Existing Medicines May Treat a Common Kidney Disease

Illustration of human kidney

A serious condition that can cause the kidneys to suddenly stop working can be treated with existing drugs, a new study has found.

New research results reveal that a serious condition that can cause the kidneys to suddenly stop working can be treated with existing drugs.

Scientists have found that drugs commonly used to treat angina and high blood pressure prevent long-term damage to the kidneys and cardiovascular system caused by acute kidney injury (AKI). The study, conducted on mice, was published in the journal Dec. 14 Science Translational Medicine.

Acute kidney injury (AKI), formerly called acute renal failure (ARF), is a sudden decline in kidney function that develops within 7 days. This condition is indicated by an increase in serum creatinine or a decrease in urine output, or both.

Experts hope the findings will pave the way for improved treatment of AKI – a common condition that occurs in around 20 per cent of emergency hospital admissions in the UK.

This condition is usually caused by other illnesses that reduce blood flow to the kidneys (such as low blood pressure, blood loss, heart attack, or organ failure) or by toxicity from certain medications.

AKI must be treated quickly to prevent death. Even with kidney recovery, AKI can cause chronic damage to the kidneys and cardiovascular system.

Of those who survive an episode of AKI, 30 percent go on to develop chronic kidney disease (CKD). The remaining 70 percent who regain full kidney function have a nearly 30-fold increased risk of developing CKD. Over time, CKD can cause the kidneys to stop working completely. This is known as kidney failure, end-stage renal disease (ESRD), or end-stage kidney disease (ESKD).

A team from the University of Edinburgh found that patients with AKI had increased blood levels of endothelin – a protein that activates inflammation and constricts blood vessels. Endothelin levels remained high even after renal function had recovered.

After finding a similar increase in endothelin in mice with AKI, experts treated the animals with drugs that block the endothelin system. The drugs – commonly used to treat angina and high blood pressure – work by stopping the production of endothelin or blocking endothelin receptors on cells.

Rats were monitored for four weeks after AKI. Those treated with endothelin-blocking drugs had lower blood pressure, less inflammation, and less kidney scarring.

Compared to untreated mice, their blood vessels were more relaxed and kidney function was also improved.

Dr Bin Dhaun, Senior Clinical Lecturer and Honorary Consultant Nephrologist at the University of Edinburgh Center for Cardiovascular Science, said: “AKI is a devastating condition, particularly in older people, and even with recovery it can have long-term effects on a person. Health Our study shows that blocking the endothelin system prevents the long-term damage of AKI in mice. Because these drugs are already available for human use, I hope we can move forward quickly to see if the same beneficial effects can be seen in our patients.”

Professor James Leeper, associate medical director of the British Heart Foundation, said: “The impaired kidney function that acute kidney injury can increase a person’s risk of developing and dying from heart and circulatory disease, so it’s important that we find ways to reduce that risk.

“This promising research suggests that widely available drugs may help counter the effects of acute kidney injury before they cause damage and further complications. Although more research will be needed to demonstrate whether this treatment is safe and effective for patients, this preliminary study is an encouraging first step.” steps.”

Reference: “Endothelin Blockade Prevents Long-Term Cardiovascular and Renal Sequelae of Acute Kidney Injury in Rats” Alicja Szopec, Rebecca Moorhouse, Peter J. Gallacher, Dan Pugh, Jessica R. Ivy, Tarik E. Farah, Emily Godden, Robert W. Hunter, David J. Webb, Pierre-Louis Thuraux, David C. Kluth, James W. Dear, Matthew A. Bailey and Neeraj Dhaun, 14 December 2022, Science Translational Medicine.
DOI: 10.1126/scitranslmed.abf5074

The study was published in the journal Dec. 14, 2022 Science Translational Medicine. It was funded by the Medical Research Council and the British Heart Foundation.


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