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Nine kidney disease research breakthroughs from 2023.

2023 was a big year for the nephrology (kidney) research field. From developments in organ transplant options to a new understanding of kidney disease risk, it can be challenging to keep up with it all. Fortunately, the American Kidney Fund (AKF) has been keeping tabs on these headlines for you. 

Here are nine of the biggest headlines from the nephrology research field from 2023.

Breakthrough #1: New atlas of human kidney cells to help unlock kidney disease research | National Institutes of Health (NIH)

In July, the National Institutes of Health (NIH) announced it had created a "comprehensive atlas of the human kidney." By comparing cells from healthy kidneys to those from diseased or injured kidneys, researchers created a "map" or model of the human kidney. This model was created as part of the Kidney Precision Medicine Project (KPMP) with support from NIH's National Institute of Diabetes and Digestive and Kidney Disease. The goal of precision medicine — and the kidney model — is to create new drugs and treatments that target the specific cause of a disease. Not all kidney diseases or acute kidney injuries affect the kidneys in the same way and this model will help scientists to better treat or prevent different types of kidney disease. 

Breakthrough #2: Report redefines overlapping risks of heart and kidney diseases | American Heart Association

The American Heart Association (AHA) submitted a presidential advisory defining and officially declaring  cardiovascular-kidney-metabolic (CKM) syndrome as a specific health condition. This condition acknowledges the overlap between cardiovascular (heart) disease, kidney disease, type 2 diabetes and obesity, breaking the condition into different stages with prevention and treatment guidelines for each stage. Find out more about what experts describe as a paradigm change in this AKF blog post .

Breakthrough #3: Feasibility of an implantable bioreactor for renal cell therapy using silicon nanopore membranes | Nature Communications

The Kidney Project — a national research project led by the University of California San Fransisco to create a bioartificial kidney — announced progress this year. The plan for the implantable device includes two key parts: (1) a bioreactor and (2) a hemofilter. The hemofilter will filter the blood to remove waste and toxins. However, the kidney performs other important functions for the body, too, including managing the level of certain hormones and reabsorbing water and other needed nutrients after the blood has been filtered. The bioreactor will perform these critical jobs, using a combination of kidney cells and silicone membranes. In August, the Kidney Project researchers published their findings that they had successfully implanted the bioreactor in healthy pigs. The next step would be FDA trials, first in animals and eventually in humans.

Breakthrough #4: Pig kidney works a record 2 months in donated body, raising hope for animal-human transplants | AP News

The University of Alabama at Birmingham (UAB) successfully transplanted a genetically modified pig kidney for the first time in August 2023 , which functioned as a healthy human kidney would for the seven days of the study. The New York University (NYU) Langone Health hospital also transplanted a pig kidney into the body of a brain-dead man, Maurice "Mo" Miller, which survived for two months . This is the longest a pig kidney has functioned in a human body to date and scientists are hopeful this may mean they can eventually begin trials to transplant one into a living human.

Breakthrough #5: Global Coalition on Aging Finds Chronic Kidney Disease A Troubling Blind Spot Among Chronic Diseases in the US - Global Coalition On Aging

The Global Coalition on Aging (GCOA), the World's Leading Business Voice on Aging, conducted a survey of 1,000 Americans 18 years and older and discovered a surprising lack of awareness and understanding about chronic kidney disease. Despite the growing rate of kidney disease in U.S., over half of the participants (58%) had no awareness of the disease at all. Even respondents who regularly saw doctors did not have an awareness of the disease. GCOA recommended several steps to increase awareness, some of which AKF has already undertaken — including bringing stakeholders together to discuss concerns within the kidney community .

Breakthrough #6: Millions of lives and billions of dollars: the need for earlier intervention in chronic kidney disease (medicaleconomics.com)

As part of the Patient Access Initiative (PAI), AKF published a white paper called "Reimagining Kidney Care: From Crisis to Opportunity," that examines the dire kidney disease trends in the U.S. The paper also highlights the potential benefits of creating policies that prioritize "upstream care." Upstream care is an approach to health care that puts an emphasis on addressing the root of a medical problem rather than the symptoms. It focuses on earlier detection and intervention of a disease rather than treating it once it has become more advanced. The paper shows how this approach could have benefits for Americans' health and its economy.  Find out more in this AKF blog post . 

Breakthrough #7: New Non-Invasive Test Uses AI and Retinal Scans To Accurately Predict Risk of Chronic Kidney Disease | AP News

A new noninvasive retinal scan that uses an artificial intelligence (AI) deep learning algorithm called Reti-CKD "showed superior prediction of future CKD risk compared to the conventional [estimated glomerular filtration rate (eGFR)] or urine test." The test can accurately predict kidney disease risk because the kidneys and retina (the light-sensitive layer of eye tissue innermost in the eye and is an extension of the brain) have similar micro blood vessels. Concerns about the micro blood vessels in the retina, therefore, can be predictive of possible problems with the micro blood vessels in the kidneys, putting the person at greater risk for kidney disease. 

Breakthrough #8: Risk Calculator for Early-Stage CKD May Soon Enter US Market (medscape.com)

Dr. Naveep Tangri, a nephrologist and professor at the University of Manitoba, is the founder of Klinrisk, Inc., a company that is developing and commercializing a new predictive tool for kidney disease called the  Klinrisk model . Using 20 lab-measured variables from routinely ordered tests, it can predict the risk of an adult with early-stage CKD developing either a 40% or greater drop in eGFR or kidney failure. Since the Klinrisk model uses information from tests a primary care doctor may already give, Dr. Tangri says it is ready for any health system, insurance company or clinic to implement.

Breakthrough #9: Exercise during hemodialysis improved physical function of patients with kidney failure

A study  found that, after 12 months, patients who participated in endurance and resistance exercises during their hemodialysis treatments had improved physical function compared to those receiving standard treatment. The study included 917 patients and found that those who did the exercises during dialysis also reported an improved quality of life and had fewer hospitalizations.

While there is no cure for kidney disease, there are ways to manage or treat it and 2023 had several exciting new developments in the advancement of drugs to treat kidney disease. These developments include FDA approvals for: 

• A  drug to slow down the decline of eGFR in people with kidney disease
• A  phosphate absorption inhibitor drug
• The  first fully-FDA-approved treatment for a rare kidney disease called IgA nephropathy  

Furthermore, a study showed overwhelmingly positive results that the active ingredient in a diabetes treatment and a weight loss drug did not further damage the heart or kidneys . Advancements like these are critical to helping the millions of people living with kidney disease manage or slow down the progression of the disease, and hopefully avoid reaching kidney failure.

You can find more headlines from throughout the year on our Renal news round up page .

We hope to see even more progress in the kidney disease research and treatment space in 2024!

Filed under

• Kidney disease
• Kidney failure
• Kidney transplant

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Scientists first in the world to regenerate diseased kidney cells

by Federico Graciano, Duke-NUS Medical School

In a world first, scientists at Duke-NUS Medical School, the National Heart Center Singapore (NHCS) and colleagues in Germany have shown that regenerative therapy to restore impaired kidney function may soon be a possibility.

In a preclinical study reported in Nature Communications , the team found that blocking a damaging and scar-regulating protein called interleukin-11 (IL-11) enables damaged kidney cells to regenerate, restoring impaired kidney function due to disease and acute injuries.

"Kidney failure is a global epidemic," said Assistant Professor Anissa Widjaja, a molecular biologist with Duke-NUS' Cardiovascular & Metabolic Disorders (CVMD) Signature Research Program. "Closer to home, Singapore ranks first in the world for diabetes-induced kidney failure and fourth in terms of kidney failure prevalence. The contribution of chronic kidney disease to mortality is rapidly increasing, suggesting there are shortcomings in current therapeutic approaches."

Searching for ways to restore the kidney's ability to regenerate damaged cells, Widjaja worked with Professor Stuart Cook, Tanoto Foundation Professor of Cardiovascular Medicine at the SingHealth Duke-NUS Academic Medical Center and the CVMD Program, and Clinician Scientist and Senior Consultant with the Department of Cardiology, NHCS, and Duke-NUS Dean Professor Thomas Coffman, a world-leading nephrologist. They teamed up with scientists in Germany to investigate the role of IL-11, which is known to trigger scarring in other organs, including the liver, lungs and heart, in acute and chronic kidney disease.

Their findings implicate the protein in triggering a cascade of molecular processes in response to kidney injury that leads to inflammation, fibrosis (scarring) and loss of function. They also discovered that inhibiting IL-11 with a neutralizing antibody can prevent and even reverse kidney damage in this setting.

"We found that IL-11 is detrimental to kidney function and triggers the development of chronic kidney disease," said Cook. "We also showed that anti-IL11 therapy can treat kidney failure, reverse established chronic kidney disease, and restore kidney function by promoting regeneration in mice, while being safe for long term use."

More specifically, the researchers showed that renal tubular cells, which line the tiny tubes inside kidneys, release IL-11 in response to kidney damage . This turns on a signaling cascade that ultimately leads to increased expression of a gene, called Snail Family Transcriptional Repressor 1 (SNAI1), which arrests cellular growth and promotes kidney dysfunction.

In a preclinical model of human diabetic kidney disease, turning off this process by administering an antibody that binds to IL-11 led to proliferation of the kidney tubule cells and reversal of fibrosis and inflammation, resulting in the regeneration of the injured kidney and the restoration of renal function.

While clinical trials of an antibody that binds to another pro-fibrotic molecule called transforming growth factor beta have been unsuccessful, this new approach brings hope of a new target.

"By boosting the kidney's intrinsic capability to regenerate, Prof. Cook and Asst. Prof. Widjaja have shown that we can restore function to a damaged kidney," said Coffman, who is also the principal investigator of the Diabetes Study in Nephropathy and other Microvascular Complications (DYNAMO), a large collaborative study that aims to find new solutions for the prevention and treatment of diabetic kidney disease.

"This discovery could be a real game-changer in the treatment of chronic kidney disease —which is a major public health concern in Singapore and globally—bringing us one step closer to delivering the benefits promised by regenerative medicine."

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A new drug candidate can shrink kidney cysts

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Autosomal dominant polycystic kidney disease (ADPKD), the most common form of polycystic kidney disease, can lead to kidney enlargement and eventual loss of function. The disease affects more than 12 million people worldwide, and many patients end up needing dialysis or a kidney transplant by the time they reach their 60s.

Researchers at MIT and Yale University School of Medicine have now found that a compound originally developed as a potential cancer treatment holds promise for treating ADPKD. The drug works by exploiting kidney cyst cells’ vulnerability to oxidative stress — a state of imbalance between damaging free radicals and beneficial antioxidants.

In a study employing two mouse models of the disease, the researchers found that the drug dramatically shrank kidney cysts without harming healthy kidney cells.

“We really believe this has potential to impact the field and provide a different treatment paradigm for this important disease,” says Bogdan Fedeles, a research scientist and program manager in MIT’s Center for Environmental Health Sciences and the lead author of the study, which appears this week in the Proceedings of the National Academy of Sciences .

John Essigmann, the William R. and Betsy P. Leitch Professor of Biological Engineering and Chemistry at MIT; Sorin Fedeles, executive director of the Polycystic Kidney Disease Outcomes Consortium and assistant professor (adjunct) at Yale University School of Medicine; and Stefan Somlo, the C.N.H. Long Professor of Medicine and Genetics and chief of nephrology at Yale University School of Medicine, are the senior authors of the paper .

Cells under stress

ADPKD typically progresses slowly. Often diagnosed when patients are in their 30s, it usually doesn’t cause serious impairment of kidney function until patients reach their 60s. The only drug that is FDA-approved to treat the disease, tolvaptan, slows growth of the cysts but has side effects that include frequent urination and possible liver damage.

Essigmann’s lab did not originally set out to study PKD; the new study grew out of work on potential new drugs for cancer. Nearly 25 years ago, MIT research scientist Robert Croy, also an author of the new PNAS study, designed compounds that contain a DNA-damaging agent known as an aniline mustard, which can induce cell death in cancer cells.

In the mid 2000s, Fedeles, then a grad student in Essigmann’s lab, along with Essigmann and Croy, discovered that in addition to damaging DNA, these compounds also induce oxidative stress by interfering with mitochondria — the organelles that generate energy for cells.

Tumor cells are already under oxidative stress because of their abnormal metabolism. When they are treated with these compounds, known as 11beta compounds, the additional disruption helps to kill the cells. In a study published in 2011, Fedeles reported that treatment with 11beta compounds significantly suppressed the growth of prostate tumors implanted in mice.

A conversation with his brother, Sorin Fedeles, who studies polycystic kidney disease, led the pair to theorize that these compounds might also be good candidates for treating kidney cysts. At the time, research in ADPKD was beginning to suggest that kidney cyst cells also experience oxidative stress, due to an abnormal metabolism that resembles that of cancer cells.

“We were talking about a mechanism of what would be a good drug for polycystic kidney disease, and we had this intuition that the compounds that I was working with might actually have an impact in ADPKD,” Bogdan Fedeles says.

The 11beta compounds work by disrupting the mitochondria’s ability to generate ATP (the molecules that cells use to store energy), as well as a cofactor known as NADPH, which can act as an antioxidant to help cells neutralize damaging free radicals. Tumor cells and kidney cyst cells tend to produce increased levels of free radicals because of the oxidative stress they’re under. When these cells are treated with 11beta compounds, the extra oxidative stress, including the further depletion of NADPH, pushes the cells over the edge. 

“A little bit of oxidative stress is OK, but the cystic cells have a low threshold for tolerating it. Whereas normal cells survive treatment, the cystic cells will die because they exceed the threshold,” Essigmann says.

Shrinking cysts

Using two different mouse models of ADPKD, the researchers showed that 11beta-dichloro could significantly reduce the size of kidney cysts and improve kidney function.

The researchers also synthesized a “defanged” version of the compound called 11beta-dipropyl, which does not include any direct DNA-damaging ability and could potentially be safer for use in humans. They tested this compound in the early-onset model of PKD and found that it was as effective as 11beta-dichloro.

In all of the experiments, healthy kidney cells did not appear to be affected by the treatment. That’s because healthy cells are able to withstand a small increase in oxidative stress, unlike the diseased cells, which are highly susceptible to any new disturbances, the researchers say. In addition to restoring kidney function, the treatment also ameliorated other clinical features of ADPKD; biomarkers for tissue inflammation and fibrosis were decreased in the treated mice compared to the control animals.

The results also suggest that in patients, treatment with 11beta compounds once every few months, or even once a year, could significantly delay disease progression, and thus avoid the need for continuous, burdensome antiproliferative therapies such as tolvaptan.

“Based on what we know about the cyst growth paradigm, you could in theory treat patients in a pulsatile manner — once a year, or perhaps even less often — and have a meaningful impact on total kidney volume and kidney function,” Sorin Fedeles says.

The researchers now hope to run further tests on 11beta-dipropyl, as well as develop ways to produce it on a larger scale. They also plan to explore related compounds that could be good drug candidates for PKD.

Other MIT authors who contributed to this work include Research Scientist Nina Gubina, former postdoc Sakunchai Khumsubdee, former postdoc Denise Andrade, and former undergraduates Sally S. Liu ’20 and co-op student Jake Campolo. The research was funded by the PKD Foundation, the U.S. Department of Defense, the National Institutes of Health, and the National Institute of Environmental Health Sciences through the Center for Environmental Health Sciences at MIT.

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Scientists Have Discovered a “Powerhouse” Gene, Opening Doors to New Treatments for Kidney Disease

The gene WWP2 regulates the energy provided to cells that cause renal failure. Drugs can be developed to inhibit this gene to slow kidney damage.

Researchers at Duke-NUS Medical School have discovered a gene, WWP2, that is key in controlling the energy flow to cells causing kidney failure. This finding presents a new avenue for developing treatments focused on reducing kidney scarring and damage.

Published in the Journal of the American Society of Nephrology , the study highlights a new approach for developing treatments and drugs to halt the progression of chronic kidney disease.

Chronic kidney disease or CKD is a global health concern contributing to high mortality rates worldwide. Singapore is particularly affected, ranking fifth in the world for new cases of kidney failure, with approximately six new patients diagnosed daily. In the advanced stage of kidney disease, kidney tissue becomes fibrotic, resulting in permanent scarring and irreversible organ damage. This condition often culminates in end-stage kidney failure, for which current treatment options are severely limited.

A New Approach to Halting Kidney Fibrosis

“Our research focused on myofibroblasts, a type of kidney cell central to the scarring of renal tissue in fibrosis. By investigating the link between the metabolic activities of these cells and the progression of the disease, we discovered that by regulating energy supply to myofibroblasts, we can control their function and potentially halt kidney fibrosis,” said Associate Professor Jacques Behmoaras from the Cardiovascular and Metabolic Disorders Programme at Duke-NUS, who is also Deputy Director of the School’s Centre for Computational Biology and co-senior author of the study.

Led by Associate Professor Enrico Petretto, director of the Centre, the research team analyzed over 130 biopsy samples from patients in China and Italy. Their findings revealed that the presence of the WWP2 gene in myofibroblasts is associated with the advancement of kidney fibrosis. The gene is crucial for regulating the mitochondria, also called the ‘powerhouses’ of the cell because they produce the energy needed for cell functions.

“In our pre-clinical models of CKD, we discovered that a higher level of WWP2 ‘re-wires’ the cell’s metabolism, contributing to the advancement of fibrosis. On the other hand, a lack of WWP2 boosts metabolism in renal cells and slows down scar formation, reducing the severity of kidney dysfunction and fibrosis,” said Dr. Chen Huimei, Principal Research Scientist with the Cardiovascular and Metabolic Disorders Programme and first author of the paper.

In earlier studies, the team had found that WWP2 controls scarring in heart disease . Targeting the gene in patients could halt the formation of excessive scar tissue and delay progression to heart failure.

Towards New Therapies for CKD

“Through our studies, we have shown that WWP2 is a new potential target for the development of drugs to halt the progression of fibrosis in several diseases. This is especially so for CKD, which can progress to renal failure and is fatal without treatment. Our findings pave the way for the design of new and promising therapies for such illnesses that would otherwise have limited treatment options,” said Assoc Prof Petretto, who is also a systems geneticist with Duke-NUS’ Cardiovascular & Metabolic Disorders Programme.

To this end, the team is in talks with venture capitalists to develop inhibitors of WWP2 to treat heart and kidney disease.

Professor Patrick Tan, Senior Vice-Dean for Research at Duke-NUS, said: “Given the rising incidence of kidney disease in Singapore, this is a groundbreaking discovery. The study not only sheds light on the genetic mechanisms underlying kidney disease but also opens up new avenues for therapeutic intervention, offering hope for millions of CKD patients worldwide.”

Reference: “WWP2 Regulates Kidney Fibrosis and the Metabolic Reprogramming of Profibrotic Myofibroblasts” by Huimei Chen, Ran You, Jing Guo, Wei Zhou, Gabriel Chew, Nithya Devapragash, Jui Zhi Loh, Loreto Gesualdo, Yanwei Li, Yuteng Jiang, Elisabeth Li Sa Tan, Shuang Chen, Paola Pontrelli, Francesco Pesce, Jacques Behmoaras, Aihua Zhang and Enrico Petretto, 19 March 2024, Journal of the American Society of Nephrology . DOI: 10.1681/ASN.0000000000000328

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Hello, my name is Renate Rosner,I am 71 years old and I have chronic kidney disease with a recent GFR of 23 My blood pressure has been treated with atacand, and has been relatively stable, last year I had an episode of increased blood pressure and my nephrologist started me on Chlorthalidone. Now, after losing about 15 pounds, I think my body is changing. I visited the doctor last week after c/o of lack of energy and dizziness. My blood ressure was 90/60, so the chlorthadione was stopped, Now a week later, I went to the lap and my GFR was 23, My GFR has ben continually dropping and I wonder if some of this is genetic, On both my parents side, they have many cardiac issure before the age of 60, my sister= 5 years younger than me, has had a total of 3 strokes and my brother died of sudden cardia arrest at age 57. I am wondering if my body produces toomuch WWP2, which I understand can lead to fibrosis and scarring. My question is –Is there a medication that could help me if this is the case, to either stop or slow down the progression of my kidney disease

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Wednesday, July 19, 2023

New atlas of human kidney cells to help unlock kidney disease research

NIH-funded effort provides interactive resource for global research community.

In a major breakthrough toward understanding and treating kidney disease, a nationwide research team funded by the National Institutes of Health has created the most comprehensive atlas of the human kidney. Data from the Kidney Tissue Atlas will allow the comparison of healthy kidney cells to those injured by kidney disease, helping investigators understand the factors that contribute to the progression of kidney disease and kidney failure or recovery from injury. The atlas, part of the Kidney Precision Medicine Project (KPMP), was supported by NIH’s National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), as published in Nature .

Due to the complexity of the kidney, scientists have struggled to develop kidney models that accurately represent human kidney structures and function. The lack of human kidney models has limited the ability to develop new drugs to treat or prevent kidney disease.

The Kidney Tissue Atlas comprises maps of 51 main kidney cell types that include rare and novel cell populations, 28 kidney cellular states that represent injury or disease, a repository of raw gene data, and interactive 3D models of cells and microenvironment relationships created from 45 healthy donor kidneys and 48 kidney disease biopsies. The atlas thus establishes a critical foundation for KPMP’s overall goal to help discover new treatments for chronic kidney disease (CKD) and acute kidney injury (AKI), medical conditions that present a significant global health burden. The publicly available data created by KPMP, including all 3D renderings and analytical tools, can be accessed at atlas.kpmp.org .

“KPMP’s new atlas represents open, public science at its best,” said Dr. Eric Brunskill, KPMP program director in NIDDK’s Division of Kidney, Urologic, and Hematologic Diseases. “With the atlas, we’ve created an interactive, hypothesis-generating resource for kidney disease investigators and clinicians around the world.”

While CKD and AKI have historically been described as single, uniform diseases, KPMP builds on growing consensus that kidney disease can have several different root causes and disease pathways leading to subgroups of CKD and AKI. Instead of a “one size fits all” approach to treating kidney disease, precision medicine explores more personalized treatments. KPMP’s kidney atlas is intended to help identify disease subgroups within CKD and AKI, leading to the discovery of new, and possibly individualized, ways to treat CKD and AKI.

The study also received support from the Human Cell Atlas initiative, an international research effort to gather information on at least 10 billion human cells, and NIH’s Human BioMolecular Atlas Program (HuBMAP). HuBMAP’s goal is to develop an open and global platform to map healthy cells in the human body; the KPMP and HuBMAP teams worked closely to align the outputs of this molecular atlas as an example of cross-consortia collaborations.

“KPMP brings together the best of new technology, patient engagement, and partnership, and represents an evolution in the way we think about kidney disease,” said NIDDK Director Dr. Griffin P. Rodgers. “We’re confident the Kidney Tissue Atlas will help us discover new ways to get the right kidney disease treatment to the right patient at the right time.”

Data related to this research are available for request at the NIDDK Central Repository .

Research reported in this study was funded by NIDDK (grants U2C DK114886, UH3 DK114861, UH3 DK114866, UH3 DK114870, UH3 DK114908, UH3 DK114915, UH3 DK114926, UH3 DK114907, UH3 DK114923 and UH3 DK114933). The research was also supported by National Institute of Health (S10 OD026929), National Cancer Institute (P30 CA91842), and National Center for Advancing Translational Sciences (UL1 TR002345). HuBMAP is supported by NIH (OT2 D033760), National Heart, Lung, and Blood Institute (U54 HL145608), and NIDDK (U54 DK134301). Additional NIH support was provided by NIDDK (K08 DK107864, R01 DK111651, P01 DK056788, U2C DK114886, U54 DK083912, P30 DK081943, K23 DK125529, and U54 DK083912), National Institute of Mental Health (U01 MH114828), and National Cancer Institute (UH3 CA246632).

About the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK): The NIDDK, a component of the National Institutes of Health (NIH), conducts and supports research on diabetes and other endocrine and metabolic diseases; digestive diseases, nutrition and obesity; and kidney, urologic and hematologic diseases. Spanning the full spectrum of medicine and afflicting people of all ages and ethnic groups, these diseases encompass some of the most common, severe, and disabling conditions affecting Americans. For more information about the NIDDK and its programs, see www.niddk.nih.gov .

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Lake BB, et al. An atlas of healthy and injured cell states and niches in the human kidney . Nature. 2023.

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FDA Approves Treatment for Chronic Kidney Disease

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Approval is First to Cover Many Causes of Disease

Today, the U.S. Food and Drug Administration approved Farxiga (dapagliflozin) oral tablets to reduce the risk of kidney function decline, kidney failure, cardiovascular death and hospitalization for heart failure in adults with chronic kidney disease who are at risk of disease progression.  

“Chronic kidney disease is an important public health issue, and there is a significant unmet need for therapies that slow disease progression and improve outcomes,” said Aliza Thompson, M.D., M.S., deputy director of the Division of Cardiology and Nephrology in the FDA’s Center for Drug Evaluation and Research. “Today’s approval of Farxiga for the treatment of chronic kidney disease is an important step forward in helping people living with kidney disease.” 

Chronic kidney disease occurs when the kidneys are damaged and cannot filter blood normally. Due to this defective filtering, patients can have complications related to fluid, electrolytes (minerals required for many bodily processes), and waste build-up in the body. Chronic kidney disease sometimes can progress to kidney failure. Patients also are at high risk of cardiovascular disease, including heart disease and stroke. 

The efficacy of Farxiga to improve kidney outcomes and reduce cardiovascular death in patients with chronic kidney disease was evaluated in a multicenter, double-blind study. In this study, 4,304 patients were randomly assigned to receive either Farxiga or a placebo. The study compared the two groups for the number of patients whose disease progressed to a composite (or combined) endpoint that included at least a 50% reduction in kidney function, progression to kidney failure, or cardiovascular or kidney death. Results showed that 197 of the 2,152 patients who received Farxiga had at least one of the composite endpoint events compared to 312 of the 2,152 patients who received a placebo. The study also compared the two groups for the number of patients who were hospitalized for heart failure or died from cardiovascular disease. A total of 100 patients who received Farxiga were hospitalized or died compared to 138 patients who received a placebo. 

Farxiga was not studied, nor is expected to be effective, in treating chronic kidney disease among patients with autosomal dominant or recessive polycystic (characterized by multiple cysts) kidney disease or among patients who require or have recently used immunosuppressive therapy to treat kidney disease. 

Patients should not use Farxiga if they have a history of serious hypersensitivity reactions to the medication or if they are on dialysis treatment. Serious, life-threatening cases of Fournier’s Gangrene have occurred in patients with diabetes taking Farxiga. Patients should consider a lower dose of insulin or insulin secretagogue to reduce the risk of hypoglycemia (low blood sugar) if they are also taking Farxiga. Farxiga can cause dehydration, serious urinary tract infections, genital yeast infections, and metabolic acidosis or ketoacidosis (acid build-up in the blood). Patients should be assessed for their volume status and kidney function before starting Farxiga. 

Farxiga was originally approved in 2014 to improve glycemic control in adults with type 2 diabetes in addition to diet and exercise.

Farxiga received Fast Track , Breakthrough Therapy and Priority Review designations for the indication being approved today. Fast track is designed to facilitate the development and expedite the review of drugs to treat serious conditions and fill an unmet medical need. Breakthrough therapy designation is designed to expedite the development and review of drugs that are intended to treat a serious condition and preliminary clinical evidence indicates that the drug may demonstrate substantial improvement over available therapy on a clinically significant endpoint(s). Priority review directs overall attention and resources to the evaluation of applications for drugs that, if approved, would be significant improvements in the safety or effectiveness of the treatment, diagnosis or prevention of serious conditions when compared to standard applications.

The FDA granted the approval of Farxiga to AstraZeneca.

Related Information

• NIH: Chronic Kidney Disease

The FDA, an agency within the U.S. Department of Health and Human Services, protects the public health by assuring the safety, effectiveness, and security of human and veterinary drugs, vaccines and other biological products for human use, and medical devices. The agency also is responsible for the safety and security of our nation’s food supply, cosmetics, dietary supplements, products that give off electronic radiation, and for regulating tobacco products.

New genetic variants for chronic kidney disease identified

Approximately ten per cent of the world's population currently suffers from chronic kidney disease (CKD). This puts people at increased risk of kidney failure, cardiovascular disease and hospitalisation -- and places a heavy burden on the healthcare system. Due to the demographic changes of an ageing population, it is predicted that CKD could become one of the five leading causes of death worldwide by 2040.

In a large-scale study, scientists from Leipzig University, in collaboration with other international study groups, investigated genetic associations between variants of the X chromosome and seven selected parameters of kidney function in men and women. The study was based on blood samples and genetic information from a total of more than 900,000 people, 80 per cent of whom were of European descent.

"We identified a total of 23 associations: 16 relate to the estimated glomerular filtration rate of the kidney and seven to uric acid," explains study leader Professor Markus Scholz from the Institute for Medical Informatics, Statistics and Epidemiology (IMISE) at Leipzig University. Along with uric acid, glomerular filtration rate is a key measure of kidney health. It shows how much blood the glomeruli -- small vessels in the kidney tissue -- can filter per unit of time.

The researchers found different effects in men and women at six positions in the genome. The scientists were able to assign functionally plausible candidate genes to the newly discovered genetic effects. "The sex-specific differences could be explained by hormonal regulation of the associated genes," reports study analyst Katrin Horn from IMISE. "This finding helps us to better understand possible mechanisms of disease development and progression," says Professor Markus Scholz: "For example, we already know that the disease is more common in women, but progresses faster in men. We now have suitable mechanisms to investigate these phenomena further."

In their analysis of X-chromosomal variants, the Leipzig scientists looked at mutations at around 270,000 positions on the chromosome and correlated these with the clinical kidney parameters. They also used tissue data to check whether and how the genetic information was actually used. A targeted search for differences between the sexes was carried out.

"We deliberately chose to analyse the more complicated X chromosome, which has not yet been sufficiently investigated in terms of genetic associations despite being very promising with regard to sex-specific differences in diseases," says bioinformatics researcher Professor Scholz. "The reason for this is that women have two of these chromosomes, but the genetic information is only partially utilised and it is not exactly understood in what way and to what extent this happens."

The method that Professor Scholz and his team have developed for this study to analyse the X chromosome in detail and identify sex-specific differences can also be used by other research teams in the future to contribute to sex-sensitive medicine for other diseases.

The study was part of the international CKDGen consortium for research into the genetics of kidney disease, which is led by Professor Anna Köttgen of the University of Freiburg, with Leipzig University as a key partner. It included data from the Leipzig studies LIFE Heart, LIFE Adult, LIFE Child and the Sorb Study, from a total of approximately 14,000 data records. The bulk of the analysis and interpretation of the data was carried out by Professor Scholz's research group.

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Story Source:

Materials provided by Universität Leipzig . Original written by Birgit Pfeiffer. Note: Content may be edited for style and length.

Journal Reference :

• Markus Scholz, Katrin Horn, Janne Pott, Matthias Wuttke, Andreas Kühnapfel, M. Kamal Nasr, Holger Kirsten, Yong Li, Anselm Hoppmann, Mathias Gorski, Sahar Ghasemi, Man Li, Adrienne Tin, Jin-Fang Chai, Massimiliano Cocca, Judy Wang, Teresa Nutile, Masato Akiyama, Bjørn Olav Åsvold, Nisha Bansal, Mary L. Biggs, Thibaud Boutin, Hermann Brenner, Ben Brumpton, Ralph Burkhardt, Jianwen Cai, Archie Campbell, Harry Campbell, John Chalmers, Daniel I. Chasman, Miao Ling Chee, Miao Li Chee, Xu Chen, Ching-Yu Cheng, Renata Cifkova, Martha Daviglus, Graciela Delgado, Katalin Dittrich, Todd L. Edwards, Karlhans Endlich, J. Michael Gaziano, Ayush Giri, Franco Giulianini, Scott D. Gordon, Daniel F. Gudbjartsson, Stein Hallan, Pavel Hamet, Catharina A. Hartman, Caroline Hayward, Iris M. Heid, Jacklyn N. Hellwege, Bernd Holleczek, Hilma Holm, Nina Hutri-Kähönen, Kristian Hveem, Berend Isermann, Jost B. Jonas, Peter K. Joshi, Yoichiro Kamatani, Masahiro Kanai, Mika Kastarinen, Chiea Chuen Khor, Wieland Kiess, Marcus E. Kleber, Antje Körner, Peter Kovacs, Alena Krajcoviechova, Holly Kramer, Bernhard K. Krämer, Mikko Kuokkanen, Mika Kähönen, Leslie A. Lange, James P. Lash, Terho Lehtimäki, Hengtong Li, Bridget M. Lin, Jianjun Liu, Markus Loeffler, Leo-Pekka Lyytikäinen, Patrik K. E. Magnusson, Nicholas G. Martin, Koichi Matsuda, Yuri Milaneschi, Pashupati P. Mishra, Nina Mononen, Grant W. Montgomery, Dennis O. Mook-Kanamori, Josyf C. Mychaleckyj, Winfried März, Matthias Nauck, Kjell Nikus, Ilja M. Nolte, Raymond Noordam, Yukinori Okada, Isleifur Olafsson, Albertine J. Oldehinkel, Brenda W. J. H. Penninx, Markus Perola, Nicola Pirastu, Ozren Polasek, David J. Porteous, Tanja Poulain, Bruce M. Psaty, Ton J. Rabelink, Laura M. Raffield, Olli T. Raitakari, Humaira Rasheed, Dermot F. Reilly, Kenneth M. Rice, Anne Richmond, Paul M. Ridker, Jerome I. Rotter, Igor Rudan, Charumathi Sabanayagam, Veikko Salomaa, Neil Schneiderman, Ben Schöttker, Mario Sims, Harold Snieder, Klaus J. Stark, Kari Stefansson, Hannah Stocker, Michael Stumvoll, Patrick Sulem, Gardar Sveinbjornsson, Per O. Svensson, E-Shyong Tai, Kent D. Taylor, Bamidele O. Tayo, Andrej Teren, Yih-Chung Tham, Joachim Thiery, Chris H. L. Thio, Laurent F. Thomas, Johanne Tremblay, Anke Tönjes, Peter J. van der Most, Veronique Vitart, Uwe Völker, Ya Xing Wang, Chaolong Wang, Wen Bin Wei, John B. Whitfield, Sarah H. Wild, James F. Wilson, Thomas W. Winkler, Tien-Yin Wong, Mark Woodward, Xueling Sim, Audrey Y. Chu, Mary F. Feitosa, Unnur Thorsteinsdottir, Adriana M. Hung, Alexander Teumer, Nora Franceschini, Afshin Parsa, Anna Köttgen, Pascal Schlosser, Cristian Pattaro. X-chromosome and kidney function: evidence from a multi-trait genetic analysis of 908,697 individuals reveals sex-specific and sex-differential findings in genes regulated by androgen response elements . Nature Communications , 2024; 15 (1) DOI: 10.1038/s41467-024-44709-1

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Accelerating New Clinical Trials and Treatments for Kidney Disease

Breakthrough research identifies key microenvironments linked to kidney injury and disease

• Download PDF Copy

A study published in  Nature Communications  provides new insight into how damaged cells interact within disease-promoting microenvironments following acute kidney injury, or AKI. With limited treatment options, AKI frequently progresses to chronic kidney disease (CKD), which affects more than 1 in 7 U.S. adults-;an estimated 37 million people.

The new findings may contribute to future efforts to prevent CKD, which can lead to kidney failure. 

The study brought together scientists from Andy McMahon's lab at USC and Long Cai's lab at Caltech, with support from a USC Broad Innovation Award that funded the cross-institutional research collaboration. 

In the study, co-first authors Michal Polonsky from Caltech and Louisa Gerhardt from USC, leveraged a cutting-edge tool, called seqFISH, developed in the Cai laboratory. With this tool, researchers can gather information about genetic activity and study cellular interactions in intact kidney tissue in mice with AKI. This allowed the scientists to analyze the precise expression of over 1,000 genes in the injured kidney tissue, identify microenvironments associated with injury, and predict cellular interactions associated with the progression to CKD.

" Dr. Cai's seqFISH technology provides unprecedented insight into the cellular interplay in the kidney following injury, " said McMahon, who is the W.M. Keck Provost and University Professor of Stem Cell Biology and Regenerative Medicine at USC and will join the faculty of Caltech in October. " A better understanding of kidney injury is needed to identify targets for preventing the progression to chronic kidney disease ."

Cai, who is a Professor of Biology and Biological Engineering, added: "We're thrilled that our technology has enabled a deeper understanding of kidney injury and disease. This study exemplifies the importance of cross-institutional and cross-disciplinary collaborations to advance biomedical research." 

In the kidney's outermost layer, the scientists identified a likely pathological microenvironment, which they dubbed "ME-5." This microenvironment contained a type of kidney cell particularly vulnerable to injury, known as a proximal tubule cell or PT. 

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In ME-5, injured PTs and neighboring connective tissue cells, known as fibroblasts, exchanged signals that could drive injury progression. Key signals involved the genes Clcf1 and Crfl1, which encode proteins that can promote inflammation and fibrosis, or scarring. Additional signals detected in ME-5 could contribute to recruitment of immune cells, thereby further contributing to development of inflammation, fibrosis and other pathological changes.

The scientists also identified another important injury-associated microenvironment, which they named "ME-16," featuring aggregations of various immune cell types called tertiary lymphoid structures that are known to contribute to chronic inflammation. Rather than being confined to a specific region of the kidney, ME-16 was distributed throughout the injured organ. 

To share their discoveries, the team constructed a comprehensive map of cellular, molecular, and structural changes following AKI, which refines our understanding of the transition to CKD. This map is publicly available at  https://woldlab.caltech.edu/ci2-celltiles/Mouse-Kidney-Fibrosis/ .

Additional co-authors are Kari Koppitch from USC; Jina Yun, Katsuya Lex Colón, Henry Amrhein, Matt Thomson, and Barbara Wold from Caltech; and Shiwei Zheng and Guo-Cheng Yuan from the Icahn School of Medicine at Mount Sinai.

In addition to the USC Broad Innovation Award, the research was supported by the National Institutes of Health (grant NIDDK UC2DK126024), German Research Foundation (grant GE 3179/1-1), and German Society of Internal Medicine (DGIM) Clinician Scientist Grant.

Keck School of Medicine of USC

Polonsky, M., et al. (2024). Spatial transcriptomics defines injury specific microenvironments and cellular interactions in kidney regeneration and disease.  Nature Communications . doi.org/10.1038/s41467-024-51186-z .

Posted in: Cell Biology | Medical Research News | Medical Condition News

Tags: Acute Kidney Injury , Biotherapeutics , Cell , Cell Biology , Chronic , Chronic Kidney Disease , Fibrosis , Genes , Genetic , Genomics , Inflammation , Kidney , Kidney Disease , Kidney Failure , Laboratory , Medicine , Research , Technology , Transcriptomics

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Kidney Disease

Normal, healthy kidneys filter about 200 quarts of blood each day, generating about 2 quarts of excess fluid, salts, and waste products that are excreted as urine. Loss of function of these organs, even for a short period of time or due to gradual deterioration, can result in life-threatening complications. Loss of kidney function is an important health challenge whether it occurs suddenly or over a long period of time.

The NIDDK supports basic and clinical research on kidney development; the causes of kidney disease; improving kidney health equity and reducing kidney health disparities; the underlying mechanisms leading to progression of kidney disease; and the development and testing of possible treatments to prevent or slow progression of kidney disease. Also of interest are studies of inherited diseases such as polycystic kidney disease, congenital kidney disorders, and immune-related kidney diseases such as IgA nephropathy and hemolytic uremic syndrome.

It has been estimated that 35.5 million American adults have chronic kidney disease (CKD). CKD has two main causes: high blood pressure and diabetes. CKD, especially if undetected, can progress to irreversible kidney failure. People with kidney failure require dialysis or a kidney transplant to live. Minority populations, particularly African Americans, Hispanic and Latino Americans, and American Indians and Alaska Natives, bear a disproportionate burden of CKD and kidney failure.

In addition, NIDDK has congressional authorization for the National Kidney and Urologic Diseases Information Clearinghouse , which provides services via the NIDDK Health Information Center. NIDDK responds to questions and provides health information about kidney disease to people with kidney disease and to their families, health professionals, and the public.

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• Scientists discover potential treatment approaches for polycystic kidney disease
• Alternatives to Race-Based Kidney Function Calculations
• New atlas of human kidney cells to help unlock kidney disease research
• Being hospitalized with acute kidney injury may increase risk for rehospitalization and death
• A Potential Explanation for Differences in Susceptibility to Kidney Complications of Diabetes

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JAMA review highlights advances in kidney cancer research and care

University of North Carolina Health Care

“The Nobel Prize in Medicine or Physiology in 2019 was awarded for the discovery of how mammalian cells sense oxygen,” said William Kim, MD, the Rush S. Dickson Distinguished Professor of Medicine at UNC School of Medicine and co-leader of the UNC Lineberger Cancer Genetics Research Program. “One of the key components of this oxygen sensing pathway is the von Hippel-Lindau tumor suppressor gene, which is mutated in approximately 90% of kidney cancers. This deep understanding of kidney cancer biology has led to several important therapeutic advances in recent years.”

Credit: UNC Lineberger Comprehensive Cancer Center

CHAPEL HILL, North Carolina — New insights into the biology of kidney cancer, including those informed by scientific discoveries that earned a Nobel Prize, have led to advances in treatment and increased survival rates, according to a review by UNC Lineberger Comprehensive Cancer Center’s William Kim, MD , and Tracy Rose, MD, MPH .

Their observations, drawn from a meta-analysis of 89 studies published between January 2013 and January 2024, were published in JAMA Aug. 28.

“The Nobel Prize in Medicine or Physiology in 2019 was awarded for the discovery of how mammalian cells sense oxygen,” said Kim, the Rush S. Dickson Distinguished Professor of Medicine at UNC School of Medicine and co-leader of the UNC Lineberger Cancer Genetics Research Program. “One of the key components of this oxygen sensing pathway is the von Hippel-Lindau tumor suppressor gene, which is mutated in approximately 90% of kidney cancers. This deep understanding of kidney cancer biology has led to several important therapeutic advances in recent years.”

Kim trained as a post-doc with William G. Kaelin, Jr., MD, who was jointly awarded the 2019 Nobel Prize for demonstrating how the von Hippel-Lindau gene influences cellular responses to changing oxygen levels.

The American Cancer Society estimates that more than 81,500 people will be diagnosed with kidney cancer in the United States this year, and the disease will cause 14,300 deaths. While the incidence of kidney cancer has been increasing by approximately 1.5% annually in recent years, deaths have decreased by about 2% each year from 2016 to 2020.

This decline in deaths is largely due to improved treatments and early detection. “The majority of kidney cancer cases are now detected incidentally, often before symptoms appear,” said Kim. He noted that the widespread use of abdominal imaging for unrelated issues has led to the incidental diagnosis of kidney cancer. “More cases are being identified in earlier stages when the cancer is typically more responsive to treatment.”

Cigarette smoking and being overweight are major risk factors for kidney cancer and are linked to nearly half of the cases in the United States. Other risk factors include high blood pressure, a family history of kidney cancer, workplace exposure to certain chemicals, and hereditary conditions, such as von Hippel-Lindau disease.

Current treatment approaches include surgery to remove part or all of the kidney, ablation using targeted heat or cold to destroy the tumor, or active surveillance with imaging technologies to monitor the tumor. For cancers that have metastasized, or spread beyond the kidney, newer treatment options include immune checkpoint inhibitors, tyrosine kinase inhibitors, or a combination of the two approaches.

“Advanced, metastatic kidney cancer is highly treatable with targeted therapy, immunotherapy or a combination of these newer therapies,” said Rose, associate professor of medicine at UNC School of Medicine. “Understanding the science underlying the disease has allowed for the rational development of therapies that have positively affected many patients the past two decades.”

10.1001/jama.2024.12848

Method of Research

Meta-analysis

Subject of Research

Not applicable

Article Title

Renal Cell Carcinoma: A Review

Article Publication Date

28-Aug-2024

COI Statement

Rose has received grant support from Merck, Bristol Meyers Squibb and Syndax. Kim has received consulting fees from Focal Medical, OncoRev, and Janssen and owns stock in AbbVie, Amgen, Apellis, Arvinas, BeiGene, Bristol Myers Squibb, Eli Lilly, ImmunityBio, Moderna, Zentalis, Focal Medical, Natera, Novo Nordisk, Revolution Medicines, Tango Therapeutics, and Viking Therapeutics.

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Donating a kidney is safer than ever, reassuring research finds

There's never been a safer time to give a kidney. 

The risk of death for people who donated a kidney has dropped by more than half in the last decade, according to a study published Wednesday. 

“It’s just becoming safer and safer for people to donate,” said Dr. Dorry Segev, a transplant surgeon at NYU Langone Health and senior author of the study. 

The overall risk of death for a kidney donor has always been low, but advances in surgery and medical care, along with more careful donor selection, have improved the odds even more. 

The kidneys play a vital role in health, responsible for filtering harmful toxins out of our blood and regulating blood pressure. As rates of chronic conditions such as diabetes and high blood pressure — both may contribute to renal disease — have increased, the need for kidney donors has become more urgent.

Nearly 90,000 people are waiting for kidney transplants in the U.S., with the average wait time around three to five years. Kidneys are the most commonly transplanted organ, with an estimated 27,000 kidney transplants performed annually.

For the new study, published in JAMA , doctors looked at data on people who died within 90 days after a kidney transplant surgery from 1993 to 2022. Data came from both the Scientific Registry of Transplant Recipients and the Organ Procurement and Transplantation Network, a nonprofit organization that administers the nation’s only transplant network authorized by the U.S. Congress.

In total, there were 164,593 kidney donors included in the study. Thirty-six died within 90 days after donation. 

From 1993 to 2002, there 13 total deaths after the procedure for a mortality rate of 3 per 10,000 people; from 2003 to 2012, there were 18 deaths, a mortality rate of 2.9 per 10,000. 

Deaths dropped significantly from 2013 to 2022, to just five, or a mortality rate of 0.9 per 10,000. 

During this time, laparoscopic surgery — a minimally invasive technique where surgeons use small incisions and specialized instruments to remove the kidney — became the standard of care, Segev said. Previously, patients underwent open donor nephrectomy, which required a much larger incision that needed longer recovery time and more risk of complications.

In previous decades, donors who were male and people with a history of high blood pressure were more likely to die within 90 days of surgery than other donors. Most of the deaths occurred in the first seven days after surgery. The most common cause of death from the procedure was excessive bleeding, or hemorrhage.

“It’s really important for us as a community that takes care of these patients to make sure the message is consistent,” said Dr. Kassem Safa, associate medical director for the kidney transplant program at Massachusetts General Hospital. “We tell them the truth about the risks they’re taking, and this study just validates the fact that it’s a very safe surgery with a very tiny risk — but not a zero risk.”

It is critical that this procedure be as safe as possible, as many patients who donate kidneys are previously healthy with no medical problems.

“The first thing we tell donors is you don’t have to do this and you’re not going to get any medical benefits from it,” Safa said.

Fortunately, long-term data from organ donors has shown that their kidney function tends to remain stable and the risk of developing chronic kidney disease is only slightly higher than in those who do not donate , Safa said. 

Doctors are hopeful that reassuring data like this will ultimately help solve the shortage of donors in the U.S. 

“Anything that comes along that says being a living donor is getting safer and safer over time will hopefully encourage more people to step forward and donate and give the gift of life,” said Dr. John Friedewald, medical director of the kidney transplant program at Northwestern Medicine.

Friedewald, who was not involved with the study, said this updated data will ultimately help doctors better consent patients who are about to undergo the procedure. 

Tracy McKibben, chair of the board of directors at the National Kidney Foundation, donated a kidney to her mother in 2009. Her mother, who was previously a very active person and a frequent traveler, had stopped doing much of what she enjoyed as she had to frequent a dialysis center three days a week. 

That all changed when McKibben gave her the ultimate gift. 

“It was just a world of difference for her and a world of difference for me,” she said. “Being able to see her have her old life that she hadn’t had for some time when she started having to undergo dialysis.”

CORRECTION:  (Aug. 28, 2024, 1:46 p.m. ET): A previous version of this article misstated the number of deaths and the death rates for kidney donors. From 1993 to 2002, there were 13 deaths and a death rate of 3 per 10,000, not a death rate of 13 per 10,000. From 2003 to 2012, there were 18 total deaths for a death rate of 2.9 per 10,000, not a death rate of 18 per 10,000. For 2013 to 2022, the death rate was 0.9 per 10,000, not 0.05 per 10,000.

Akshay Syal, M.D., is a medical fellow with the NBC News Health and Medical Unit. 

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Travere Gains 11% on Securing Full FDA Nod for Kidney Disease Drug

September 09, 2024 — 11:58 am EDT

Written by Zacks Equity Research for Zacks  ->

Travere Therapeutics TVTX announced that the FDA granted full approval to its oral non-immunosuppressive drug Filspari (sparsentan) in IgA nephropathy (IgAN) indication, a rare progressive kidney disease.

Following this decision, Filspari is approved for slowing kidney function decline in adults with primary IgAN who are at risk of disease progression. The FDA’s decision also makes Filspari the only non-immunosuppressive medication in the IgAN space.

Filspari was initially granted accelerated approval in February 2023 to reduce proteinuria (protein in the urine) in adults with primary IgAN who are at risk of rapid disease progression.

Travere’s shares were up nearly 11% on Friday after the announcement. Investors were impressed with Filspari’s label expansion as it expanded the drug’s total addressable patient population. Before full approval, the drug was approved only to treat patients at higher risk of disease progression. The drug is approved to treat patients who are at risk of disease progression — including individuals at low risk of disease progression.

Year to date, the stock has increased 22.1% against the industry ’s 2.8% fall.

Did Travere’s Filspari Meet Study Goals?

The approval is based on data from the pivotal phase III PROTECT study, which evaluated Filspari against irbesartan head-to-head in adults with primary IgAN for more than two years. Data from the study showed that treatment with Filspari demonstrated long-term kidney function preservation in IgAN patients compared with irbesartan.

The above data is based on a modified intention to treat (ITT) analysis, which included data from all patients, even those who stopped treatment. This approach was also favored by the FDA.

We remind investors that Travere Therapeutics reported the PROTECT study last year in September, wherein the study results narrowly missed out on failing to meet the key secondary endpoint of the estimated glomerular filtration rate (eGFR) total slope. This endpoint is required to be achieved for a regulatory review in the United States. The study did meet the other confirmatory secondary endpoint of the eGFR chronic slope, which is necessary for regulatory purposes in the European Union.

The modified analysis of data helped the PROTECT study achieve the eGFR total slope endpoint. Patients who received Filspari achieved a mean eGFR slope of -3.0 mL/min/1.73 m 2 /year from baseline to Week 110 compared with -4.2 mL/min/1.73 m 2 /year for irbesartan.

Monitoring For Liver Diseases & Child Defects

Despite the full approval, the drug has been added to the FDA’s Risk Evaluation and Mitigation Strategies (REMS) program. Doctors must monitor patients' liver enzymes before starting treatment, every month for the first year and then every three months during treatment. Travere is planning to engage in discussions with the FDA to remove Filspari from the REMS program eventually.

Filspari also comes with a boxed warning for severe birth defects in case the drug is taken during pregnancy.

Other Players in the IgAN Space

Apart from TVTX, the space is dominated by Calliditas Therapeutics CALT , which markets Tarpeyo, the first fully-approved FDA drug for IgAN based on a measure of kidney function. The approval history of CALT’s Tarpeyo is similar to Filspari — the drug was granted full approval by the FDA in December 2023 for an indication similar to Filspari.

In July, Calliditas announced that it had secured full marketing authorization for Tarpeyo in IgAN indication. The drug is being marketed by its commercial partner, STADA Arzneimittel AG, under the trade name Kinpeygo.

Last month, pharma giant Novartis NVS also entered the IgAN market after the FDA granted accelerated approval to Fabhalta for reducing proteinuria in adults with primary IgAN at risk of rapid disease progression. This approval marks the first FDA nod for Novartis’ renal pipeline. Fabhalta was initially approved by the FDA in paroxysmal nocturnal hemoglobinuria (PNH) indication.

Apart from Fabhalta, Novartis is also developing other candidates in IgAN indication. The company’s acquisition of Chinook Therapeutics last year added late-stage candidates atrasentan and zigakibart to its pipeline, both of which are being developed in IgAN indication. An FDA filing is currently under review seeking approval for atrasentan in adults with IgAN.

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Current progress in CAR-based therapy for kidney disease

Affiliations.

• 1 Department of Nephrology, Affiliated Hospital of Xuzhou Medical University, Xuzhou, China.
• 2 Department of Internal Medicine and Diagnostics, Xuzhou Medical University, Xuzhou, China.
• 3 Clinical Research Center For Kidney Disease, Xuzhou Medical University, Xuzhou, China.
• PMID: 39234257
• PMCID: PMC11372788
• DOI: 10.3389/fimmu.2024.1408718

Despite significant breakthroughs in the understanding of immunological and pathophysiological features for immune-mediated kidney diseases, a proportion of patients exhibit poor responses to current therapies or have been categorized as refractory renal disease. Engineered T cells have emerged as a focal point of interest as a potential treatment strategy for kidney diseases. By genetically modifying T cells and arming them with chimeric antigen receptors (CARs), effectively targeting autoreactive immune cells, such as B cells or antibody-secreting plasma cells, has become feasible. The emergence of CAR T-cell therapy has shown promising potential in directing effector and regulatory T cells (Tregs) to the site of autoimmunity, paving the way for effective migration, proliferation, and execution of suppressive functions. Genetically modified T-cells equipped with artificial receptors have become a novel approach for alleviating autoimmune manifestations and reducing autoinflammatory events in the context of kidney diseases. Here, we review the latest developments in basic, translational, and clinical studies of CAR-based therapies for immune-mediated kidney diseases, highlighting their potential as promising avenues for therapeutic intervention.

Keywords: T lymphocytes; autoimmune diseases; cell immunotherapy; chimeric antigen receptor T cell therapy; kidney disease.

Copyright © 2024 Zhang and Sun.

PubMed Disclaimer

Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

A representation of various immune-mediated…

A representation of various immune-mediated kidney diseases including systemic antibody-induced vascular damage (ANCA-associated…

CD19 CAR-T cells are able…

CD19 CAR-T cells are able to eliminate pathologic B cells in B cell-mediated…

The mechanism of action of…

The mechanism of action of CAAR-T cells in immune-mediated kidney diseases. (A) CAAR-T…

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• Petr V, Thurman JM. The role of complement in kidney disease. Nat Rev Nephrol. (2023) 19:771–87. doi: 10.1038/s41581-023-00766-1 - DOI - PubMed
• Floege J, Barbour SJ, Cattran DC, Hogan JJ, Nachman PH, Tang SCW, et al. . Management and treatment of glomerular diseases (part 1): conclusions from a Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference. Kidney Int. (2019) 95:268–80. doi: 10.1016/j.kint.2018.10.018 - DOI - PubMed
• Kant S, Kronbichler A, Sharma P, Geetha D. Advances in understanding of pathogenesis and treatment of immune-mediated kidney disease: A review. Am J Kidney Dis. (2022) 79:582–600. doi: 10.1053/j.ajkd.2021.07.019 - DOI - PubMed
• Hartinger JM, Kratky V, Hruskova Z, Slanar O, Tesar V. Implications of rituximab pharmacokinetic and pharmacodynamic alterations in various immune-mediated glomerulopathies and potential anti-CD20 therapy alternatives. Front Immunol. (2022) 13:1024068. doi: 10.3389/fimmu.2022.1024068 - DOI - PMC - PubMed

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Mayo Clinic Q&A: Diagnosed with chronic kidney disease. Now what?

I have high blood pressure and was just diagnosed as having chronic kidney disease. i am disheartened by this news, but i also am determined to do more to improve my health. i know i may not be able to reverse my condition, but i am hoping to avoid dialysis or a kidney transplant for as long as possible..

DEAR MAYO CLINIC: I have high blood pressure and was just diagnosed as having chronic kidney disease . I am disheartened by this news, but I also am determined to do more to improve my health. I know I may not be able to reverse my condition, but I am hoping to avoid dialysis or a kidney transplant for as long as possible.

ANSWER:  Your determination will help you manage your chronic kidney disease by following recommended treatments and making lifestyle changes.

As you know, kidneys remove waste and fluids from the body through urination. With chronic kidney disease, kidney function is gradually lost. End-stage renal failure is when dialysis or a kidney transplant is needed to stay alive.

Similar to how high blood pressure is called a silent killer, many people don't know they have chronic kidney disease until it is discovered during a lab test for another reason. Because kidney disease usually doesn't cause symptoms in earlier stages, it often is not discovered until later in the course of the disease process. In fact, one in nine people may not know they have chronic kidney disease, but it affects about 14% of the population. That's more than 30 million people in the U.S.

Your healthcare professional will discuss what's best to help slow progression of kidney disease in your situation, but some recommendations typically include:

Follow a kidney diet

One key dietary adjustment to prevent the development or progression of chronic kidney disease is sodium restriction . Some people cook with a lot of salt and often add more salt at the table. Many processed foods also have added salt.

Reduce sodium intake by limiting convenience foods, salty snacks and processed meats and cheeses. Overall, try to eat fresher foods rather than foods that come out of a can or a bag. You can still enjoy many foods .

Increase fluid intake as well. Lack of fluid can lead to disease progression and affect how well medications work.

Address underlying conditions

Treatments for chronic kidney disease usually involve tackling the underlying issue. One of the most common causes of chronic kidney disease is high blood pressure, also known as hypertension.

High blood pressure relates to the pressure inside of blood vessels when the heart is pumping and when it relaxes. That pressure can increase as we age. A number of medical problems are associated with increases in blood pressure over time, which can lead to cardiovascular disease and chronic kidney disease. Controlling those disease processes is extremely important.

High blood pressure responds to our lifestyle choices, including getting regular exercise, avoiding processed foods, reducing sodium intake and eating more fruits and vegetables. All of these things reduce high blood pressure without medications.

Sometimes those lifestyle changes aren't enough. These are the patients who need medications to help with blood pressure control. The patient with chronic kidney disease typically has a goal blood pressure of 130/80 mm Hg.

Some risk factors for kidney disease we can't control, such as our age and race. Being Black, Native American or Asian American, for example, increases the risk of kidney disease. But some risk factors can be controlled. Managing diabetes , quitting smoking or tobacco use and maintaining a healthy weight are important steps to help control kidney disease. — Ivan Porter II, M.D. , Nephrology and Hypertension, Mayo Clinic, Jacksonville, Florida

Mayo Clinic Q&A is an educational resource and doesn’t replace regular medical care. Email a question to MayoClinicQ&[email protected]. For more information, visit www.mayoclinic.org .

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