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Mayo Clinic Minute: Game-changing treatment for chronic kidney disease could slow down progression of the disease

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About 15% of adults in the U.S. are  estimated  to have chronic kidney disease — that's about 37 million people.

What if those people could be treated with medication that could slow the progression of their disease, and help avoid the need for dialysis and kidney transplantation altogether?

Dr. Naim Issa , a Mayo Clinic transplant nephrologist says there is a class of medications to help people with chronic kidney disease that does just that. He says Mayo Clinic has been incorporating these medications to help patients for the last few years.

March 9 is World Kidney Day, a day aimed at raising awareness about the importance of the kidneys.

Watch: The Mayo Clinic Minute

Journalists: Broadcast-quality video (1:03) is in the downloads at the end of this post. Please courtesy: "Mayo Clinic News Network." Read the script .

Most people don't have symptoms of chronic kidney disease until it's at an advanced stage.

"Early detection of chronic kidney disease may help us actually treat and prevent patients ahead of time before the need for dialysis or kidney transplantation," says Dr. Issa.

He says a new class of drugs,  SGLT2 inhibitors , is being called a game changer. The drugs were originally designed to treat diabetes — a main cause of chronic kidney disease.

Medicines in the SGLT2 inhibitor class include canagliflozin , dapagliflozin and empagliflozin.

"In large trials , we observed groundbreaking success with those medications in slowing down the progression of chronic kidney disease, to the extent of avoiding dialysis and the need for kidney transplantation," Dr. Issa says.

The medications are used whether the patient is diabetic or not.

"They are actually game-changer medications that help us prevent the progression of chronic kidney disease," says Dr. Issa.

You can help yourself by following a low-sodium, moderate-protein diet, avoid smoking and getting plenty of exercise.

Dr. Issa says it is important that patients with chronic kidney disease work with their primary care physician and health care team to monitor and check blood pressure, urine analysis and bloodwork.

Related posts:

• Lifestyle changes can be critical for kidney transplant patients’ long-term survival
• Mayo Clinic Minute: What is chronic kidney disease?
• Diets higher in calcium and potassium may help prevent recurrent symptomatic kidney stones, Mayo Clinic study finds

For the safety of its patients, staff and visitors, Mayo Clinic has strict masking policies in place. Anyone shown without a mask was recorded prior to COVID-19 or recorded in an area not designated for patient care, where safety protocols were followed.

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News Release

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 .

About the National Institutes of Health (NIH): NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.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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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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Research Ties Gut Microbial TMAO Pathway to Chronic Kidney Disease

New findings from Tufts University and Cleveland Clinic researchers show high blood levels of TMAO (trimethylamine N-oxide) predicts future risk of developing chronic kidney disease over time.  

The findings build on several years of research between investigators at the  Friedman School of Nutrition Science and Policy at Tufts University  and the  Cleveland Clinic  related to the gut microbiome’s role in cardiovascular health and disease, including the adverse effects of TMAO, a byproduct formed by the gut bacteria from nutrients abundant in red meat, eggs and other animal source foods.  

The current study,  published in the  Journal of the American Society of Nephrology ,  measured blood levels of TMAO over time in two large National Institutes of Health populations and followed the kidney function of more than 10,000 U.S. adults with normal kidney function at baseline over an average follow-up period of 10 years. The investigators found that participants with elevated TMAO blood levels were at increased risk for future development of chronic kidney disease. 

Higher TMAO levels were also associated with a faster rate of declining kidney function in people with normal or impaired kidney function at baseline. These associations were independent of sociodemographic characteristics, lifestyle habits, diet and other known risk factors for kidney disease. The findings also are consistent with earlier reported preclinical model studies showing TMAO directly fosters both kidney functional decline and tissue fibrosis. 

“Our study is a crucial complement to studies in preclinical models supporting TMAO as a novel biological risk factor for chronic kidney disease,” said  Meng Wang , first author and research assistant professor at the Friedman School. “TMAO levels are highly modifiable by both lifestyle-like diet and pharmacologic interventions. Besides using novel drugs to lower TMAO in patients, using dietary interventions to lower TMAO in the general population could be a cost-efficient and low-risk preventive strategy for chronic kidney disease development.” 

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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 37 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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New £10.4 million research centre will unlock new tests, treatments and cures for people living with rare kidney diseases.

Press release issued: 23 April 2024

Thousands of people living with rare kidney disease will get access to improved diagnostics, treatments and potentially cures, thanks to the creation of a new research centre, involving experts from the University of Bristol.

In 2023, a major report from Kidney Research UK showed that kidney failure could overwhelm the health care system within ten years. The LifeArc-Kidney Research UK Centre for Rare Kidney Diseases is being launched to provide urgent focus and resource. It will unite researchers, patients and healthcare professionals and build on strong established resources, including the national registry of rare kidney diseases (RaDaR), the national renal sample biobank (NURTuRE) and care guidelines. It will signal the start of a transformation in all of the 13 of the UK’s children’s kidney centres to embed a culture of research by connecting the systems to accelerate discoveries and advance the treatment of rare kidney diseases.

The new translational centre is jointly funded by the medical research charity, LifeArc, who are investing £9.4 million in partnership with Kidney Research UK which is contributing an additional £1 million to be used to support the work of the centre over the next five years. It will be led by  Dr Louise Oni, Senior Lecturer in Paediatric Nephrology at the University of Liverpool and honorary consultant paediatric nephrologist at Alder Hey Children’s Hospital.

Dr Louise Oni said: “It is a privilege to be leading this exciting transformation on behalf of the entire kidney community. We are incredibly grateful for the opportunity to establish the LifeArc-Kidney Research UK Centre for Rare Kidney Diseases with the support of our charity partners Kidney Research UK. This UK wide project aims to create a culture of constant learning to bring rapid advances to patients of all ages living with kidney diseases. The project will start by focusing on children with rare kidney diseases to attempt to halt the journey to kidney failure and then upscale into adult patients. Through collaboration, the templates presented by these rare disease centres will support mass transformation to benefit many other patients.”

Dr Aisling McMahon, executive director of research at Kidney Research UK, said: “Ensuring that everyone has equal access to innovations and new therapies designed to benefit kidney patients is a key priority for Kidney Research UK. We are delighted to be co-funding this new centre with LifeArc and working in partnership with them and the renal research community to deliver this exciting project. This new collaboration will ensure that patients of all ages with rare kidney diseases not only benefit from new approaches to prevention, diagnosis and treatment, but also become active partners in the research process.”

Kathryn Croker faced kidney failure after being diagnosed with the rare disease IgA vasculitis, aged just 13. Following a successful kidney transplant from her dad in 2013, she went on to volunteer with Kidney Research UK and now shares her own experiences to help shape research projects, including this new centre. She said: “If there was a way to treat rare diseases before they get to that point of causing kidney failure and needing a transplant, that would just be incredible because it changes the course of your life. It’s exciting to be involved in a project with doctors and researchers focused on kidney disease in children, as typically research involves adults. Hopefully in the next 20 years or less, what I’ve experienced since childhood will be a thing of the past because I don’t want anyone to go through what I have. This new research centre is an exciting opportunity to achieve that.”

Moin Saleem , Professor of Paediatric Renal Medicine at Bristol Medical School: Translational Health Sciences (THS) and Director of Bristol Renal , and one of the Bristol leads for the new centre added: “The Bristol team are delighted to be core part of this transformative project. The kidney community in the UK (patients, clinicians, researchers) has several unique world-leading strengths, and is perfectly poised for this collaborative lead from Dr Oni to bring together these resources into a cohesive unit.

“Bristol Renal was the originator of the UK renal rare disease registry as well as the national biobank (NURTuRE), and contributes world-leading translational science in kidney disease. Rare disease requires cooperation above all, and this exciting collaboration will markedly accelerate key scientific and infrastructure advances for the benefit of patients who have a huge unmet need."

The new LifeArc-Kidney Research UK Centre for Rare Kidney Diseases is one of four new centres to be funded by the non-profit medical charity, LifeArc, with the aim of overcoming these barriers that ordinarily prevent new tests and treatments reaching patients. Globally, there are more than 300 million people living with rare diseases. However, rare disease research can be fragmented. Researchers can lack access to specialist facilities, as well as advice on regulation, trial designs, preclinical regulatory requirements, and translational project management, which are vital in getting new innovations to patients.

Dr Catriona Crombie , Head of Rare Disease at LifeArc, continued: “We are extremely proud to be launching four new LifeArc Translational Centres for Rare Diseases. Each centre has been awarded funding because it holds real promise for delivering change for people living with rare diseases. These centres also have the potential to create a blueprint for accelerating improvements across other disease areas, including common diseases.”

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New modelling reveals the escalating toll of chronic kidney disease on patients, planet and economies

Impact ckd model projects up to 16.5% of the population across eight countries to suffer from chronic kidney disease by 2032.

A new modelling analysis by AstraZeneca, IMPACT CKD, forecasts up to 16.5% of the population across eight countries will suffer from chronic kidney disease (CKD) by 2032, including a rise of up to 59.3% in advanced-stage. 1 Presented at the 2024 ISN World Congress of Nephrology (WCN’24) in Buenos Aires, the study highlights an urgent and growing global health crisis with profound economic and environmental implications. 1 IMPACT CKD is the first study to examine and forecast the vast, multi-dimensional impact of CKD over a 10-year time horizon across eight countries — the United States, Brazil, the United Kingdom, Spain, Germany, the Netherlands, China, and Australia. 1

The research estimates nearly 125 million people across these countries will suffer from advanced CKD by 2032, marking a 25% increase since 2022 when the model began. 1 The economic toll of renal replacement therapy, including dialysis and transplant, is anticipated to reach approximately $186 billion, and dialysis requirements are expected to surge by over 75%, contributing significantly to healthcare's carbon footprint — equivalent to adding approximately 17.3 million cars' worth of CO2 emissions. 1

Ruud Dobber, Executive Vice-President, BioPharmaceuticals Business Unit, AstraZeneca, highlights: “Our modelling emphasises the enormous impact CKD could have on patients, economies and the environment. But this future is not inevitable. At AstraZeneca, we are committed to working with global policy makers to reduce the world-wide impact of end-stage CKD and drive earlier diagnosis and treatment to slow or halt progression of disease.”

The IMPACT CKD study is part of AstraZeneca’s Accelerating Change Together (ACT) for CKD initiative, aiming to improve understanding and outcomes of CKD worldwide. Through the ACT on CKD programme, AstraZeneca, alongside the Global Patient Alliance for Kidney Health (GloPAKH), has launched ‘ Make the Change for Kidney Health ’ campaign. This initiative seeks to elevate CKD on the global policy agenda, advocating for comprehensive and effective disease management strategies to combat this escalating health challenge.

CKD    CKD is a serious, progressive condition defined by decreased kidney function (shown by reduced eGFR or markers of kidney damage, or both, for at least three months). 2  Nearly 850 million people worldwide are affected by CKD, 3 with the majority undiagnosed. 2 The most common causes of CKD are diabetes, hypertension and glomerulonephritis .4  CKD is associated with significant patient morbidity and an increased risk of cardiovascular (CV) events, such as heart failure (HF), which drives premature death. 5 In its most severe form, known as kidney failure, kidney damage and deterioration of kidney function have progressed to the point where dialysis or kidney transplantation are required .6  The majority of patients with CKD will die from CV causes before reaching kidney failure .7 

IMPACT CKD IMPACT CKD is an innovative study that incorporates a sophisticated simulation model to unveil a holistic projection of the extensive impacts of chronic kidney disease (CKD) across clinical, economic, societal, and environmental dimensions. 1 This landmark analysis delivers the first-ever, 10-year outlook on the impact of CKD, providing insight for the United States, Brazil, the United Kingdom, Spain, Germany, the Netherlands, China, and Australia. 1 Emphasizing the critical importance of early CKD detection and treatment, the study offers strategic insights aimed at substantially mitigating the disease's multi-dimensional burden. 1

ACT on CKD ACT on CKD is a programme by AstraZeneca to transform kidney health through partnerships aimed at reducing the proportion of patients progressing to kidney failure by 20% by 2025. To realise this ambition, the programme supports initiatives that aim to raise awareness of the burden of CKD and its consequences, expand early detection and drive optimisation of treatment to improve patient outcomes. To further support people at risk of CKD, we also look to achieve sustainable change through health policy reforms. 

We want to provide patients, healthcare providers (HCPs) and decision makers with the necessary information to drive change. As a part of our broader contribution to building knowledge around CKD we continue to generate evidence to help advance clinical practice: DISCOVER-CKD shows a lack of urine albumin-creatinine ratio (UACR) testing and adherence to Kidney Disease Improving Global Outcomes (KDIGO) guidelines; REVEAL-CKD shows the extent of the gaps in early detection of CKD and the clear benefits of diagnosing early; INSIDE-CKD shows the unsustainable future burden of CKD and potential benefits to the healthcare system of improved management; PACE-CKD shows CKD is associated with a poorer quality of life not only for patients but also their carers; and IMPACT CKD provides modelling of the future CKD burden for public health policy planning, including societal and environmental impact.

The World Congress of Nephrology (WCN) The World Congress of Nephrology (WCN) is the annual scientific, educational, and networking meeting of the International Society of Nephrology (ISN). 8 The ISN is a global professional association dedicated to advancing kidney health worldwide since 1960 through education, grants, research, and advocacy .8

AstraZeneca in CVRM Cardiovascular, Renal and Metabolism (CVRM), part of BioPharmaceuticals, forms one of AstraZeneca’s main disease areas and is a key growth driver for the Company. By following the science to understand more clearly the underlying links between the heart, kidneys, liver and pancreas, AstraZeneca is investing in a portfolio of medicines for organ protection by slowing or stopping disease progression, and ultimately paving the way towards regenerative therapies. The Company’s ambition is to improve and save the lives of millions of people, by better understanding the interconnections between CVRM diseases and targeting the mechanisms that drive them, so we can detect, diagnose and treat people earlier and more effectively. 

AstraZeneca AstraZeneca (LSE/STO/Nasdaq: AZN) is a global, science-led biopharmaceutical company that focuses on the discovery, development, and commercialisation of prescription medicines in Oncology, Rare Diseases, and BioPharmaceuticals, including Cardiovascular, Renal & Metabolism, and Respiratory & Immunology. Based in Cambridge, UK, AstraZeneca operates in over 100 countries and its innovative medicines are used by millions of patients worldwide. Please visit  astrazeneca.com  and follow the Company on social media  @AstraZeneca

Contact For details on how to contact the Investor Relations Team, please click here . For Media contacts, click here . 

1. Rao N, et al. Multidimensional Burden of Chronic Kidney Disease in Eight Countries: Insights from the IMPACT CKD Study. Presented at: WCN 2024, 13-16 April 2024, Buenos Aires, Argentina.

2. Bikbov B, et al. Global, regional, and national burden of chronic kidney disease, 1990–2017: a systematic analysis for the Global Burden of Disease Study 2017. Lancet. 2020;395(10225):709-733.

3. Jager KJ, et al. A single number for advocacy and communication-worldwide more than 850 million individuals have kidney diseases. Nephrol Dial Transplant. 2019;34(11):1803-1805.

4. National Kidney Foundation [Internet]. Chronic Kidney Disease (CKD); [cited 2024 March 25]. Available from: https://www.kidney.org/atoz/content/about-chronic-kidney-disease.

5. Centers for Disease Control and Prevention (CDC) [Internet]. Chronic Kidney Disease: Common - Serious - Costly; [cited 2024 March 25]. Available from: https://www.cdc.gov/kidneydisease/prevention-risk/CKD-common-serious-costly.html.

6. Centers for Disease Control and Prevention (CDC) [Internet]. Chronic kidney disease in the United States; 2021 [cited 2024 March 25]. Available from: https://www.cdc.gov/kidneydisease/pdf/Chronic-Kidney-Disease-in-the-US-2021-h.pdf.

7. Briasoulis A, et al. Chronic kidney disease as a coronary artery disease risk equivalent. Curr Cardiol Rep. 2013;15(3):340.

8. WCS [Internet]. ISN World Congress of Nephrology (WCN’24) Abstract Embargo Policy [cited 2024 March 25]. Available from: https://www.theisn.org/wcn/wp-content/uploads/sites/6/2023/06/WCN24-Abstract-Embargo-Policy.pdf.

Veeva ID: Z4-63620 Date of Preparation: April 2024

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New insights on kidney disease in African Americans could lead to therapies

by Sarah Avery, Duke University

In a finding that could help reduce the racial disparity in kidney disease, Duke Health researchers have detailed how two common gene variants among African Americans can cause kidney failure.

The finding, reported in the Journal of Clinical Investigation , could point to new treatment approaches and advance investigational therapies that block the gene.

"African Americans develop end stage kidney disease at four times the rate of white Americans and represent more than 30% of people on dialysis," said lead author Opeyemi Olabisi, M.D., Ph.D., associate professor in the Department of Medicine at Duke University School of Medicine.

"For more than a decade, we have known that two APOL1 gene variants account for much of the excess risk of non-diabetic kidney failure in African Americans, but we have only a limited understanding of how these variants work. Our study provides that insight."

Two variants in the APOL1 gene—G1 and G2—are known risk factors for kidney disease. These variants arose 5,000 years ago among people in West Africa to provide immunity against African sleeping sickness.

Today, 13% of African Americans carry these two APOL1 gene variants. Approximately 20% of them will develop kidney disease in their lifetime, making APOL1 the most common genetic driver of racial kidney health disparity in the U.S.

Using mice and human cell lines, Olabisi and colleagues found that the APOL1 G1 causes kidney disease by increasing the flow of sodium into and potassium out of a type of cell in the kidney called the podocyte, which forms a protective barrier in the kidney.

This increased flow of sodium and potassium triggers a series of events that damage the kidney. The researchers were able to reduce that damage using an investigational molecule that blocks the function of the APOL1 protein.

"Insights from this work support ongoing therapeutic strategies testing this APOL1 blocker," Olabisi said. "Additional cellular mechanisms that we've identified could also be explored as new therapeutic targets to treat APOL1-mediated kidney disease, with the hope of reducing the high burden of kidney disease in African Americans."

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New £10.4 million research centre will unlock new tests, treatments and cures for people living with rare kidney diseases

Professor Jonathan Barratt

Thousands of people living with rare kidney disease will have access to improved diagnostics, treatments and potentially cures, thanks to the creation of a new research centre, involving experts from the University of Leicester.

It follows a major report from Kidney Research UK which showed that kidney failure could overwhelm the health care system within ten years.

The LifeArc-Kidney Research UK Centre for Rare Kidney Diseases will provide urgent focus and resource, uniting researchers, patients and healthcare professionals and building on strong established resources, including the national registry of rare kidney diseases (RaDaR), the national renal sample biobank (NURTuRE) and care guidelines. 

It signals the start of a transformation in all 13 of the UK’s children’s kidney centres to embed a culture of research by connecting the systems to accelerate discoveries and advance the treatment of rare kidney diseases.

Medical research charity, LifeArc, has invested £9.4 million into the new translational centre, with a further £1 million contribution from Kidney Research UK to support work over the next five years. 

It will be led by Dr Louise Oni, Senior Lecturer in Paediatric Nephrology at the University of Liverpool and honorary consultant paediatric nephrologist at Alder Hey Children’s Hospital.

Professor Jonathan Barratt leads the Renal Research Group within the University of Leicester. His research is focused on a bench to bedside approach to improving understanding of the pathogenesis of IgA nephropathy – a common global cause of kidney failure. As such he will be heavily involved in the new centre and said: “It will offer a transformative approach to the study and care of children with rare kidney diseases.

“Having worked with Louise to help develop the LifeArc proposal it is clear to me that this programme of work has the potential to transform how adult and paediatric nephrologists work together to find cures for rare kidney diseases. 

“LifeArc will leverage the 25 years plus expertise we have in Leicester in the study of IgAN and IgA vasculitis, two rare causes of kidney disease that affect both adults and children, and will utilise the cutting-edge technologies we have available in The Mayer IgA Nephropathy Laboratories to study changes at the molecular level in the kidneys of children with these diseases.” 

Dr Louise Oni said: “This UK wide project aims to create a culture of constant learning to bring rapid advances to patients of all ages living with kidney diseases. It will start by focusing on children with rare kidney diseases to attempt to halt the journey to kidney failure and then upscale into adult patients. Through collaboration, the templates presented by these rare disease centres will support mass transformation to benefit many other patients.”

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Kidney disease ends here .

New £10.4M research centre will unlock new tests, treatments and cures for people living with rare kidney diseases

Thousands of people living with rare kidney disease will get access to improved diagnostics, treatments and potentially cures, thanks to the creation of a new research centre co-funded by Kidney Research UK and medical charity LifeArc .

In 2023 our major report showed that kidney failure could overwhelm the health care system within ten years. The LifeArc-Kidney Research UK Centre for Rare Kidney Diseases is being launched to provide urgent focus and resource. It will unite researchers, patients and healthcare professionals and build on strong established resources, including the national registry of rare kidney diseases (RaDaR), the national renal sample biobank (NURTuRE) and care guidelines. It will signal the start of a transformation in all of the 13 of the UK’s children’s kidney centres to embed a culture of research by connecting the systems to accelerate discoveries and advance the treatment of rare kidney diseases.

The new translational centre is jointly funded by LifeArc, who are investing £9.4M, in partnership with Kidney Research UK. We are contributing an additional £1M to be used to support the work of the centre over the next five years. It will be led by Dr Louise Oni, senior lecturer in paediatric nephrology at the University of Liverpool and honorary consultant paediatric nephrologist at Alder Hey Children’s Hospital.

Dr Louise Oni says “It is a privilege to be leading this exciting transformation on behalf of the entire kidney community. We are incredibly grateful for the opportunity to establish the LifeArc-Kidney Research UK Centre for Rare Kidney Diseases with the support of our charity partners Kidney Research UK.

"This UK wide project aims to create a culture of constant learning to bring rapid advances to patients of all ages living with kidney diseases. The project will start by focusing on children with rare kidney diseases to attempt to halt the journey to kidney failure and then upscale into adult patients. Through collaboration, the templates presented by these rare disease centres will support mass transformation to benefit many other patients.”

Ensuring equal access for people living with kidney disease

Dr Aisling McMahon, executive director of research at Kidney Research UK, said: “Ensuring that everyone has equal access to innovations and new therapies designed to benefit kidney patients is a key priority for Kidney Research UK. We are delighted to be co-funding this new centre with LifeArc and working in partnership with them and the renal research community to deliver this exciting project. This new collaboration will ensure that patients of all ages with rare kidney diseases not only benefit from new approaches to prevention, diagnosis and treatment, but also become active partners in the research process.”

The impact for patients

Kathryn Croker faced kidney failure after being diagnosed with the rare disease IgA vasculitis, aged just 13. Following a successful kidney transplant from her dad in 2013, she went on to volunteer with us and now shares her own experiences to help shape research projects, including this new centre.

She says: “If there was a way to treat rare diseases before they get to that point of causing kidney failure and needing a transplant, that would just be incredible because it changes the course of your life. It’s exciting to be involved in a project with doctors and researchers focused on kidney disease in children, as typically research involves adults. Hopefully in the next 20 years or less, what I’ve experienced since childhood will be a thing of the past because I don’t want anyone to go through what I have. This new research centre is an exciting opportunity to achieve that.”

One of four new centres

The new LifeArc-Kidney Research UK Centre for Rare Kidney Diseases is one of four new centres to be funded by the non-profit medical charity, LifeArc, with the aim of overcoming these barriers that ordinarily prevent new tests and treatments reaching patients. Globally, there are more than 300 million people living with rare diseases. However, rare disease research can be fragmented. Researchers can lack access to specialist facilities, as well as advice on regulation, trial designs, preclinical regulatory requirements, and translational project management, which are vital in getting new innovations to patients.

Dr Catriona Crombie, head of rare disease at LifeArc, says: “We’re extremely proud to be launching four new LifeArc Translational Centres for Rare Diseases. Each centre has been awarded funding because it holds real promise for delivering change for people living with rare diseases. These centres also have the potential to create a blueprint for accelerating improvements across other disease areas, including common diseases.”

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New research sheds light on the potential cause of diabetic kidney disease

September 20, 2023 • 1:13 p.m.

New paper describes the existence of a new version of diabetes—innate immune-driven Diabetes Mellitus caused by uPAR-D2D3

For years, researchers have worked to understand why some people with diabetes get kidney disease while others do not. A paper published in today’s edition of Science Translational Medicine may have uncovered the reason: the existence of a new type of diabetes.

In 2022, the Centers for Disease Control and Prevention estimated that 37.3 million Americans had been diagnosed with diabetes, making it one of the world’s most persistent metabolic endocrine illnesses. About a third of patients with diabetes will develop kidney disease in their lifetimes.

“In addition to Type I and Type II Diabetes Mellitus, our paper suggests the existence of a third type,” said Dr. Sanja Sever, an associate professor at Harvard Medical School and a senior corresponding author of the paper. “It’s an innate, immune-driven Diabetes Mellitus caused by a protein known as uPAR-D2D3.”

Researchers found that D2D3, an enzymatic fragment of uPAR, circulates in blood and binds to insulin-producing beta cells in the pancreas, thereby reducing insulin production. It also targets kidney cells which triggers kidney disease.

“We have always wondered why only a third of patients with Diabetes Mellitus get kidney disease,” said Dr. Jochen Reiser, president of the University of Texas Medical Branch and a senior corresponding author of the paper. “Our paper might have an explanation because uPAR-D2D3-driven pancreatic injury comes with kidney disease, harming both organs simultaneously.”

As a renowned physician-scientist, Reiser has been leading the effort to define the implications of uPAR—and its soluble form suPAR—in renal and cardiovascular diseases for more than 20 years.

While circulating suPAR is known to be a kidney disease risk factor, uPAR-D2D3 appears to be the culprit for mainly diabetic kidney disease, said Dr. Ke Zhu, a scientist at Rush University Medical Center in Chicago and one of the study’s lead authors.

“Our findings also indicate that an antibody that blocks the D2D3 protein can rescue the diabetic phenotypes in a novel mouse model, thus, opening a new avenue for drug therapy”,  said Zhu. “This is an astonishing discovery, as it could help in the development of a new treatment that can potentially reverse the damage caused by the uPAR-D2D3 protein, which may be a direct cause for diabetes and chronic kidney disease. These diseases continue to grow at an alarming rate with no new adequate treatments in sight, so this is good news for patients whose diabetes and kidney disease are caused by uPAR-D2D3 protein.”

“Our study posits that the D2D3 protein may serve as a potential therapeutic target,” said Dr. Kamalika Mukherjee, a co-first author of the study at Massachusetts General Hospital and Harvard Medical School.

The findings described in the study could have implications beyond diabetes and kidney disease, said Dr. Salim Hayek, a cardiologist who is the medical director of the University of Michigan Health Frankel Cardiovascular Center Clinics and another lead author of this project.

“This research dives into the notorious nexus of inflammation, diabetes and kidney disease,” said Hayek. “These conditions are strongly linked to cardiovascular disease, and our team has recently identified a role for suPAR in the pathophysiology of cardiovascular disease . Our discovery delineates the strong connections between these conditions and cardiovascular disease—a convergence orchestrated by suPAR. Recognizing suPAR as the common denominator could pave the way for revolutionary therapies that alleviate not just one, but a spectrum of interconnected ailments, fundamentally enhancing the wellbeing and health prospects for countless individuals.”

“Decades  of studies on uPAR and suPAR from us and others have revealed an enormous potential of regulating the interaction between the immune system and the kidney,” said Dr. Changli Wei, a professor at Rush University Medical Center who was part of initial effort to characterize uPAR-D2D3. “It is very exciting and energizing to see suPAR science coming closer to patients with each new study.”

Other contributing authors include and Mehmet M. Altintas from Rush University Medical Center; Agnieszka Collins, Changkyu Gu and Kristin Corapi from Harvard Medical School; Yong Wang from the University of Virginia; Sushrut S. Waikar from Boston University; Antonio C. Bianco from the University of Chicago; Alexander Koch from University Hopsital Aachen in Aachen, Germany; and Frank Tacke from Universitätsmedizin Berlin in Berlin, Germany.

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The unexpected health benefits of Ozempic and Mounjaro

Research is showing that these new weight-loss drugs can help treat conditions from addiction to kidney disease—and may even be contributing to a boom of “Ozempic babies.”

Casey Arnold, who lives in a suburb of Houston, spent years trying to quit smoking. She’d tried nicotine patches. That failed. She tried quitting cold turkey but that made her short tempered. On other occasions the idea of quitting made her so anxious, she smoked more to ease her fears.

By the time she permanently gave up cigarettes in the winter of 2023, at age 55, she’d been smoking for four decades and was up to two packs a day. But this time it was a new type of weight loss drug that helped her quit.

GLP-1, short for glucagon-like peptide 1, is a natural hormone that stimulates the production and release of insulin, slows digestion, curbs appetite, and blunts the brain’s focus on food. GLP-1 agonist drugs, like exanetide, tirzepatide and semaglutide, mimic this hormone. They were originally developed as diabetes treatments, but as more people began taking them, researchers observed these medications are effective for many more conditions than just diabetes and weight loss.

The FDA recently approved semaglutide, the active ingredient of Wegovy, for the treatment of obesity and for reducing the risk of heart attack and stroke in patients with obesity and heart disease . But as the number of people taking these drugs grows, physicians and researchers are learning about unanticipated health benefits for conditions where treatments have been limited, such as addiction, heart failure, and kidney disease.

( Ozempic is a serious drug with serious risks. Here’s what to know. )

Arnold quit smoking while participating in a clinical trial examining the potential of GLP-1 agonists as a treatment for smoking addiction.

“It was totally opposite of when I tried to quit in my previous years,” Arnold says. “I was shocked at how calm I was, compared to how I used to think about quitting.” Instead of anxiety and rage, she felt at peace, and her cravings faded.

“It’s just been an avalanche across the different patient populations,” says Mark Petrie , a cardiologist at the University of Glasgow, whose research focuses on the use of GLP-1 agonists in patients with heart failure. “It’s just good news all around.”

Heart failure with preserved ejection fraction

More than six million Americans are living with heart failure , a condition where the heart progressively loses the ability to pump enough blood to the rest of the body. Of these patients, approximately half have a type known as heart failure with preserved ejection fraction , in which the heart can pump normally but is too stiff to fill up with blood.

In a study published last year , researchers tested semaglutide as a treatment for heart failure with preserved ejection fraction in patients who were not diabetic. The result: patients who received the drug showed fewer symptoms and reported a better quality of life, compared to those who received the placebo. Patients who received the drug had lower levels of C-reactive protein, which is a marker for inflammation.

“This is a big finding,” says James de Lemos, a cardiologist at UT Southwestern Medical Center, in Dallas, Texas, who was not associated with the study. The study was too small to determine if semaglutide can reduce the risk of hospitalization or death but given the stark improvement in patient quality of life, it’s promising.

Although some of these benefits are likely due to weight loss, that’s just part of what makes this treatment effective.

These medications are also cardioprotective and reduce inflammation, which is known to be a driver of heart failure, says Amanda Vest , a cardiologist at the Cleveland Clinic, who specializes in treating patients with heart failure. “We must continue to think more expansively than just about the number on the scale,” Vest says.

For patients with the other major type of heart failure—heart failure with reduced ejection fraction—there is less evidence, so far, that these drugs are effective. More trials are in the works to determine which types of patients will benefit from the use of these medications.

Kidney disease

An estimated 850 million people worldwide are living with chronic kidney disease ,   but there are few effective treatments. Historically, the main strategy has been to stall kidney failure for as long as possible and then move the patient to dialysis or wait for a kidney transplant. But nine out of 10 patients die of complications before reaching that point.

For patients with severe chronic kidney disease, “you are looking at a mortality rate that’s 10 to 20 percent a year,” says Katherine Tuttle , a nephrologist at the University of Washington Medicine. “This is on par with the worst malignancies.”

As a couple of recent studies have shown , the GLP-1 agonist dulaglutide helps patients who suffer from chronic kidney disease and diabetes. In a recent trial looking at the effect of semaglutide on patients with chronic kidney disease and type 2 diabetes, the treatment was so effective at delaying the progression of chronic kidney disease that the clinical trial was stopped early so that all the trial patients could benefit from the drug.

“It’s the only semaglutide trial that was stopped early for efficacy,” says Tuttle, who is on the executive committee for the trial. “To stop a trial early for efficacy, the bar is set really high,” which includes strong enough evidence for its efficacy that it would be no longer considered ethical to continue giving patients the placebo.

( New obesity drugs are coming. Here's how they could change everything. )

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As Tuttle notes, the effects on the kidneys is only partially due to reductions in risk factors such as blood pressure, blood sugar, and weight. Other benefits are likely to result from reduced inflammation.

“They have a profound anti-inflammatory effect,” Tuttle says. “Our field is really under recognizing the importance of inflammation, particularly in kidney damage caused by diabetes.”

Results from the trial will be published later this year.

Effects on fertility

For a growing number of patients on GLP-1 agonists, such as Ozempic or Mounjaro, one surprising side effect has been unexpected pregnancy, which for some patients, has come after years of struggling with infertility. Although more research is needed to explore the link between GLP-1 agonists and pregnancy, it’s become enough of a phenomenon that ‘Ozempic babies’ has become a trending phrase. Meanwhile, experts think there are several factors responsible.

The first factor is the fact that GLP-1 agonists cause a delayed gastric emptying, which can cause oral contraception pills to be absorbed by the body at a slower rate. “These drugs are altering that particular part of the drug absorption phase,” says Archana Sadhu , an endocrinologist at Houston Methodist Hospital, adding that this effect can be particularly prominent during dosage increases. This means that oral birth control may not be as effective.

The second factor is the link between polycystic ovarian syndrome (PCOS)—the leading cause of infertility in women—and insulin resistance.

“Insulin resistance will dysregulate the ovarian cycle,” Sadhu says. Insulin resistance can lead to infertility by disrupting hormones such as estrogen and testosterone, which are related to fertility; and it can affect the release of eggs from the ovaries. When patients start taking GLP-1 agonists, this reduces their insulin resistance, which boosts fertility.

However, the effects of these drugs on pregnancy are still unknown, which means that it’s important for patients to talk with their doctors about any plans for becoming pregnant, as well as strategies for contraception, which may include adding in a second method to augment oral contraceptive pills, or switching to a different method.

Treating addiction

Since Ozempic and Mounjaro have been become more common, patients have been reporting several unexpected side effects, such as a diminished desire to smoke or drink. Although more research is needed, it’s thought that the part of the brain that is responsible for food cravings overlaps with the part of the brain that is responsible for cravings for substances of abuse, says Luba Yammine, an addiction researcher at UTHealth Houston.

For doctors working in the field, earlier versions of these GLP-1 drugs showed tremendous potential as anti-addiction medications.

“We have far fewer medications available” for treating addiction and many patients report difficulties accessing these, says Christian Hendershot, an addiction researcher at the University of North Carolina School of Medicine. The field also receives less research funding compared with other diseases.

For Yammine, she first became interested in studying the effect of GLP-1 agonists on addiction while working in primary care, where she had several patients who were smokers with diabetes. Yammine would counsel her patients on quitting smoking, prescribing nicotine patches or the medication buproprion, to help them quit. But most of the time these strategies failed.

“It’s hard to quit smoking, period,” Yammine says. “The vast majority of smokers want to quit, but even with the use of these therapies, many of them are not successful.”

To help these smokers with their diabetes she would prescribe GLP-1 agonist medications, only to discover when they returned for a follow-up that they had quit smoking. When she asked them what happened, their answer was that suddenly their cravings vanished. “That was a very interesting finding,” Yammine says.

This happened often enough that Yammine decided to explore the impact of these GLP-1 receptor agonists on addiction through a clinical trial.

Yammine and her collaborators led a pilot study , in which 46 percent of the participants who received exanetide, plus nicotine patches and smoking cessation counseling, were able to quit, compared to 26 percent of participants who received nicotine patches, counseling, and a placebo. Yammine and her collaborators are now following up with a larger trial. They are also planning a separate trial with semaglutide.

For the patients in the study who received exanetide, their post-cessation weight was 5.6 pounds lower than those who received the placebo, a side effect that can help offset the weight gain that is often associated with quitting smoking.  

“This weight gain is very problematic,” Yammine says, adding that many patients are either afraid to quit or relapse due to concerns about weight gain, while it can also put them at heightened risk for developing weight-related conditions, such as type 2 diabetes.

For Arnold, who was enrolled in a follow up trial that Yammine is conducting, the months in which she was participating in the trial was characterized both by a calmness surrounding her efforts to quit, as well as minimal weight gain. Since the trial has ended, she’s been able to maintain her efforts to quit smoking, although she gained a little weight. “I don’t have cravings,” Arnold says. “It’s this weight gain that is bothering me.”

Arnold, who works for an HVAC company, would really like to go back on exanetide, but as is the case with so many other patients who have experienced benefits from GLP-1 receptor agonists, she’s finding that it’s too expensive to do so. Just one month’s supply costs about $1,000, and without FDA approval for its use as an anti-addiction drug, most health insurance companies won’t pay for it.

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Should Kidney Donors Be Paid?

A guest essay argued in favor of payments. Readers, including donors, offer divergent views.

To the Editor:

Re “ We Should Be Allowed to Sell Our Kidneys ,” by Dylan Walsh (Opinion guest essay, April 4):

I’ve seen firsthand how kidney transplants can transform the lives of patients living with debilitating renal disease who are often forced to spend hours each week in painful and exhausting dialysis treatments. Mr. Walsh is correct that we need to greatly boost the number of living organ donors. But before we consider paying people for their kidneys, we need to ensure that every potential donor has an equitable chance to also receive a lifesaving organ transplant.

Even though undocumented people can and do donate organs, far too many of the undocumented, Black and low-income clients we serve with severe renal disease are unable to receive treatment at transplant centers run by private hospitals, despite many of them being excellent medical candidates for a successful transplant.

It would be grossly unethical for our government to encourage them to sell their organs when they receive far less than an equitable share of needed organs.

There are many steps the federal and state governments can take to gather data on transplant equity and require tax-exempt health systems to provide fair and equitable access to transplant care, regardless of immigration or insurance status, income or race. We must create a fair system before we consider a market for organs.

Karina Albistegui Adler New York The writer is co-director of health justice for New York Lawyers for the Public Interest.

As president of the American Society of Transplantation, I know there is an extreme need for additional organs to support lifesaving organ transplantation. Dylan Walsh aptly describes the challenge.

We at the A.S.T. support the author’s intent to increase living donation. However, A.S.T. policy opposes direct remuneration for organs, as it would encourage donations for financial rather than altruistic reasons, thereby propagating disparities. Instead, we aim to remove disincentives that prevent living donors from providing a lifesaving gift.

The A.S.T. is advancing effective solutions. The Living Donor Protection Act , which ensures that life, disability and long-term care insurers cannot discriminate against living donors, has bipartisan support. Other legislation provides a one-time tax credit for living donors that would offset donors’ expenses without providing perverse incentives. The A.S.T. also encourages companies to offer paid leave for living donors through our Circle of Excellence initiative.

Living donors alone cannot meet demand. The A.S.T. is engaged in ongoing work with the Health Resources and Services Administration, patients and other stakeholders to optimize the existing system for deceased donor transplantation, maximize the use of all available organs and minimize non-use.

These activities, along with research on the best strategies to remove disincentives, will result in meaningful progress. Selling organs is not the answer we need now.

Josh Levitsky Chicago The writer is a professor of medicine, surgery and medical education at Northwestern University Feinberg School of Medicine.

Five years ago I donated my left kidney to a stranger after seeing his flyer posted in Starbucks. I was not paid money for my efforts. Yet it was one of the most rewarding endeavors in my life. Throughout the process, I learned many of the lessons that Dylan Walsh discusses.

Even though it’s too late for me to benefit financially, I strongly support the idea of paying future donors. The criticism that rich, powerful people will take advantage of the poor or vulnerable is based on the incorrect assumption that it’s not a rational decision to incur personal risks for financial and other benefits.

It is legal for women to act as paid surrogates carrying a pregnancy that poses at least as many potential medical risks as the nephrectomy. Paying people for kidneys is no different.

As a social worker who has worked with vulnerable people for decades, I believe it’s possible to create safety protocols to ensure that no one is making a decision that is coerced or lacking proper informed consent. There is no better reward than the good feeling of saving a life. Paying someone to do it is just icing on the cake.

Catherine Pearlman Laguna Niguel, Calif.

Nineteen years ago, I donated a kidney to my younger sister with the hope she would live another 10 good years. She had 12 good years, two not so good, and died at the age of 63. I am now 72 and have no regrets, but I remain strongly opposed to the concept of selling kidneys.

The organ transplant community tells only half the story, which is that donors should expect to live well with just one kidney. The other half of the story is what might be involved in recuperating from major surgery. To those involved in physical labor, I would tell them to be prepared to lose your livelihood for up to a year. Sure, there will be anecdotes like “I was mowing my lawn a week later!” But for me, even months later, my children told me that I walked funny.

With a Ph.D. in ethics, I am well aware of the ongoing debate of autonomy versus paternalism on all kinds of subjects. It’s too simplistic to say, “People should be allowed the personal freedom to sell a kidney.” We live in a society that limits our choices in all kinds of ways and for good reason.

In this case, I don’t see the transplant community ever being fully transparent about all the consequences of making this choice, just as they weren’t with me.

Thomas P. Roberts Hillsborough, N.C.

Dylan Walsh’s essay struck a chord. I have failing kidneys, brought on by being one of the millions of Americans with diabetes. Now 75, I long ago made major changes relating to diet, weight and exercise. Unfortunately, my progressive chronic kidney disease refused to get better.

So many of those thousands of Americans who are on waiting lists are young people deserving of so much more life to live. With so few donor kidneys available even for them, at my age I’ve made the decision not to seek a donor kidney, not to add my name to the waiting list. It would not be fair for those who have yet to experience a full life to miss out because I was next in line.

Would I like more time to enjoy life, love, family, etc.? Of course. If Mr. Walsh’s piece gains traction, and one day there are donor kidneys aplenty, I look forward to changing my mind.

Esteban S. Corona, Calif. The writer’s full name is not being used to protect his medical privacy.

The essay by Dylan Walsh highlights the travesty of our kidney transplant program. We are allowed to sell our blood, serum, sperm or ova but not kidneys, which are in short supply.

In addition to Mr. Walsh’s suggestion I would add another: Trade a kidney to stay out of jail. If select first offenders were given the opportunity to avoid a prison sentence by donating a kidney, they would benefit immediately by avoiding incarceration.

Society would benefit from obtaining a young healthy kidney while avoiding the cost of prison sentences. The offender/donor would avoid the many negative aspects of imprisonment. The kidney donation will save the life of someone who might otherwise die of kidney failure.

The experience of saving a life might also contribute to the rehabilitation of a first offender.

Robert W. Morgan Vero Beach, Fla. The writer is an epidemiologist.

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Chronic kidney disease: highlights from research

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