peripheral edema and even the development of ascites or pleural effusion which can manifest as shortness of breath known as this near the reduction in the blood levels of albumin causes the oncotic pressure of the blood 24 meaning fluid will more readily leak into the surrounding tissues causing edema this is sensed as hypovolemia because less fluid is in the vessels which then triggers the renin-angiotensin-aldosterone system causing retention of salt and water this is known as the underfill hypothesis while another is the Learn more about your ad choices. Visit megaphone.fm/adchoices
"...chronic kidney disease or chronic renal failure is a progressive irreversible condition characterized by either a reduction in kidney function or kidney damage as a result of any cause that a present for more than 3 months it is divided into stages based on the glomerular filtration rate which is a measure of how well the kidneys are functioning it shows the flow rate of filtrate through the glomerulus of the Nephron into the Bowman's capsule and ultimately through the renal tubules the stages are labeled 1 to 5 with 2 groups in stage 3 the definition of a reduced GFR is below 60 milliliters per minute but in groups 1 and 2 the GFR may actually be above 60 but there is evidence of kidney damage end-stage renal disease is classed as a GF are below 15 or the need for renal replacement therapy like dialysis or renal transplant kidney damage can be defined as signs of damage seen on Imaging or on testing such as a high albumin to creatinine ratio which is a measurement of the amount of protein lost in the urine in fact in combination with GFR these patients are divided into three food groups based on the albumin creatinine ratio with higher values indicating more damage and an increased likelihood of progression initially chronic kidney disease may not cause many problems and it is often asymptomatic however as it progresses it brings with it several significant complications these can include an elevated cardiovascular risk with patients are 5 to 10 times more likely to die from cardiovascular disease than end-stage renal disease the risk of stroke has been found to increase as the GFR lowers around seven percent for every 10 ml per minute lost this may also be the result of CKD contributing to hypertension as well as being caused by it this can be due to activation of the renin-angiotensin-aldosterone system and can also be because as the disease progresses the kidney is less able to excrete leading to retention and subsequent fluid overload signs of fluid overload could be dismissed near due to pulmonary edema or a fusion and peripheral edema or ascites anemia is also common which contributes to disappear and can come from a reduction in erythropoietin from the..." Learn more about your ad choices. Visit megaphone.fm/adchoices
"...nephritic syndrome is a collection of signs and symptoms that result from glomerulonephritis which is inflammation of the kidney specifically the glomerulus this could be remembered because it means inflammation rather than being a disease itself nephritic syndrome is the manifestation of an underlying disease that causes the inflammation and there are many of these causes it is easily confused with nephrotic syndrome which instead is a collection of signs and symptoms resulting from a high amount of protein being lost through the kidneys in the urine this leads to hypoalbuminemia meaning low levels of albumin in the blood these are the two defining features in nephrotic syndrome there is some overlap but nephritic syndrome is different in that the degree of proteinuria is lower and there is the dozens of hematuria meaning blood in the urine which could be microscopic or macroscopic red blood cell casts in the urine sterile / urea which is the presence of white blood cells without evidence of bacteria hypertension and oliguria which is a reduced urine output typically between 80 and 400 ml per day the functional unit of the kidney is the Nephron which includes the glomerulus and modified capillary surrounding this there are multiple layers which together form a filter these include a fenestrated endothelium the glomerular basement membrane and the foot processes of podocytes which are cells that wrap around the capillary in most cases of nephritic syndrome there is a trigger causing inflammation in this area overall featuring cellular proliferation complement activation recruitment of leukocytes and production of proteases and free radicals that ultimately lead to injury of the kidney this then leads to the characteristic features for example injury to the glomerular filtration membrane allows protein to leak into the urine though not as much as is seen in nephrotic syndrome red blood cells can also pass through causing hematuria and they can be dysmorphic with a camping sites in particular suggesting glomerular injury red blood cells can also Clump together within the tubules forming cylindrical structures called castes in fact this is considered suggestive of glomerulonephritis the injury and inflammation means white blood cells are recruited and can pass into the urine and as we said it's termed sterile pyuria because there..." Learn more about your ad choices. Visit megaphone.fm/adchoices
"...chronic kidney disease or chronic renal failure is a progressive irreversible condition characterized by either a reduction in kidney function or kidney damage as a result of any cause that a present for more than 3 months it is divided into stages based on the glomerular filtration rate which is a measure of how well the kidneys are functioning it shows the flow rate of filtrate through the glomerulus of the Nephron into the Bowman's capsule and ultimately through the renal tubules the stages are labeled 1 to 5 with 2 groups in stage 3 the definition of a reduced GFR is below 60 milliliters per minute but in groups 1 and 2 the GFR may actually be above 60 but there is evidence of kidney damage end-stage renal disease is classed as a GF are below 15 or the need for renal replacement therapy like dialysis or renal transplant kidney damage can be defined as signs of damage seen on Imaging or on testing such as a high albumin to creatinine ratio which is a measurement of the amount of protein lost in the urine in fact in combination with GFR these patients are divided into three food groups based on the albumin creatinine ratio with higher values indicating more damage and an increased likelihood of progression initially chronic kidney disease may not cause many problems and it is often asymptomatic however as it progresses it brings with it several significant complications these can include an elevated cardiovascular risk with patients are 5 to 10 times more likely to die from cardiovascular disease than end-stage renal disease the risk of stroke has been found to increase as the GFR lowers around seven percent for every 10 ml per minute lost this may also be the result of CKD contributing to hypertension as well as being caused by it this can be due to activation of the renin-angiotensin-aldosterone system and can also be because as the disease progresses the kidney is less able to excrete leading to retention and subsequent fluid overload signs of fluid overload could be dismissed near due to pulmonary edema or a fusion and peripheral edema or ascites anemia is also common which contributes to disappear and can come from a reduction in erythropoietin from the..." Learn more about your ad choices. Visit megaphone.fm/adchoices
"...nephritic syndrome is a collection of signs and symptoms that result from glomerulonephritis which is inflammation of the kidney specifically the glomerulus this could be remembered because it means inflammation rather than being a disease itself nephritic syndrome is the manifestation of an underlying disease that causes the inflammation and there are many of these causes it is easily confused with nephrotic syndrome which instead is a collection of signs and symptoms resulting from a high amount of protein being lost through the kidneys in the urine this leads to hypoalbuminemia meaning low levels of albumin in the blood these are the two defining features in nephrotic syndrome there is some overlap but nephritic syndrome is different in that the degree of proteinuria is lower and there is the dozens of hematuria meaning blood in the urine which could be microscopic or macroscopic red blood cell casts in the urine sterile / urea which is the presence of white blood cells without evidence of bacteria hypertension and oliguria which is a reduced urine output typically between 80 and 400 ml per day the functional unit of the kidney is the Nephron which includes the glomerulus and modified capillary surrounding this there are multiple layers which together form a filter these include a fenestrated endothelium the glomerular basement membrane and the foot processes of podocytes which are cells that wrap around the capillary in most cases of nephritic syndrome there is a trigger causing inflammation in this area overall featuring cellular proliferation complement activation recruitment of leukocytes and production of proteases and free radicals that ultimately lead to injury of the kidney this then leads to the characteristic features for example injury to the glomerular filtration membrane allows protein to leak into the urine though not as much as is seen in nephrotic syndrome red blood cells can also pass through causing hematuria and they can be dysmorphic with a camping sites in particular suggesting glomerular injury red blood cells can also Clump together within the tubules forming cylindrical structures called castes in fact this is considered suggestive of glomerulonephritis the injury and inflammation means white blood cells are recruited and can pass into the urine and as we said it's termed sterile pyuria because there..." Learn more about your ad choices. Visit megaphone.fm/adchoices
"...nephritic syndrome is a collection of signs and symptoms that result from glomerulonephritis which is inflammation of the kidney specifically the glomerulus this could be remembered because it means inflammation rather than being a disease itself nephritic syndrome is the manifestation of an underlying disease that causes the inflammation and there are many of these causes it is easily confused with nephrotic syndrome which instead is a collection of signs and symptoms resulting from a high amount of protein being lost through the kidneys in the urine this leads to hypoalbuminemia meaning low levels of albumin in the blood these are the two defining features in nephrotic syndrome there is some overlap but nephritic syndrome is different in that the degree of proteinuria is lower and there is the dozens of hematuria meaning blood in the urine which could be microscopic or macroscopic red blood cell casts in the urine sterile / urea which is the presence of white blood cells without evidence of bacteria hypertension and oliguria which is a reduced urine output typically between 80 and 400 ml per day the functional unit of the kidney is the Nephron which includes the glomerulus and modified capillary surrounding this there are multiple layers which together form a filter these include a fenestrated endothelium the glomerular basement membrane and the foot processes of podocytes which are cells that wrap around the capillary in most cases of nephritic syndrome there is a trigger causing inflammation in this area overall featuring cellular proliferation complement activation recruitment of leukocytes and production of proteases and free radicals that ultimately lead to injury of the kidney this then leads to the characteristic features for example injury to the glomerular filtration membrane allows protein to leak into the urine though not as much as is seen in nephrotic syndrome red blood cells can also pass through causing hematuria and they can be dysmorphic with a camping sites in particular suggesting glomerular injury red blood cells can also Clump together within the tubules forming cylindrical structures called castes in fact this is considered suggestive of glomerulonephritis the injury and inflammation means white blood cells are recruited and can pass into the urine and as we said it's termed sterile pyuria because there..." Learn more about your ad choices. Visit megaphone.fm/adchoices
Coming to you from SCBIO's 2023 annual conference, Matthew and Heather chat with Lou Kennedy, the Owner and CEO of Nephron Pharmaceuticals and a champion of the life sciences industry in South Carolina! We dive into the expanding life sciences opportunities in the state, engaging young people in the industry, and more. You don't want to miss this exciting conversation with a trailblazing force in the industry - Tune in now!
Nephron is someone endowed with music. He's also an instrumentalist at church. He started playing piano when He was young. He discovered the singing talent at church when he was given the opportunity to sing in the absence of the church singer.
Ein riesiger Energieaufwand und ein toller technischer Trick! Dein Körper ist eine Meisterleistung! Pflege ihn!
While FSGS was once thought to be a single disease entity, it is now understood to be a pattern of injury caused by diverse mechanisms, but classifying FSGS accurately can be challenging. In this episode, we provide an overview of these classifications and risk factors that can help stratify disease progression risk and assist with determining management approaches. To help understand how we can most effectively and accurately classify FSGS, we are joined by Professor An De Vriese, who is head of the Division of Nephrology and Infectious Disease at the AZ Sint-Jan hospital in Bruges, Belgium. By completing this activity you can qualify for 0.25 CME credits. To claim your credits, you must listen to the podcast and successfully pass the post-module assessment at nephrology.knowledgeintopractice.com, where you can find all past episodes of the podcast as well as other free CME resources. References: 1. De Vriese AS et al. Differentiating primary, genetic, and secondary FSGS in adults: A clinicopathologic approach. J Am Soc Nephrol 2018;29(3):759-774. 2. KDIGO 2021 Clinical Practice Guideline for the Management of Glomerular Diseases. Kidney Int 2021;100(4S):S1–S276. 3. Jacobs-Cachá C et al. Challenges in primary focal segmental glomerulosclerosis diagnosis: from the diagnostic algorithm to novel biomarkers. Clin Kidney J 2020;14(2):482-491. 4. Friedman DJ & Pollak MR. APOL1 nephropathy: From genetics to clinical applications. CJASN, 2021;16(2):294-303. 5. Zee J et al. APOL1 genotype-associated morphologic changes among patients with focal segmental glomerulosclerosis. Pediatric Nephrology. 2021;36(9):2747-2757. 6. Shabaka A et al. Focal segmental glomerulosclerosis: State-of-the-art and clinical perspective. Nephron 2020;144(9):413-427. Disclosures: Prof. An De Vriese has no disclosures to announce. Liberum IME staff, ACHL staff and others involved with the planning, development, and review of the content for this activity have no relevant affiliations or financial relationships to disclose. The Academy for Continued Healthcare Learning (ACHL) requires that the faculty participating in an accredited continuing education activity disclose all affiliations or other financial relationships (1) with the manufacturers of any commercial product(s) and/or provider(s) of commercial services discussed in an educational presentation and (2) with any commercial supporters of the activity. All conflicts of interest have been mitigated prior to this activity. Funding: This independent educational activity is supported by an educational grant from Travere Therapeutics. The educational content has been developed by Liberum IME in conjunction with an independent steering committee; Travere Therapeutics has had no influence on the content of this education.
In this podcast, Dr. Kim Thielen, a nephrologist/kidney specialist with Minnesota Kidney Specialists joins us today to continue part 2 of our discussion on acute kidney injury, as we wade further "into the weeds" discuss intrinsic renal disease. This episode will break down hallmark urinary findings and further subdivide intrinsic concerns into bland, nephrotic and nephritic, various causes, and treatment. Enjoy the podcast! Objectives: Upon completion of this podcast, participants should be able to: State the 3 types of urinary analysis findings related to instrinic acute kidney injury. Describe etiology of presentation of each type of intrinsic acute kidney injury. CME credit is only offered to Ridgeview Providers & Allied Health Staff for this podcast activity. Complete and submit the online evaluation form, after viewing the activity. Upon successful completion of the evaluation, you will be e-mailed a certificate of completion within approximately 2 weeks. You may contact the accredited provider with questions regarding this program at rmccredentialing@ridgeviewmedical.org. To receive continuing education credit for this activity - click the link below, to complete the activity's evaluation. CME Evaluation (**If you are listening to the podcasts through iTunes on your laptop or desktop, it is not possible to link directly with the CME Evaluation for unclear reasons. We are trying to remedy this. You can, however, link to the survey through the Podcasts app on your Apple and other smart devices, as well as through Spotify, Stitcher and other podcast directory apps and on your computer browser at these websites. We apologize for the inconvenience.) DISCLOSURE ANNOUNCEMENT The information provided through this and all Ridgeview podcasts as well as any and all accompanying files, images, videos and documents is/are for CME/CE and other institutional learning and communication purposes only and is/are not meant to substitute for the independent medical judgment of a physician, healthcare provider or other healthcare personnel relative to diagnostic and treatment options of a specific patient's medical condition; and are property/rights of Ridgeview Medical Center & Clinics. Any re-reproduction of any of the materials presented would be infringement of copyright laws. It is Ridgeview's intent that any potential conflict should be identified openly so that the listeners may form their own judgments about the presentation with the full disclosure of the facts. It is not assumed any potential conflicts will have an adverse impact on these presentations. It remains for the audience to determine whether the speaker's outside interest may reflect a possible bias, either the exposition or the conclusions presented. Ridgeview's CME planning committee members and presenter(s) have disclosed they have no significant financial relationship with a pharmaceutical company and have disclosed that no conflict of interest exists with the presentation/educational event. Thank-you for listening to the podcast. SHOW NOTES: *See the attachment for additional show information. Intrinsic Kidney Injuries: Urinary analysis findings- Bland Urine: no protein - Nephrotic: protein - Nephritic: protein and blood Hallmark Urinary Findings: Casts - Tamm Horsfall Protein : Mucoprotein made by tubular epithelial cells that precipitate out and congeal to form casts on whatever is in the cells at the time. (i.e. RBCs, WBCs, tubular debris) Bland Urine States- Crystalline Induced Renal Injury: obstruction and infllamatory response - Uric Acid Neuropathy (Most common) - Cancers, lymphomas, etc. - Drugs: acyclovir, methotrexate, protease inhibitors, etc. - Toxins: Ethylene glycol - Bland Urine Disease states: results from injury to tubules, instertim or pre glomerular blodd vessels, not the filters of the kidney - Interstital Nephritis - Hallmark: pyuria and WBC casts - Biopsy: inflammatory infiltrate - Causes: viral, PPIs, Adenover, mizalamin, etc., Checkpoint inhibitors - Acute Tubular Necrosis - Hallmark: tubular epithelial cell cast - Granular: (course or fine) diagnostic of ATN - Biopsy: denuded dilated tubular cells - Causes: #1: Ischemia; toxins, drugs, contrast dye; pigment injury. myoglobin - What about contrast dye? - Categorized under ATN - Per Dr. Thielen, plays a role, but injury is not solely dependent on dye alone. - Hepatorenal Syndrome: ischemic injury to the kidney due to unopposed vasocontstriction - Ace inhibitors cause unopposed efferent vasoconstriction + nonsteroidals cause unposed afferent vasoconstriction = no glomerular perfusion pressure - Multiple Myeloma - Hallmark: Light chain cast nephropathy or myeloma kidney - Light chains precipitate out causing obstruction, inflammatory response and causes tubular damage - Presentation: older possibly with anemia, bone pain and elevated creatinine with a bland urine. - Protein to creatinine ratio: + for protein (non albumin) - Dipstick: (which measures for albumin and not light chains) will be negative for protein aka bland urine - Hypertensive Nephrosclerosis - Small vessel vascular disease - Blood vessels prematurely atherosclerosis causing glomerular drop out and scarring of the interstim - Scleroderma - Limited cutaneous systemic sclerosis - Diffuse cutaneous systemic sclerosis: 60-80% have renal injury from disease state itself - FANA positive - Concern for Scleroderma Renal Crisis = medical emergency - AKI, moderate to severe HTN and bland urine - Uncontrolled accumulation of collage, thickens vascular walls, narrowing and renal ischemia - Occurs in 10-15% of those with Diffuse Cutaneous Systemic sclerosis and happens early in disease - Left untreated: renal failure in 1-2 months and death in 1 year - Treatment: ACE Inhibitor Nephrotic Urine States - Urine protein: albumin excretion greater than 3.5g in 24 hours - Nephrotic Syndrome: - Present with 3 things (nephrotic range protein, hypoalbuminemia, peripheral edema) - Hyperlipidemia: due to increased hepatic lipogenesis - Increased risk of renal disease and arthroscleratic - Venous thrombotic disease: - Loose proteins other than albumin and develop a hypercoagulale state - Renal and peripheral venous thrombosis - Lipiduria (forms fatty casts, looks like a latese cross under microscope) -Pathophysiology or nephrotic syndrome - Glomerular capillary wall - 3 layers that work as a glomerular filtration and responsible in the filtration between blood and urine - Fenestrated Capillary Enothelial cells (fenestrations allow plasma through to the basement membrane) - Glomerular Basement Membrane (maintains glomerular filtration barrier; negatively charged, repels albumin) - Epithelium: Podocytes (Have highly specialized foot processes that connect and form slit diaphragms; Slit diaphragm important for the efficient flow of small solute and water) - Anything that messes with any of these layers: nephrotic proteinuria - Nephrotic Disease States: - Biopsy: anyone with nephrotic proteinuria (besides diabetics) 1) Light microscopy: high overview 2) Immunofluorescens: looks for nephritic component and identif immunce complexes 3) Electron microscopy: (EM) helps look at the ultrastructure and better identify immune deposits - Diabetic nephropathy - Leading cause of kidney disease in U.S. and western society - Responsible for 30-40% of all ESRD causes - Hyperglycemia: produces inflammatory responses, oxidative stress, and injures the podocytes and deposits that charge and affect the ability of the kidney to filter. - Amyoidosis - Organize into betapleted sheets and produce spikes of the capillary uniion and poke through the GF membrane - Easily identified by apple green birefringence on congo red - Terminal illness - Present with HTN, cardiac effects and elevated creatine - Nephrotic Disease states based of histologic appearance - Diagnosed by histologic appearance but does not determine the etiology - Minimal Change Disease - Fairly common - Minimal change under light microscope - EM: podocytes are abnormal, fused, no unique cell-cell junction - Primary: Immune generated circulating facture; alters the cytoskeleton of the podocytes - Secondary - Nonsteriodal - most common cause of secondary minimal change disease - Gama interferon - Hodgkin's lymphoma - Allergy: 30% of minimal change have associate allergy (mechanism unknown) - Presentation - Sudden onset (days to weeks) - Marked edema and hypoablbuminemia - 60% have normal blood pressure, 82% have normal creatinine - Focal Segmental Glomerulosclerosis (FSGS) - primary and secondary - Most common cause idopathic nephrotic syndrome in adults - Primary glomerulonephritis in the US that causes ESRD - Widespread podocyte injury - Primary: circulating factor that messes with regulation of foot process and adhesion to the glomerular basement membrane (afffect all podocytes) - Present with nephrotic syndrome and rapid progression - HTN and elevated creatinine - Secondary: the visceral epithelial cells don't replicate - Nephron loss or obesity or direct foot process injury - Cannot replicate (podocytes), leads to decreased to podo denisty at specific areas (focal injury) - 2/3 of all cases FSGS - Present: with slowly increasing proteinuria and kidney impairment over time - Causes: interferon, bisphosphonates, talc, anabolic steroids - Genetics: gene mutations that encode for the slit diaphragms of the podocytes (affect all podocytes) - Present in Childhood: full blown nephrotic and progress rapidly to ESRD Membranous Nephropathy - Most common cause of nephrotic syndrome in caucasion adults - 80% present with nephrotic but develops more slowly to ESRD - Primary: Major antigen identified - antibody to trans-membrane receptor that is highly expressed on the glomerular podocyte - Secondary: Cancers (lung, breast, GI), Lupus, Thyroiditis, Hep B, Syphilis, Nonsteroidals, Monoclonal Antibodies Nephritic Syndrome - Hematuria and proteinuria - Hematuria: blood from kidney or outside the kidney - Outside the kidney: look the same - Inside the kidney: dysmorphic red cells - Present: - Renal impairment for days to weeks - Edmatous, HTN and look critically ill - Vasculitis, sinusitis, oral ulcers - Pulmonary renal syndrome: short of breath or hemoptysis - Skin changes: bruising , bleeding, purpura - Myalgias and arthritis - Urine: - Hallmark: red blood cell casts (polymorphic red cells) - dipstick + for blood - elevated proteinuria - Biopsy: nephritic and + urine Nephritic Disease States (based on immunofluorescence staining) - Pauci Immune Disease - Ankle vasculitis, common - A paucity (little amount) of immune complexes - See black on imaging - Lab work: check on ANCA and peripheral eosinophils - Anti-GBM Disease - Renal limited, or classic pulmonary renal: Good Pasture's - linear staining of the glomerular basement with anti IGG (looks like a ribbon on a package) - Treat with cytotoxic agents - Immune Complex - Starry sky pattern - Glomerulus looks dotted with stars - Stars = immune complex definition - Diseases: Lupus (FANA), Post Infectious GN, Membranous Proliferative GN - IGA Nephropathy - Most common cause of glomerulonephritis in the world - Presentation: - Peak incidence is the 2nd and 3rd decades of life - 40-50% gross hematuria with upper respiratory and GI illness - Risk Factors for Progression: - younger age or hypertension at time of presentation - > 1g proteinuria - Elevated creatinine at time of presentation Thanks for listening.
Speaker: Thomas F. Kolon, MD
In this video, we explore the urinary system! As we observe the kidneys, we will delve into the nephron & understand how the kidneys filter our blood to create urine.
In this episode, we review the high-yield topic of The Nephron 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
References for Chapter 5--the Distal NephronRoger pointed out the fact that the distal nephron can achieve very low urinary sodium as evidenced by observations in people from the Yanomamo tribe Blood pressure and electrolyte excretion in the Yanomamo Indians, an isolated population in this report, 84% of the participants had urinary sodium < 1mmol/24 hours. Information about the Yanomamo Tribe. It looks like they're starting to make chocolate, now! YanomamiThe Yanomami are great observers of natureThe Amazon's Yanomami utterly abandoned by Brazilian authorities: ReportYanomami Amazon reserve invaded by 20,000 miners; Bolsonaro fails to actI believe this is the original study looking at urine sodium and blood pressure in the Yanomamo Indians, but the INTERSALT trial linked above I believe had more robust urine dataThis study mentions the average lipid profile for men and women along with BMI. I didn't mention in the “Voice of God” overview, but there is some interest looking at the Yanomamo and rate of cancer as it relates to the correlation with intracellular potassium to sodium ratiosJosh referred back to his notes and realized that the tightest junctions are in the TOAD not FROG bladders Physiology and Function of the Tight JunctionAn excellent review from McCormick and Ellison on the Distal convoluted tubule in Comprehensive Physiology.We flirt with the disorder of Gordon's syndrome: Familial Hyperkalemic Hypertension | American Society of Nephrology and its alter ego, Gitelman syndrome: Gitelman Syndrome | HypertensionJC spoke about this beautiful report on how calcineurin inhibitors lead to hyperkalemia (and mimic Gordon's syndrome). The calcineurin inhibitor tacrolimus activates the renal sodium chloride cotransporter to cause hypertensionThis superb review of the DCT includes all the highlights of Rose's chapter 5 with a modern lens including “braking” from DCT hypertrophy Distal Convoluted Tubule | American Society of NephrologyEchos of the lessons learned in the DCT can be seen in this review: Diuretic Treatment in Heart Failure | NEJMAnna reminds us of the ALL HAT trial which showed that chlorthalidone was superior to the lisinopril and amlodipine groups (and the alpha blocker dropped out earlier) Major Outcomes in High-Risk Hypertensive Patients Randomized to Angiotensin-Converting Enzyme Inhibitor or Calcium Channel Blocker vs DiureticNice review of drug induced Hyperuricemia with a deep dive into the mechanisms of diuretic induced Hyperuricemia. Drug-induced hyperuricaemia and goutPlus, despite the concerns that thiazides are weaker than loop diuretics and may not work in CKD, this report suggests that it can still be of use. Chlorthalidone for poorly controlled hypertension in chronic kidney disease: an interventional pilot studyIf you love diuretics, you will love this classic paper from Craig Brater on diuretics Diuretic Therapy | NEJM which also includes the t1/2 of various diuretics and points out that chlorthalidone's half life is 24-55 hours so eliminated after 4-10 days. The hypercalcemia seen in some patients who take thiazides may be the unmasking of primary hyperparathyroidism Thiazide-Associated Hypercalcemia: Incidence and Association With Primary Hyperparathyroidism Over Two DecadesAs we discussed the relative importance of DCT vs Proximal tubule for the hypercalcemia seen with thiazides, Amy reminded us of about the TRPV5 knockout mice: JCI - Renal Ca2+ wasting, hyperabsorption, and reduced bone thickness in mice lacking TRPV5 JC mentioned the defect in TRPM6 that can cause severe hypomagnesemia: Novel TRPM6 Mutations in 21 Families with Primary Hypomagnesemia and Secondary HypocalcemiaWe enjoyed talking about Liddle syndrome Hypertension caused by a truncated epithelial sodium channel γ subunit: genetic heterogeneity of Liddle syndromeWe wondered about the role of pendrin which was discovered after this book was published. Here's a nice review: The role of pendrin in renal physiology and also a potential therapeutic target for pendrin: Pendrin—A New Target for Diuretic Therapy? | American Society of NephrologyBradykinen Bradykinin B2 receptor antagonist increases chloride and water absorption in rat medullary collecting ductMore Bradykinen Chronic Overexpression of Bradykinin in Kidney Causes Polyuria and Cardiac HypertrophyWe ended on a high note when we considered the urothelium of the American black bear. These magnificent creatures have aquaporins 1 &3 that allow them to reabsorb their own urine during hibernation. The urothelium of a hibernator: the American black bear
This Podcast talks about the different CILIOPATHIES, that are Genetic conditions related to Cilia in Nephron of Kidney. Explaination of its pathophysiology, investigation to perform, treatment offered in Modern Medicine are covered in the podcast. Do Listen to it as it will surely help you to increase your knowledge and give a better understanding of disease condition. I am here to share my part of knowledge in regards to subject MEDICINE. Do spread this podcast by sharing my podcasts with your friends and colleagues. Thank you for listening.
Madrazo-Ibarra A, Vaitla P. Histología, Nephron. [Actualizado el 7 de diciembre de 2020]. En: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 enero-. Disponible en: https://www.ncbi.nlm.nih.gov/books/NBK554411/?report=classic --- Send in a voice message: https://anchor.fm/las-poderosas-celulas-nk/message
Today we talk with Matt Crawford with the Montgomery Company in South Carolina about what is happening in the Columbia Market. We cover everything from the way he works, economic and employment trends, taxes, the current level of competition, and other things that make Columbia an investor's market. --- Transcript Michael: Hey, everybody, welcome to another episode of The Remote Real Estate Investor. I'm Michael Albaum and today I'm joined by my co hosts, Tom Schneider and Mark Woodling. And we have a very special guest with us today, Matt Crawford is an agent out of Columbia, South Carolina. And today Matt's gonna be giving us a market overview and talk about some of the things that he and his team are able to assist buyers and sellers in doing in that market. So let's get into it. Awesome. So Matt Crawford, thank you so much for taking the time to join us today. Really appreciate you being on the show. Matt: Excellent. Thank you, Mike. Glad to be here. Michael: And so you're out in Columbia, South Carolina. Is that right? Matt: Yeah, Sunny Columbia mass about 85 degrees, you know, beautiful state born and raised about an hour north of here. So fantastic market, man, it's a good place to be. Michael: Awesome. And I'm curious, Matt, who are you an agent with. Matt: So right now, my agency is hung under the Montgomery company, which is a pretty interesting story. And just to quickly unpack that, Matt Montgomery, he's a great friend of mine. He runs a massive construction business here in the southeast. And just for the conveniency of our partnership, I ended up creating a brokerage with him. And I'm really sort of the head of the firm, sole proprietor of that brokerage, which I moved my company under, which is technically not a capital in southern capital brothers, which is our investment brokerage underneath this umbrella. Tom: That's a perfect segue, Matt, and, you know, before jumping into Columbia, South Carolina, I'd love to learn a little bit more about yourself and your background and how you got to where you're at today. Matt: Yeah, 100% time, you know, it's a, it's been a journey, you know, as we all are inclined to take. And so, you know, I'm going to probably take this back five years, you know, I'm in Denver, Colorado, man, loving life, sort of so in the proverbial oats of a new broker. And I started really getting into cahoots with a lot of the investors out in Colorado, a lot of these guys were doing huge land acquisitions, building massive multifamily complexes, as well as doing something that I'd never heard of, which was institutional capital investing. So they were piecing together these massive SFR, BTR portfolios, renting them out, stabilize them, and then doing the disposition strategy. And I was like, what a awesome niche within the real estate arena to start cutting my teeth on. And so we got licensed in Colorado started working with these guys, the barrier to entry there for a new young agent in his 20s was so massive, and like, man, it'd be great if I had $600,000 for my first rental, not the case. So I look back to my roots back here in Columbia, South Carolina, where I can get that first rental for about 50,000. And so jumped over here about four years ago, and started building some institutional funds with a previous venture, we built that went to about 2200 homes deployed around 220 million over 24 months. I don't think I slept much. I probably lost a little bit of weight. But I learned a lot, you know, and, and from there, you know, there was a talk about destiny, talk about fate, you know, the pandemic arose, a created a little bit of space, to sort of see where I wanted to navigate. And, you know, I decided with a few of my other founders, Jordan, and Alex Fisher, to start our own company. And that's sort of how we got here today, Tom: I had a boss who had a pretty funny joke. I was like, working a lot of hours. And he's like, Hey, good news. Tom, you're getting credit for two years of work, which is one year by working, you know, every day, 100 hour weeks, you know, yes. Matt: It is a journey man is like, you know, you know, first and last out, but we had the, the gusto of, you know, being passionate and, and finding, you know, a purpose within the the jumble of real estate, not at one point, I thought it was so binary, you know, it's just traditional transactions between buyers and sellers, and then start unpacking that man, I'm like, oh, man, if you can sell one home, you could sell a portfolio of 1000 homes. And so that's what brought us here. Tom: Let's, let's learn a little bit more about the practice today. Your guyses brokerage today. Matt: Yep, yep. So, you know, we really have pivoted to fly a new banner. That banner is called Southern capital. It's a company that we've had for many years. And what that really does is it pieces together investment clients, like you guys have it Roofstock with really high profile properties here in the southeast. And if we can drill down even more granular, you know, Colombia has been our top market. And it's just so funny how it happened. You know, when I, when I ended here, I wasn't thinking, Oh, Colombia is going to be the most fantastic rental market ever. But it is just really happen that way, the average property value in ratio to the average rent rate is just so incredibly strong, that it's created a lot of attraction. So at Southern capital, I have Jordan shots, he's just like our tech, no, not man, this guy is building these fantastic databases. He's bifurcating all these beautiful codes on the back end, that parallels the software that you guys have, you know, shout out to Andy, and Danielle, for Roofstock. And it's just played so well in our court. And then Alex Fisher, the guys basically like a pseudo General of the military. And he's just running fantastic operations, and allowing me to sort of be on the forefront, gaining knowledge, making really strategic connections, and providing the utmost service to the clientele. And so Southern capital sort of walks that fine line of servicing large institutional clients. But I've really, really enjoyed the opportunity that mark and Matt and you all at rusak have provided us, which is working really intimately with people from all around the world. I mean, we've had, we've closed deals in India now, like doing five day meltaways. And I'm like, this is awesome, man. Because with the with the large institutional space, you know, with any kind of maybe corporate structure, you almost become a data point. You know, they're they're really looking hard at performance underwriting sheets, which I'm fine with. And I love the scalability of numbers. But there's something beautiful about that connection of getting on the phone with someone who's buying their first rental or their 10th rental, looking at looking at their projected rent rates. And that's sort of what we're doing in a nutshell, on the day to day here. Mark: Let me kind of unpack it, as Matt Crawford would say, in a sense of connecting why Matt's here with us today, because, you know, Matt's one of our prized certified agents that Roofstock has partnered with, he's the one that's actually handpicking properties to bring over to Roofstock select. So we don't just treat Matt like he's a partner, but he is sitting in the same arena with us, he is there rolling up his sleeves every single day, and really bringing properties a Roofstock. So we want to give Matt a shout out bring him on the podcast because a he's an expert in Columbia, South Carolina, we want people to understand it, but he's the guy that's handpicking the properties for the Select program. So if anybody likes what you're doing, they're going to see your work. It's almost like artwork that's going up on Roofstock. So great job, thanks for all your participation. And again, I would love to love to get into the market when when we do really unpack it for for the crowd, because there's a lot of things happening in South Carolina, but specifically your market. Matt: I love it. I love it. Mark within let's uh, let me let me switch some gears real quick. Now you guys have started getting the creative juices flowing. So let's talk about the masterpiece, the artwork, and that breaks down to the underwriting that goes into these problems. So all that history that we just covered, taught us one thing, and that's how to underwrite really well to be the best underwriters, right? In South Carolina, you know, putting that out there into the universe. And so it is an art form. You know, we're looking at a ton of different data points. We're looking at so many different comps, whether it's purchase comps, rent comps, we're looking at outlier data that we're pulling off Airbnb, err, DNA that we're trying to figure out how many data points can I put on this one property to make it a sure bet for an investor. And that really is what's given us the success with the Roofstock program, you know, as Mark mentioned, you know, we're looking at these properties every single day, manually underwriting them, you know, which is a huge, huge help from Jordan, my partner, you know, really appreciate you, Jordan when you see this, but we're getting on there, and everything is converting, because we've already done that heavy lifting upfront, you know, and I think that's sort of the secret sauce here, as well as being so intimate with the market here. And that's just the beauty of painting this piece for you guys. Michael: Matt. So if we can peel back another layer of this proverbial onion here, what are you seeing? Are you able to get a finger on what makes great investment properties in Colombia? Matt: 100%, like, you know, it's, it's gonna come down like the easiest way is my hot zones. You know, there's a, there's zip codes, no 29209, 29206, you know, 29203 I want to stay away from except if I'm on this one side of the street. And so just being able to speak on the micro locality. I think that's such an important word here is a huge service to these investors. And then, you know, like any, you know, skilled tradesmen of his craft, you get to a point where you can Almost looking at property, as long as sort of meets the actual locale checkbox, in my mind, I can tell you, this is going to be a great rental. And I can also tell you if the area is going to have a specific tenant demographic that's going to play in to the longevity of your asset. And that simply just comes from experience from data, you know, those probably now 25 different homes that we've managed to underwrite, put in a pipeline, put a tenant in there and have it stabilized. And so that really has allowed us to speak really clearly to the Rootstock clientele. Michael: that's such a good point. Because like we've sent out other episodes, you know, the, the what the one thing you can never change about a property's location. So getting that right off the bat is so critical. Matt: Oh, man. And and and, you know, I'm not gonna lie. It's sort of fun. Because you go across the bridge here in Colombia, you have you have greater Colombia, then you have West Columbia, which is a whole different municipality, and it's split by a huge river called the Congo. Five years ago, there was no one saying, hey, let's head across the river, it was almost like that was a less developed obtuse area. Well, now, these veterans just came in, they put $4 million dollars into a brand new brewery right on the river. And so I'm doing reconnaissance, hitting up the brewery, checking out all the properties around there and then actually sourcing data, you know, so it's, it's a lot of give and take, but you know, it's how creative can you get with your market? Know, your market in my eyes is a product, you know, how can you literally turn these widgets polish this product to make it presentable and digestible from somebody who's investing all the way from California? And that's what we do. Tom: Would love to hear about some of the broader kind of like macro tailwind. So Colombia is the capital of the state. What other you know, how else would you describe this sort of, you know, general kind of tailwinds. Beyond, behind the Columbia, South Carolina market, like what are the major employers all that good stuff? Matt: Yeah. Awesome, awesome question time. And it's, it's so just, to me, it's a beautiful thing, what's happening here, so an hour north of here you have Charlotte, North Carolina 2018, ranked the number one city for millennial retention in the US. You know, two and a half, two and a half hours east of here yet Charleston, South Carolina, ranked the number one best small town in the US of this several years in a row. If you go an hour and a half Northwest, you're in Greenville, South Carolina, which is also have gone through this huge development curve. And then you have Little Columbia right in the smack middle of the state that has been like overseen for the last seven years as each one of these towns develops. And we're now starting to see this huge shift of people being priced out of assets and Charlotte green go in Charleston. And so all that wealth is coming right to the center of the state now, and this is super evident. And probably the last three to four years, like you know, call it serendipity or what may have you but right when I moved here, it was the first time institutional capital really got into this market. And now it is just turning in two parallel that the big players are now coming to town, these huge multinational conglomerates, just to rattle a few law, we have Prisma health Prisma health basically aggregates massive hospital systems, puts them under the Prisma banner sort of puts a new culture and spin on the health care that has exploded here. They bone up everything and Columbia and Lexington and irmo. With that medical Lance now on Columbia, Nephron pharmaceuticals, one of the largest pharmaceutical manufacturers in the country, actually opened up their HQ here in Lexington. I think it brought around like 12,000 jobs to town. I mean, you cannot go out and meet somebody Now, that doesn't have a gig at nephron. So those two players really showed that Columbia can get out of sort of the Capitol education scene, and now we're having huge entities pick up. So outside of the medical field, of course, you're gonna have education, you have the University of South Carolina, for all you awesome investors out there. This is a cash grab of amazing students as fantastic business program and a law program that sort of as you can sort of insinuate is going to feed into the rentals, especially if we're going to be plotting these five to 10 miles outside of downtown Columbia. And I would say probably the third is going to be your, your political and your military industry. We have Fort Jackson right here. It's the largest trainee base in all of the US, I believe, for new recruits. So what we've done as well is we pivoted to the industry. So on my personal portfolios, we're actually doing a majority of short term rentals Airbnb models, which is something that you know if you guys are ever interested in I'd love to also unpack that to sort of look at the underwriting scales between a 12 month long term lease versus if we put this into a another tier of short term leases. But all those things just play perfectly together with the assets that are available in Colombia. Mark: So Matt, I always like to play around with the Economic Development Council websites and like, really dig into what's happening, like, how are these? How is the local city trying to draw in outside business? Right. And so they're always putting a ton of numbers up there. So I see that there's a ton of renters, there's a young population. But tell me, one thing I didn't see on there is tech, what's happening in the tech scene out there? What kind of jobs do you think are being developed? And maybe are there a ton of startups moving in or Yeah, go into a little detail about that. Matt: 100%. And I think that's also the beauty of a lot of people, especially in the startup world, you know, being a entrepreneur myself, you know, might not have that $50,000 liquid to plop down on a $220,000 starter home. Or, in fact, they might have used that liquid to actually inject into their business or building. And we're seeing an explosion of that community here. Maybe it's because FCRA is a huge grantee here in Columbia, South Carolina, they're getting everything from 20,000, up to $200,000 startup grants. So people are just flooding this town, seeking those grants, you know, there's low, low barrier to entry. This is not Charlotte, this is not Atlanta. So you really can get great visibility into the market without having all the noise of similar competitors. Everything from five bubble five bubble was a fantastic tech startup here. Shout out to those guys. We meet with them all the time. And then even more so mark, to your point, because of that community, because of that influx that's now happening and putting this polish on this town, there's a massive tech, what would you call this, like a, like, tech village, man, it's probably like, I don't know, a million square feet total. But it's going to be housing. Tons and tons of startups that come in and basically have office space for Mark: Basically like an incubator where everybody can come together, exchange ideas, and magic happens in those kinds of environments. Matt: It's massive. And I think I can add one more layer to that as well is that at the key here, you know, Tom and Mike to fill you guys in this is a true tertiary market, right? You know, this is tertiary being that we have moderately low purchase prices, and comparative to the historical rent rates. And so in any kind of investors mind, you really want to be searching for that true tertiary market, but not only got a tertiary market, but a evolving tertiary market that's about to flip over into the secondary category, secondary, secondary, meaning you have a little bit more modernize commercial entities, we have a lot more retention of your population that is grown there, then you have just a average household income starting to rise and a gradual slope. That literally is happening right now. And that's what's helping retain startups retain the young millennials that are getting out of their MBAs or college. And we're bout to flip into a true secondary market, whereas Charlotte, Charleston, Atlanta, I would say a primary, you know, they have massive, massive inventory, but also high purchase prices, we're bouncing the ball, which that secondary market, which I think is the perfect time to start planting some seeds and dollars here, because in three to five years, this, this city is going to have a total different culture, a different field. And as you guys would, you know, understand a totally different marketplace. And that's what makes it so healthy right now to invest in. Michael: So Matt, let's let's unpack that a little bit further and talk about some specifics. So if somebody is just a first time investor looking at different markets, which is a question we get all the time, and the Roofstock Academy is, hey, what market should I be looking at? Can you give us an idea of what that entry purchase price looks like? And what someone could expect for rent, and maybe give us an idea of some different neighborhoods to look at at a different price point and rental amounts. Matt: Oh, let's rock and roll. Michael, you know, for everyone out there watching, you know, my two senses. Let's get started. Right? Come on. Like, we will literally show you the ins and outs of this marketplace. But it's easy to have analysis paralysis, you know, especially or building a portfolio or investing, you know, hard earned capital or anything. I understand that there's this level of nervousness. How do I choose between San Antonio or do I look in California? I've never even heard of Columbia, South Carolina. But I can tell you if you guys just give us the opportunity to show you the ins and outs. You'll see exactly why this is the number one market The Roofstock buyer program right now. And that's because you can come in, you can buy a house for $80,000. For 80k, if we have it in the bank account, collectively, I'm going to put this over in West Columbia, I'm going to literally draw you a circle that is probably around five minutes from the actual river front. And so the fact that we can get that close to a beautiful amenity, you're about to be 10 minutes from downtown for $80,000, it's going to run out conservatively probably 1200 to 1250. Now if we come in there, we slap granite, stainless steel appliances, maybe put some LVT on the flooring, that $80,000 property, literally now could probably fetch $1500 for a modest three bed two bath, and I am hard pressed to find a another market that can support such high rent rates with such low barrier to entry and the purchase price without maybe going to specific places in Birmingham, Alabama, or what have you. But that's the beauty of Columbia right now. Tom: As we're talking I'm like looking over Zillow in the area. And man, I love how I love how self serving this podcast is. It was will definitely be talking after math like, I don't know, I'm gonna love the thesis on like this. Matt: It's a beautiful thing. Mark Well, what I love about it's a state capitol, right, and you have a major college there. I live in Dallas, near Austin, Texas. And it's like the two things I see with Austin are the same exact thing that you would see in Columbia, it's just it may be years behind. So people move to affordable areas and where they can stay young, right? You get out of college, you find a good job, you can stay hanging around your friends if you really wanted to. So there could be some really cool things I see in Colombia happening. Matt: Massive and Mark, I can even add some two cents there. And that can parallel it to with your point, Mike about, you know, what are some micro neighborhoods to start really searching in and so if anybody's taking notes, Rosewood, you know, rosewood is where you want to be it's literally maybe what happened to Austin five years ago before Austin became keep Austin weird. Like, that's what's happening in Rosewood right now. We have world renowned graffiti artists, you know, tagging massive walls, like the coolest stuff that you know, really did not reflect in Colombia, even two years ago, even like pre pandemic like there was no, no justified culture. There certainly wasn't an art area. You know, I think back to Denver, Colorado when the river North District, which is now this huge art conglomerate, that literally is happening here. So if you're ever searching for properties, massive, massive student population, it's going to be in the Rosewood neighborhood area. And it really is following that path like Austin is of creating its own personality, its own culture, and its own distinctive. Tom: Where is rosewood? I'm looking at my map right now. And this is probably for helpful people pulling up their map where is rosewood relative to the center of Colombia, maybe like near a freeway or where is Yeah. Matt: But I'm looking at the center of Columbia, like, literally pinpoint the very center actually is the state capitol. It is three miles to the right. So literally, if you just look to the right, I'm pretty sure the zip code is 29204. Nope, internet 206. But there is a main bang, there it is. It's literally called… Tom: Inside of 77, just south of 378. Is that right? Cool. Matt: Yep, that is 100%. Right. And it's just like, it's the coolest spot man. There's like a 19 hundred's airstrip that's been this like massive hangout spot on they actually converted the hangar into a state of the art brewery. And so using those like outlier data points, like, especially with something as commodity commoditized, as a brewery, I've been seeing values on these properties jumped up 10 to 13%, year after year, just because it was getting to attain more and more populations. And it's becoming hit, you know, for whatever arbitrary. Tom: Looking at the great school ratings, I'm seeing an elementary school and an eight, which is incredibly high and middle school to five in Dre, her high school at a seven those are those are fantastic school scores. And that's one of my big criteria that I look at. So we might need to you know, hide this part of the podcast because Mark: Or let's do the opposite. So after this, you have you have full control, go ahead and post some properties on a roof stock in the rosewood neighborhood. And let's let's see it through the roof stock lens. So I think we're onto something here. Matt: Absolutely. And then, you know, Tom, now that you're sort of looking into the map, you know, I'm going to sort of drive us down. I 26. This head west probably about 13 minutes. I'm getting off at exit 103 B and I'm in Lexington, South Carolina. You know, so a lot of people, a lot of people will come in and say that tell me about Colombia. So the big four that you want to really start investing in, that's going to be Colombia proper. West Colombia, KC, which is right parallel to West Colombia, and Lexington man, Lexington is like Hotlanta, baby, but a lot smaller. And it's just fantastic. It's created its own culture. It's right beside Lake Murray, which for this area, you know, is literally as I'm sweating in my back, I'm glad you can always see my front right now is a beautiful thing to have. And these, you know, you're gonna have a little bit more competition, but anywhere in Lexington, especially centralized and looking East fantastic inventory. Michael: So Matt, this is this is really great. And I love that delta between the purchase price and the rental amount. I mean, that sounds like it's really, really strong. Something that our investors see is either able to make or break these deals as an investment is often Pentagon property taxes. Can you talk to us a little bit about how property taxes work in the Columbia market? Matt: Yes, 100%. And it may or Benjamin, you're watching this, please answer my emails, because the taxes are tough man, you know, it really is, it's the double edged sword. You know, with such a fantastic market such beautiful rent rates and purchase prices, of course, there has to be some catch. And that is going to be the non owner occupied property taxes, you know, and these are going to really come in roughly around 3% of your gross purchase price. So, you know, on a four bed two and a half bath, beautiful new bill, that's, you know, 210,000, man, you're gonna get slapped with, like $5700 tax bill. So I mean, if your cash flowing, you know, a couple 100 bucks a month, that means you're probably only gonna net maybe four to five to 6k annually. It eats up a lot of the margin. So Mayor Benjamin, please, can we change that law and attract more beautiful investors in estate. But what we're doing to offset that is looking for those lower purchase price assets. Right. So a lot of people they want the new builds, you know, they sound sexy on paper. But, you know, to win to win in this market, need to combat, that 3%, non owner occupied property tax, you know, let's play in the 120 to $150,000 range. So now your taxes are three grand, and we're going to get that thing rented at 1500 to 1800. That's how we can combat such a tax problem. Michael: And just as a kind of a point of reference. So folks understand why people might be continuing to move to Colombia. What is the tax rate for an owner occupant? Matt: Oh, man, it's less than half man. It's like, you're not really paying much. You know, and there's a ton of grants out here as well, to incentivize people to move to Colombia. You know, and I can even go into a little bit of deeper history of why that is. So, you know, the 1980s, the sort of the war on drugs really hit Columbia hard, because this is this is historically a new labor force town, you know, we have a massive flour mill in the heart of downtown that now it's become sort of a legacy item, no, people have weddings on top of it now. So that demographic really was affected by the 1980s pandemic itself. And a lot of the assets in the single family units sort of were deteriorated, especially in some zip codes, nobody would move there and develop them. And so now the state is giving tons of grants for people to come in and give more life to this city, as we're sort of pulling out of that prior, that prior culture that really stuck around really, until today, there's still pockets and 29203 that are, you know, less than desirable, because the demographic there has sort of been inundated with the ancestral baggage that came from a few years ago. Tom: This is awesome. Michael, do you have any more questions or mark, anything else you want to touch on? I'm, this has been? Yeah, I'm, I'm a fan. I don't know. I've been looking at market for a while. And this kind of conversation really is drawing me in a little bit. A little bit closer for sure. Michael: Yeah, I guess my only other question that would be kind of on that on the example you gave previously. Were you getting in for 80k? Putting in that granite countertops and stainless steel now that thing could rent is renting at 1500? Is there any type of reassessment that the county is going to do in any kind of regular frequency? Or is your property tax truly tied to the purchase price at acquisition? Matt: Boom! So everybody, Let's get some house hacking skills ready? Because it's tied to that gross acquisition price. And so that's how you get to beat the market here is you can get by a distressed property for 60k You know, that's so 20 $25,000 into it, you know, Sue Paint windows flooring kitchen. And that thing's now gonna appreciate and appraise probably at 120 125k ran out for 1500. But now we're only tied to that $60,000 original purchase price, we're going to let it season we're going to refi our money, and we're going to keep it rolling. And that's exactly what we did in tranches of 100 properties, every 100, we do that exact strategy, pull that cash out, recycle that it's your, your, your gilded, BRRRR strategy, and it works perfectly for this market. And so, actually, Mark is very well aware of this, that there are a few individuals that have come to this, this market space through you guys. And we're actually doing that right now. So, you know, Southern capital, we are a acquisition renovation management company. And so we have what I literally would crowned the best crew, because we have cycled through the last years of who guys can keep up with the scalability, that consistency and the sourcing of these renovations. And that's where Matt Montgomery, who we mentioned at the very start of this cast, that company now supports all of our innovations. And so, guys, if you're interested in the Columbia market, you want to find a way to get around the property taxes, you know, my resources are your resources, I'm more than happy to have a scope built for you completely itemized with timelines. General rule of thumb is for every $1,000 renovation, it's about one day. So a $30,000 job should take us about a solid month to do. But that is one really great way to start cash flow and quickly here in Colombia. Michael: That's great. And let's just kind of highlight that again, Matt. So if I'm an investor, I'm interested in doing some kind of value, add renovation, and then putting a long term tenant in place, I can do that all with you and southern capital, you'll take care of the acquisitions, you'll assist in the renovations, and then you'll manage the property once I've got it completed. Matt: 100%. So that was the whole idea of creating a holistic turnkey investment centric brokerage. That is a mouthful, but basically, we're here to be your best friend. And not only that, but we have the opportunity and the blessings of working with people like Mark, yourself, Michael, yourself, Tom, the whole team at Rootstock. So their back office, our front office and operations literally have made such matrimony moving forward that we're here to help. Michael: I love it. Tom, like you said, I got to make a couple phone calls over the over to Matt's office here after we hop off. Yeah. Matt: Come on the ship is sailing, baby. Mark: Got one last question. Now that I think about one last question for you, Matt. So buyers can really understand what you know, what the competition level is there? Are you seeing multiple offer situations on every property? Or is it less frequent, like we see in like Birmingham right now where almost every property has multiple offers? Matt: Awesome, awesome. Question mark. And so Phil, you know, everybody tuning in, you know, it's, you know, we're almost 50% maybe the last that I checked, 48% less inventory, then last April of 2020. So every offer is almost I would say 95% a multiple offer situation. But this is what we're going to do. You know, we're going to get your offer, we're going to expedite it being built out signed by you. I literally pick up my call and just being a player here in Colombia. I know a lot of the brokers say Hey, man, this is one of my investment clients, you know, you know, I know you love your your buyers and sellers, but I really value these people and their trust, can you please put me at the top of the pile. And so that's, that's me. I'm kissing babies and shaking hands. And so I really push it as far as I can. But if you guys are coming in, we really have, I would say one shot to get it right. But that's not the case. Because if I know that we're not the highest and best, I'm gonna allow us that window, you know, and a lot of times they say, hey, Matt, we're sorry, the sellers didn't even you know, want a call for highest and best but I'm pressing these people I'm following up. I'm texting them say Hey, man, before you accept, you got to give me some feedback. So that's number one. So guys, if you come in know that we're going to be right at ask, you know, if not five to 7% over ask. But that's not the end of the story. There's a beautiful part. And this is really what I think makes us dangerous is our off market channel. So for the last several years, I've amassed this massive contacts through asset managers to different real estate lawyers from local investors portfolios, trust funds, and say, Hey, guys, like funnel your inventory through me and I can bring a really, really healthy productive investment base to buy these acquisitions. And so I think that's what makes Columbia stand out from the rest is that we're uploading exclusive off market properties every single day that are not publicly facing and not on Zillow. They're not on the MLS stay get the sort of forsee that wave of multiple offer situations and avoid it completely. And that's something that we've done tons of transactions With the Roofstock clientele as well. Mark: And just to fill in on that, so you're doing that through our BYOB program, right the bring your own property, so you can send our private link, because otherwise we can't post those because they're not on the MLS. And we don't have the listing, which would be the ones that go on our exclusive marketplace. But there's still a way for buyers to get access to that inventory through you. So if they want to reach out, you can show them some of those properties, but still use the roof stock lens, so they can get the roof stock guarantees if if the properties are in the right condition. Matt: 100% Mark, and you know, you know, Fred Haines, I hope you're watching this podcast, he just picked up four off markets from us here in Colombia. The guy is a champion, Fred, thank you so much pleasure to work with you. And we're going to get those things closed here in the month of May. Michael: Oh, that's so exciting. So Matt, if folks do want to reach out to you or southern capital or have questions about you know, reaching out, purchasing properties, getting rehab or management services, what's the best way for folks to get in touch with you? Matt: Man, I love the email. So MCrawford@roofstock.com shoot me an email, I'll shoot you a calendly link we'll get a phone call. I absolutely love that discovery phase, to sort of hear what your investment footprint is. What you are looking from this market that's gonna help me perform for you guys. Michael: Alrighty, everybody that was our episode a big big big thank you to Matt for coming on the show a lot of fun. Kudos to you for crushing it out there with the roofstock select program as a certified agent. We definitely look forward to having you on again. If you'd like the episode, feel free to leave us a rating or review wherever it is your podcasts. And as always, we'd love to hear new episode ideas, topics feedback in the comment section. If you want to hear about a particular episode. Again, thank you all for watching. We look forward to seeing on the next one. Happy investing
The exciting conclusion to Chapter Two: Renal Circulation and Glomerular Filtration Rate - Determinants of GFR - First step in making urine is separation of an ultrafiltrate - Governed by starling forces - Balance of hydraulic and osmotic forces - GFR = LpS (P gc – P us - Osmotic Pressure Cap p) - Normal GFR 95 in women, 120 in men - Cap Hydrolic pressure remains constant - glom cap Oncotic progressively rises - Due to filtration of protein free fluid (protein concentration rises in the capillary) - Filtration gradient begins at 13 mmHg and falls to zero after filtration of 20% or RPF! - GFR is capped at 20% of RPF called filtration equilibrium - So GFR is dependent on RPF, unless you can change glomerular hydraulic pressure - Glomerular hydraulic pressure is controlled by balance of twin arteriole (afferent and efferent) - Constriction of afferent arteriole reduces RPF, GFR, and glom pressure - Dilation of afferent arteriole increases RPF, GFR, and glom pressure - Constriction of the efferent arteriole increases Glom pressure, increasing GFR - Besides glom hydrostatic pressure the other starlings forces are rarely relevant to changes in GFRLetty says: referred to this NEJM review article later JC thought she was referring to something else -see #2- and then Roger referred to this again)Normotensive Acute Renal Failure from Gary Abuelo in NEJM 2007. https://www.nejm.org/doi/10.1056/NEJMra064398 (note in this article, Dr. Abuelo acknowledges the newer terminology of the time, AKI rather than ARF but chooses not to embrace it). In figure 2, he highlights the classic examples of how autoregulation can be affected. In the table, additional examples are provided but all within the framework of alterations related to autoregulation and the interplay between the two resistance vessels.- Regulation of GFR - Autoregulation - The ability to keep glomerular pressure constant over wide range of systemic arterial pressure - When pressure < 70 autoregulation fails and GFR will fall with decreases in systemic pressure - When pressure falls below 40-50 GFR ceases - At least some of this autoregulation is mediated with Ang2. Giving ACEi markedly disrupts autoregulation - Nitric oxide, not important - TGF - Chloride in macula densa - Blocked by furosemide - Group affect of nephrons - Ang 2 sensitizes - Adenosine mediates - Function of TGF - 90% of filtrate is reabsobed in PT and LOH - 10% is reabsobed dismally - Need to control the amount of fluid delivered distally to prevent overwhelming the resorptive capacity of the distal nephron - Talks about acute renal success without naming it (but did reference it) - Mentions glucosuria blunts TGF. Hmmm... - Neurohormonal influences - Volume changes in ang2, sympathetic NS - Role of PGE - Interesting discussion of change of the nephrons perfumed with volume depletion, shifting of blood from outer coretex to inner medullary cortical gloms with their long loops - Dopamine and ANP both increased with volume up - Dopamine causes vasodilation of afferent and efferent arteriole - ANP causes afferent vasodilation and efferent vasodilation constriction, increasing GFR without affecting RPF - Glomerular hemodynamics and renal failure - Decreased glomerular mass results in hyperfiltration of remaining gloms - Mediated through afferent vasodilationJC talks about this classic study in critical care: High vs. Low blood pressure target in Septic Shock. https://www.nejm.org/doi/pdf/10.1056/NEJMoa1312173In this multi-center open label trial of 776 patients randomized to either a MAP of 65-70 or 80-85 with the primary endpoint of mortality. There was no difference in mortality at 28 days between the two groups (but a small difference in AKI in the patients who had chronic HTN- in the higher BP target, there was a decrease in need for RRT; there was also a higher incidence of afib in the high target group overall). - Results in compensation and stable GFR in short term, long term maladaptive - Reason for ACEi- Clinical Evaluation of Renal Circulation - Concept of clearance and measurement of GFR - GFR as an index of functioning renal mass - Had a patient today s/p nephrotomy, 72 years old, Cr0.9!Melanie referred to this article in Circulation which demonstrates that SGLT2 inhibitors do decrease single nephron GFR (in mice) and that this is related to a decrease in the afferent arteriole diameter and then they show that this is related to a local increase in adenosine. Kidokoro K, Cherney DZI et al. Evaluation of glomerular hemodynamic function by empagliflozin in diabetic mice using in vivo imaging Circulation 140 (4) 2019https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.118.037418 - Fall in GFR earlier and only sign of renal disease - Serial monitoring is used to assess severity and follow the course of disease - GFR is useful for dosing drugs - How to measure GFR - Consider fructose polysaccharide inulin (love the parenthetical, not insulin) - Inulin filtered = inulin excreted - Filtered inulin = plasma inulin concentration x GFR - Inulin excreted = urine concentration x urine volume - Use Alber a to get GFR = [Urine]insulin x urine volume / [plasma]inulin - GFR = inulin clearance - There is not an available assay for inulin - Creatinine clearance - Freely filtered - Not reanbsorbed - Not metabolized - Small amount excreted - CrCl exceeds GFR by 10-20%Roger says the SGLT2 inhibitor story is about the afferent arteriole and he thought it reminded him of the MDRD study and the concept that the lower protein intake would be protective and delay the progression of CKD. The concept was that low protein diets would decrease glomerular pressure by decreasing the intake of amino acids that lead to arteriolar vasodilation and increased GFR. Klaur S, Levey AS et al. The effects of Dietary Protein Restirciton and blood-pressure control on the progression of chronic renal disease. NEJM 1994 330:877-884. https://www.nejm.org/doi/full/10.1056/nejm199403313301301 - Compensated for by noncreatinine chromogens (acetone proteins, as Orbi acid, pyruvate) that over estimate Cr by 10-20% - Cr Cl = [Urine]cr x urine volume / [Plasma]cr - Two major limitations - Incomplete collections - 20-25 mg/kg in adult men - 15-20 mg/kg in adult womenThe term “Acute renal success” comes from Thurau K and Boylan JW. Acute renal success. The unexpected logic of oliguria in acute renal failure. Am J Med 1976 61(3): 3038-15. - Falls by 50% from age 50 to 90 to 10 mg/kg - Increased tubular secretion with decreased kidney function - GFR of 40-80 cr secretion may account for as much as 35% of creatinine excretion - In some cases CrCl can exceed GFR by a factor of 2 - Give cimetidine 1200 mg! - It is important to appreciate however that exact knowledge of GFR is not required. More important to know if GFR is changing - Why is radio labeling the solution DTPA and iothalamate? - Talks about the reality of progressive disease despite stable GFR and CrCl - On to plasma Cr and GFRIf you think placing dialysis lines is too easy, here is a wonderful review of micropuncture technique in the kidneys by Volker Vallon.Micropuncturing the Nephron. Pflugers Arch 2009 458(1): 189-201. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2954491/ - Creatinine excretion = creatinine production (and this is constant) - Creatinine excretion = [Cr] x GFR = constant - If GFR falls in half, creatinine excretion will fall in half, while creatinine production remains the same, so creatinine will rise and rise until [Cr] x GFR = creatinine production and then it will level off. - Changes in creatinine load - High protein diet can increase it - Vegetarian diet can decrease itJC brought up studies on fenoldopam, of which there are many. This is one such study in patients undergoing cardiac surgery. JAMA 2014 Bove T et al. Effect of fenoldopam on use of renal replacement therapy among patients with acute kidney injury after cardiac surgery: a randomized clinical trial https://pubmed.ncbi.nlm.nih.gov/25265449/ - Cooked meat can increase Cr by 1 mg/dL - Talks about need for steady state to assess GFR - Talks about the curvilinear relationship - Then he talks Cockcroft GaultThe one, the only: The Cockcroft Gault: Prediction of creatinine clearance from serum creatinine. Nephron 16: 31–41, 1976 https://pubmed.ncbi.nlm.nih.gov/1244564/ - Cirrhosis masks kidney insufficiency, low meat intake, low BUN production - Can someone explain what we are supposed to take from figure 2-12 - Stable Cr does not mean stable kidney diseaseRoger describes the study design for the seminal paper on the use of ACE inhibitors to slow the decline in renal function in diabetic kidney disease (then called diabetic nephropathy) and the decision to use the doubling of the serum creatinine as an endpoint. Lewis EJ The effect of Angiotensin-converting-enzyme inhibition on diabetic nephropathy NEJM 1993 https://www.nejm.org/doi/full/10.1056/NEJM199311113292004 - Ketoacidosis can raise the Cr 0.5 to 2.0mg/dL - On to BUN - Destination of amino acids produces ammonia - We detoxify ammonia by converting to urea - Increased with increased protein load - Increased catabolismMelanie mentioned an old study on ingestion of expired blood: Cohen TD. Induced azotemia in humans following massive protein and blood ingestion and the mechanism of azotemia in gastrointestinal hemorrhage. AM J Med Sci 1956 https://pubmed.ncbi.nlm.nih.gov/13302213/ - Tetracycline causes decreased anabolism - Trauma - Steroids - Urea excretion is variable and tied to hydration and FF - Renal plasma flow and PAH
This episode covers high yield topics related to the renal system. Make sure to check out the visual aid. Also good luck to everyone starting dedicated! GI is coming soon! Notes: https://documentcloud.adobe.com/link/track?uri=urn:aaid:scds:US:1acb8de2-6419-4fb8-9803-e3ccc9689ac9 Outline: https://documentcloud.adobe.com/link/track?uri=urn:aaid:scds:US:1201019c-bd9a-4e0f-b788-cb832b4b1922 Basics and the Nephron (0:19), Urine (4:46), Blood Supply (7:59), Embryology (11:10), U/A and microscopy (17:30), See This Think This (19:52)
Because studies predict one in nine Americans will face some level of disease of the kidney, understanding kidney development and nephron function is key. Professor Lori O'Brien discusses her research into kidney processes, describing How kidney development progresses in utero and what are the two main type of progenitor cells, What are the stages of kidney disease and how effective are dialysis and kidney transplantation, and What are challenges to kidney organoid development such as how to rid the organoid of filtrate. Lori O'Brien is a principal investigator and assistant professor in the Department of Cell Biology and Physiology at the University of North Carolina Kidney Center. In this podcast, she discusses the focus of her work, namely to understand the development of a kidney to better understand what goes wrong in kidney disease. This work informs efforts to eventually manufacture a renal replacement, and she explains that scientists need to understand its basic biology as much as possible to do so. She also explains the damage of kidney disease as well as the mistaken notion that dialysis treatment is somehow a cure. Rather, on average, most dialysis patients will only survive about five years because dialysis treatment only mimics about 10% of what a kidney actually does for the body. She then describes her work more specifically around pluripotent stem cells that lead to the two different cell populations in the kidney: cells that eventually make nephrons and those that make up the connecting duct system. She describes challenges to each cell type, the complex specialization of the cell types, and how they work in the body along with the vascular and nerve network in a way that's hard to reproduce with organoids. She describes some advances therein and various ways they hope to problem solve. For more, see her UNC website at med.unc.edu/cellbiophysio/directory/lori-obrien-phd/, and her lab's website at obrienlab.web.unc.edu. Available on Apple Podcasts: apple.co/2Os0myK
Crush Step 1: The Ultimate USMLE Step 1 Review (An InsideTheBoards Podcast)
This episode contains the first section of the Nephrology chapter from Crush Step 1, covering topics such as: - Anatomy - Physiology Overview and Terminology Glomerular Filtration Rate Clearance and GFR The Glomerulus and Filtration - The Nephron and it's Segments Proximal Tubule Body Fluid Compartments and Maintenance Other Endocrine Functions of the Kidney pH Homeostasis and Acid-Base Disturbances Get a discount on best selling study resources from Elsevier ITB listeners can get 30% off of books like Crush Step 1, USMLE Step 2 Secrets, Netter’s Anatomy Coloring Book, and more! Head over to us.elsevierhealth.com/insidetheboards and use the code ITB30 at checkout. About the Crush Step 1 Podcast With a focus on teaching you to “think like a question writer”, InsideTheBoards is the leading producer of medical education podcasts. The Crush Step 1 podcast, the second collaboration between InsideTheBoards and Elsevier, features a totally free, audio optimized, complete narration of Crush Step 1: The Ultimate USMLE Step 1 Review by Ted O'Connell, Ryan Pedigo, and Thomas Blair. Crush Step 1 features up-to-date, easy-to-read (or listen to), high yield info on all the material tested on the exam with topics selected by a review board of current medical students and residents who scored in the 99th percentile on the USMLE Step 1. The Crush Step 1 podcast is the perfect companion for your dedicated prep time. InsideTheBoards Study Smarter Podcast Each year during the dedicated prep time we run a “Study Smarter Series for the USMLE Step 1 and COMLEX Level 1” on our Study Smarter Podcast with a focus exclusively on breaking down USMLE style questions. Click here to check it out on iTunes or visit our BRAND NEW Website ITB Audio Qbank and iOS Beta App The Audio Qbank by InsideTheBoards mobile app has both free and premium features and is available on both Android and iOS. To get started, first, create a Boardsinsider Account on our website insidetheboards.com Free Features All of our podcasts in one place organized into playlists for easy studying (also with less ads and exclusive content) Mindfulness meditations designed specifically for medical students A monthly offering of high yield content (questions dissections, audio qbank samples) available only on our mobile app. Early Access and exclusive content like a preview of the soon to be released "Crush Step 1" podcast and the "Inside ITB" podcast where we "get real" about the challenges of building ITB and the day to day behind the scenes stuff. Premium Features Subscribe to an ITB premium account and get additional features Access to 500+ audio optimized board style practice questions in our Audio Qbank. The Step 1 version is powered by Exam Circle and the Step 2 Version is powered by OnlineMedEd. New questions added each month. High Yield Pharmacology (powered by Lecturio) with 100 of the top pharm questions you need to know for both Step 1 and Step 2 Audio Flashcards (coming soon) Our audio qbank is PERFECT for studying for the boards on the go. And we're adding content and improving it all the time. Learn more about the Audio Qbank by InsideTheBoards mobile app here InsideTheBoards, Elsevier and their collaborators are not affiliated with the NBME, USMLE, COMLEX, NBOME or any professional licensing body. InsideTheBoards and its partners fully adhere to the policies on irregular conduct outlined by the aforementioned credentialing bodies.
(Part 1) Episode 20 dives into the anatomy and physiology of the kidneys. We specifically discuss the nephron and the sites of ion transport. Be sure to look out for episode 21 where we build on this information and discuss the medications and diseases associated with the renal system. To become a premium member go to Patreon.com, search "student nurse anesthesia" and become a member. You will then have access to all of our episodes right here on Apple Podcasts!
Kara and Burnie talk BEES, plus a few things that make Nephron kind of unique.. (0:20). Interview with Nephron Pharmaceuticals President & CEO Lou Kennedy (1:13) - talking pre-coronavirus investments and production (2:50), Nephron's teacher-hire program (4:15), adjusting production for COVID-19 response (5:57), advice for companies looking to make adjustments (12:22), U.S. vs. overseas pharmaceutical production (16:22), importance of investing in health/life sciences and rural broadband (19:39).
From innovative new work programs, to investing in education and the push for tax reform in South Carolina we talk with the always candid Lou Kennedy.
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. Chapter 23: Role of Kidneys in Metabolism; 309-319. Copyright 2014, Elsevier Limited. Available at: www.clinicalkey.com. Accessed 6/9/2014. Bellizzi V. Low-protein diet or nutritional therapy in chronic kidney disease? Blood purification. 2013;36(1):41–6 Bellomo R, Ronco C, Kellum JA, Mehta RL, Palevsky P. Acute renal failure - definition, outcome measures, animal models, fluid therapy and information technology needs: the Second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group. Critical care (London, England). Aug 2004;8(4):R204-212. Bertelli AAE, Migliori M, Panichi V. Resveratrol, a component of wine and grapes, in the prevention of kidney disease. Ann N Y Acad Sci. 2002;957:230–8 Brodin EE, Braekkan SK, Vik A, Brox J, Hansen JB. Cystatin C is associated with risk of venous thromboembolism in subjects with normal kidney function--the Tromso study. Haematologica. Jul 2012;97(7):1008-1013. Busch M, Franke S, Ruster C, and Wolf G. 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. Implications of magnesium deficiency in type 2 diabetes: a review. 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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. 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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. 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Nephron Pharmaceuticals Corporation is located in Cayce, South Carolina. They are a global leader in manufacturing generic respiratory medications and also contract manufacturing.
Dr Segun Simon talks about the specialty of Nephrology, having a passion, the business opportunities, working as a solo practitioner, the variety of cases seen in Nephrology, the new innovations and the subspecializations within Nephrology.
Dr Segun Simon talks about the specialty of Nephrology, having a passion, the business opportunities, working as a solo practitioner, the variety of cases seen in Nephrology, the new innovations and the subspecializations within Nephrology.
Today I want to turn our discussion to Kidney Cancer. According to the National Cancer Institute there are three main types of kidney cancer. Renal cell cancer is the most common type in adults and Wilm's tumors are the most common in children. These types form in the tissues of the kidney. Transitional cell cancer, the same type of cancer that can form in the bladder, forms in the renal pelvis and ureter, the funnel shaped drainage system from the kidney. According to the American Cancer Society, in the United States in 2017, about 64,000 new cases of kidney cancer and renal pelvis cancer are expected and will lead to more than 14,000 deaths. Statistically, about 1 out of every 63 people will get a kidney cancer within his or her lifetime For today's discussion, I want to focus specifically on Renal Cell Carcinoma, the most common type of kidney cancer in adults. Renal Cell Carcinoma is responsible for over 90% of all cases of kidney cancer. Renal Cell Carcinoma accounts for about 4% of all the adult malignancies and is in the top ten malignancies for both men and women. A man is 1.5 times more likely to get kidney cancer than is a woman. Risk factors for Renal Cell Carcinoma include the following: smoking, obesity and high blood pressure. Extensive use of NSAIDS has also been implicated. It goes without saying, of course, but I am going to say it anyway. Stop smoking, watch your weight, and control your blood pressure. A family history of renal cell cancer also predisposes you to a risk of kidney cancer. Genetic variants have been identified as the cause of inherited cancer risk in some Renal Cell Carcinoma–prone families; these pathogenic variants are estimated to account for about 5% of Renal Cell Carcinoma cases. Furthermore, having certain conditions or syndromes can also lead to Renal Cell Carcinoma such as von Hippel-Lindau disease, Birt-Hogg-Dubé syndrome, hereditary leiomyomatosis, and tuberous sclerosis. Patients with kidney cancer may present with the so-called “classic triad” of symptoms: blood in the urine, pain in the flank or abdomen, and a palpable mass. But this presentation is only common when the tumor is very large. Renal Cell Carcinoma has also received the moniker, “the internist's tumor” because an interesting facet of kidney cancer is that it may manifest first in something called a “paraneoplastic syndrome” that seems unrelated to the kidney: hypercalcemia (pseudohyperparathyroidism), erythrocytosis, hypertension, and gynecomastia are all related to hormone like substances made some renal cell carcinomas. More commonly in the day of advanced imaging such as CT or MRI kidney tumors are discovered incidentally (i.e. an incidentaloma) when a person has the imaging done for other reasons and a small, asymptomatic tumor is seen in the kidney. Tumors found incidentally may be very small, even as small as 1 cm, the size of a pea. A CT scan also called computerized axial tomography or CAT scan is an x-ray that makes a series of detailed pictures of areas inside the body by computing x-ray pictures taken from many different angles. A dye may be injected into a vein or swallowed to help the organs or tissues show up more clearly. An MRI or magnetic resonance imaging is a procedure that uses a magnet and a computer to make a series of detailed pictures. Both the CT and the MRI create a very detailed image of the kidneys and can determine if a tumor is cystic (typically benign) or solid (can be benign or cancerous). A CT scan or MRI cannot tell you if a tumor is cancerous; a cancer can only be diagnosed by biopsy of the tumor or after the tumor is removed. A Renal Cell Carcinoma (RCC) originates from the lining of the proximal convoluted tubule, a part of a series of small tubes in the kidney that filter the blood and then concentrate and transport urine to the renal pelvis and ureter. But doctors didn't always know that this tumor found in the kidney actually started in the kidney. In fact, the origin of kidney cancer, where it came from in the body, was not known for many years, and was one of the longest controversies in surgical pathology. The debate started with Dr. Paul Grawitz, a German pathologist, when in 1883, he published his observations on small, yellow renal tumors that had previously been described as lipomas or fatty tumors. Dr. Grawitz compared these small tumors to the normal adrenal gland and hyperplasia of the adrenal gland, and concluded that they represented small ectopic adrenal rests (struma suprarenalis aberrata). Dr. Grawitz consolidated his theory with further illustrations of intrarenal ectopic adrenal tissue. Dr. Grawitz's theory stimulated considerable interest and was widely, but not universally, accepted. Other doctors supported the adrenal rest theory by coining the term hypernephroid tumor, which was later amended to “hypernephroma”, to describe these tumors. Vigorous criticism of Grawitz was provided by Oskar Stoerk in 1908, who considered the adrenal origin of renal tumors to be unproved. He compared the relative frequency of renal tumors with the scarcity of malignant epithelial tumors of the adrenal gland and commented on the lack of histological similarity between a hypernephroma and adrenal gland cancer. It wasn't until 1959 that convincing evidence to settle the debate was offered in the Journal Nature(1960, 186: 402-403) by Dr. Oberling C who studied the ultrastructure of clear cells from eight renal carcinomas and found that the tumor cell cytoplasm contained numerous mitochondria and deposits of glycogen and fat, with occasional cells containing microvilli along free borders and concluded that these features were more consistent with the epithelial cells of the renal convoluted tubule. Although renal cell carcinoma is now recognized as starting in the kidney, renal cell carcinoma is still sometimes referred to incorrectly as a hypernephroma or a Grawitz tumor. Doctors continue to learn more and more about different types of kidney cancer. In The 2004 World Health Organization (WHO) classification of genitourinary tumors recognized over 40 subtypes of renal neoplasms, and several more have been added since that time. Let's transition to how we treat Kidney Cancer. I want to begin by quoting another author. “The treatment for Renal Cell Carcinoma, both, primary and secondary growths, continues to be surgical…a review of the literature indicates that the hope of cure in this tumor lies in the hand of the surgeon.“ Thus begins an article in the Journal of Urology when, in 1964, Dr Charles Robson reviewed 88 cases of kidney cancer that he treated surgically during a 15 year span between 1949 and 1964. Robson's article is published, along with other groundbreaking articles in Urology, in an anniversary edition of the Journal of Urology, this year celebrating its centennial. You can find the article at www.JU100.org. What was true in 1964 is still true today. The best hope of cure of Renal Cell Carcinoma is to catch it early and remove it, almost regardless of subtype or predisposing condition. The recommended treatment for renal cell cancer is surgical removal of all or part of the kidney. Different procedures, radical nephrectomy vs. partial nephrectomy, open vs. laparoscopic or robotic, removal of adrenal glands and lymph nodes, may all be appropriate depending on circumstances, tumor size, location and a patient's other medical problems. A "radical" nephrectomy removes the entire affected kidney including Gerota's fascia (the fat around the kidney), and may also include the adrenal gland which is on the same side as the affected kidney, and the regional retroperitoneal lymph nodes. This technique is most often used when there is a large tumor present in only one kidney. It is important to note that the other kidney must be fully functional and the patient must be healthy enough to undergo a major surgery and associated risks and complications both during and after the surgery. Smaller renal tumors (usually < 4 cm) are treated by “partial” nephrectomy when possible. The partial nephrectomy involves the removal of the affected tissue only, sparing the rest of the kidney, Gerota's fascia and the regional lymph nodes. This allows for more renal preservation as compared to the radical nephrectomy, and this can have positive long-term health benefits. Nephron-sparing partial nephrectomy is especially important when the patient has other medical concerns such as diabetes or hypertension. Larger and more complex tumors can also be treated with partial nephrectomy by experienced surgeons. Cryotherapy or other ablative techniques can also be done on smaller lesions with good long-term success if chosen for the right patient. Surgery is increasingly being performed via laparoscopic and robotic techniques. Laparoscopic or robotic surgery does not have the large incisions seen in a classically performed radical or partial nephrectomy, but still successfully removes either all or part of the kidney. Visualization and dissection is performed using small incisions (one of my partners calls them “poke holes”) through which we pass high definition cameras and dissecting instruments. Robotic surgery has an advantage over laparoscopic surgery because of the increased dexterity afforded by the robotic instruments. I discussed robotic surgery with one of my partners in episode of this podcast. Laparoscopic and robotic surgery is associated with shorter stays in the hospital and quicker recovery time. Most cases that I perform are done robotically, with a preference for a partial nephrectomy if possible. Last week I was involved with 5 different operations for renal masses. One of the operations was a radical nephrectomy, 4 others were done as robotic partial nephrectomy. The nephrectomy done last week was for a very large renal mass and required an incision, the first incision I have made for my practice in several months. In 1964 Dr. Robson used the thoraco-abdominal or trans-peritoneal abdominal approach to remove a kidney, and his name became almost synonymous with a thoraco-abdominal incision, an incision that opens the chest cavity as well as the abdominal cavity. Urologists rarely use the thoraco-abdominal approach today, but use an abdominal incision only when a large incision is needed. He described the operation succinctly but effectively and I will read from his article. “After reflection of the colic flexure, dissection should begin on the medial border of the tumor. The renal vein is identified and the renal artery is dissected free from its posterior aspect. The artery should be ligated before the vein wherever this is possible, thus disturbing the hemodynamics as little as possible. The value of a preoperative aortogram, besides its diagnostic features, might be emphasized here, because it will definitely identify the position of the renal artery and, also, if there is an accessory artery present or if there is an abnormal division of the renal artery, the surgeon is forewarned. The perinephric fat and overlying peritoneum are removed with the primary growth and, where possible, the para-aortic and para-caval lymph nodes from the bifurcation of the aorta to the crus of the diaphragm. If the tumor is very large, it may be necessary to remove it before the gland dissection is carried out.” The principles that Robson defines in his brief description of the operation, specifically understanding the vascular anatomy prior to the operation and early identification and ligation of the renal artery still hold today, and are the foundation for today's careful anatomical dissection and improved outcomes, regardless of whether the procedure is done robotically or with a large incision. As I read through his description I realized that with the exception of the extended lymph node dissection, last week I used a trans-peritoneal subcostal incision and performed the surgery just as he described. Dr. Robson argued in his article that the prognosis for renal cell carcinoma is dependent upon 5 factors and/or a combination of these: 1) involvement of adjacent structures by direct extension, 2) presence or absence of distant metastases, 3) involvement of the regional lymph nodes, 4) gross invasion of the renal vein or its main tributaries and 5) histological grade of the tumor. Robson created a staging system with 4 different stages based on whether the tumor was in the kidney or invaded the perirenal fat, had lymphatic or vascular involvement, or had metastasized. We now use a more detailed TNM Staging System, but there are still 4 stages of cancer. A tumor confined to the kidney and less than 7 cm across is Stage 1, if it is greater than 7 cm it is stage 2. Stage 3 is a tumor of any size that is invading the fat around the kidney or resides in a nearby lymph node. Stage 4 is any invasion into the adrenal gland, distant lymph nodes or other metastasized to other organs. Taken as a whole, if cancer is only in the kidneys, it can be cured roughly 80-90% of the time with surgery. More specific subsets show a five-year survival rate of around 90–95% for tumors less than 4 cm. For larger tumors confined to the kidney without venous invasion, survival is still relatively good at 80–85%. For tumors that extend through the renal capsule and out of the local fascial investments, the survivability reduces to near 60%. Survivability decreases significantly in cases where the cancer is stage 4 or metastasized. But even in cases of metastatic disease, long term prognosis continues to improve with changing chemotherapy regimens. Factors such as general health and fitness or the severity of their symptoms at presentation impact the survival rates. The earliest reference suggestive of tumor arising in the kidney was made by Daniel Sennert in his text Practicae Medicinae, first published in 1613. Sennert wrote, “Moreover the hard swelling of bad kidneys which has the capacity to throw a person into cachexia and dropsy, is for the greater part incurable”. That is not true today. Today with advanced techniques and diagnostic tools we are able to find kidney cancers early and remove them or control them effectively if they have spread. And, as I said, we are still learning. Dr. Robson's article in 1964 advanced our knowledge and surgical expectations for patients with kidney cancer. Laparoscopy, robotic surgery, advanced CT, MRI and Ultrasound imaging have also moved us forward. Newer chemotherapy and immunotherapy regimens will continue to improve the survivability of the disease but, for now, I will leave you quoting Dr. Robson again, “…the hope of cure in this tumor lies in the hands of the surgeon.” https://en.wikipedia.org/wiki/Paul_Grawitz http://uscapknowledgehub.org/site~/98th/pdf/companion09h02.pdf https://www.cancer.gov https://www.iarc.fr/en/publications/pdfs-online/pat-gen/bb7/BB7.pdf
In this episode, I discussed various aspects of nephron physiology, segment by segment, and I threw in some examples of pathophysiology as we went along. Enjoy! The Med School Phys podcast discusses topics in human physiology. Our primary aim is to help medical students learn/review high yield material for their classes and board exams. Hopefully listeners find that this alternative audio-based learning format works for them. This podcast is intended to be educational and all the information shared herein is publicly available through the internet. Med School Phys is an independent project and currently shares no affiliation with other organizations, companies, or academic institutions.-You can email me questions or constructive feedback at medschoolphys@gmail.com -Check out my book, Read This Before Medical School: https://www.amazon.com/dp/B07YCXZM3X/ref=docs-os-doi_0 -Episode transcriptions can be found at: https://drive.google.com/drive/folders/12QQSFho-ThIIeZuulsblGSnnNL8oJ7ag?usp=sharingDISCLAIMER: All information, content, and materials published by the Med School Phys podcast are for informational purposes only and are NOT intended to serve as a substitute for the consultation, diagnosis, and/or medical treatment of a qualified healthcare provider. Please consult your healthcare provider regarding personal medical decisions.
In this episode, I discussed various aspects of nephron physiology, segment by segment, and I threw in some examples of pathophysiology as we went along. Enjoy! The Med School Phys podcast discusses topics in human physiology. Our primary aim is to help medical students learn/review high yield material for their classes and board exams. Hopefully listeners find that this alternative audio-based learning format works for them. This podcast is intended to be educational and all the information shared herein is publicly available through the internet. Med School Phys is an independent project and currently shares no affiliation with other organizations, companies, or academic institutions.You can email me questions or constructive feedback at medschoolphys@gmail.comYou can share a link to our episodes via Spreaker or encourage others to listen on their podcasting app of choice: https://www.spreaker.com/user/medschoolphysFind our Youtube channel at: https://www.youtube.com/channel/UCXEEgC1JZysYsKy9NRYisEQEpisode transcriptions can be found at: https://drive.google.com/drive/folders/12QQSFho-ThIIeZuulsblGSnnNL8oJ7ag?usp=sharingDISCLAIMER: All information, content, and materials published by the Med School Phys podcast are for informational purposes only and are NOT intended to serve as a substitute for the consultation, diagnosis, and/or medical treatment of a qualified healthcare provider. Please consult your healthcare provider regarding personal medical decisions.
How are substances reabsorbed and secreted along the nephron to create urine? How do diuretics work?
John He and Ravi Iyengar talk about their use of proteomic analysis and computational methods to identify potential targets for reversing kidney damage.
Tubular Transport in the Nephron
Tubular Transport in the Nephron
Tubular Transport in the Nephron
Medizinische Fakultät - Digitale Hochschulschriften der LMU - Teil 02/19
Die Ionenkanäle des renalen Tubulus- und Sammelrohrsystems bestimmen die Funktion der adulten Säugetierniere. Sie müssen mit der Entwicklung der permanenten Niere (Metanephrogenese) erworben werden und können auch entwicklungsspezifische Aufgaben haben. Ziel dieser Arbeit ist die erstmalige systematische Beschreibung der Expression und entwicklungsspezifischen Rolle von Ionenkanälen während der Metanephrogenese. Methoden: Die ontogenetische mRNA-Expression der Kir Kalium-Kanal-Untereinheiten Kir6.1, SUR2 und ROMK1-3 (Kir1.1a-c) wurde mittels RT-PCR von Primärkulturen im Sammelrohrepithel quantifiziert, die ontogenetische Kir6.1- und ROMK-Protein-Expression mittels Immunhistochemie in Sammelrohr- und Nephron-Epithelien untersucht. Der Effekt von cAMP auf die ROMK-mRNA-Expression wurde gemessen und der Einfluss von Kalium-Kanalmodulatoren auf das Wachstum von Nephron-Kulturen in vitro und von HEK293 Nierenepithel-Zellen bestimmt. Ferner wurde die ontogenetische mRNA-Expression des ENaC-Natrium-Kanals und der Chlorid-Kanäle CFTR, CLC-2 und ICLn mittels RT-PCR im Sammelrohrepithel quantifiziert. Alle Experimente wurden an Ratten oder Mäusen durchgeführt. Ergebnisse: (i) Die mRNA der KDNP-(KATP)-Kanaluntereinheiten Kir6.1/SUR2 war in frühen Ureterknospen-Generationen (embryonaler Tag E14) hoch exprimiert und nach der Geburt herunterreguliert. In gleicher Weise war Kir6.1-Protein im embryonalen Sammelrohrepithel und Nephron ubiquitär apolar exprimiert. Im Gegensatz hierzu war Kir6.1 im adulten Nephron ausschließlich im Proximalen Tubulus nachweisbar (apikal > basolateral). Die spezifische Aktivierung von KNDP-(KATP)-Kir6.1/SUR2-Kanälen in Nephronkulturen und HEK293-Zellen steigerte die Zellproliferation, was auf eine wachstumsregulierende Rolle der frühen Kir6.1/SUR2-Expression hinweist. Somit könnten zelluläre Entwicklungsprogramme der Niere die Wachstumsrate über die Expression von Kalium-Kanälen regulieren. (ii) Die mRNA des apikalen sekretorischen Sammelrohr-Kalium-Kanals ROMK2(Kir1.1b) war von Beginn der Entwicklung an in Ureterknospen/Sammelrohrepithelien exprimiert und stieg während der Reifung des Kortikalen Sammelrohrs um den Faktor 4 an (postnatale Tage P7-28). Diese Zunahme spiegelt den Erwerb der adulten Natrium-retinierenden Funktion des Sammelrohrepithels wider. Die Protein-Expression von ROMK war in embryonalen Nierenepithelien ubiquitär und apolar nachweisbar, jedoch postnatal auf die apikale Plasmamembran des aufsteigenden Teils der Henle'schen Schleife und des Sammelrohrs beschränkt. Die ROMK-mRNA-Expression in embryonalen Sammelrohrepithelien war durch cAMP stimulierbar. (iii) Während der frühen Genese des Sammelrohrsystems wurden die mRNAs der Chlorid-Kanäle CFTR, CLC-2 und ICLn exprimiert, die sehr wahrscheinlich an der aus Ureterknospen bekannten hohen fraktionellen Chlorid-Leitfähigkeit beteiligt sind. Während der postnatalen Sammelrohrepithel-Reifung wurde die mRNA des apikalen Natrium-Kanals ENaC transkriptionell hochreguliert. So kann rechtzeitig die NaCl-resorbierende Funktion der Niere des Neugeborenen sicher gestellt werden (zusammen mit der Heraufregulation von ROMK).
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