According to a new study showing that a serious disease that can cause the kidneys to stop working suddenly could be treated with existing drugs.
New research findings reveal that a serious disease that can cause the kidneys to stop working suddenly could be treated with existing drugs.
Scientists have found that drugs commonly used to treat angina and high blood pressure prevent much of the long-term damage to the kidneys and cardiovascular system caused by acute kidney injury (AKI). The study, which was conducted on mice, was published Dec. 14 in the journal Science Translational Medicine.
Acute renal failure (ARI), formerly known as acute renal failure (ARI), 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 results will pave the way for improved treatment of ARI – a common condition which occurs in around 20% of emergency room admissions in the UK.
The condition is usually caused by other diseases that reduce blood flow to the kidneys (such as low blood pressure, blood loss, heart attack, or organ failure), or due to toxicity of certain medications.
ARI must be treated quickly to avoid death. Even if the kidneys recover, ARI can cause lasting damage to the kidneys and cardiovascular system.
Among those who survive an episode of ARI, 30% suffer from chronic renal failure (CRI). The remaining 70% who recover full kidney function have an almost 30 times greater risk of developing CKD. Over time, CKD can lead to kidneys that stop working altogether. This is called kidney failure, end-stage renal disease (ESRD) or end-stage renal disease (ESKD).
A team from the University of Edinburgh found that patients with ARI had increased blood levels of endothelin – a protein that activates inflammation and causes blood vessels to constrict. Endothelin levels remained elevated long after renal function was restored.
After seeing the same increase in endothelin in mice with ARI, the experts treated the animals with drugs that block the endothelin system. The drugs – normally used to treat angina and high blood pressure – work by stopping endothelin production or blocking endothelin receptors in cells.
The mice were monitored over a period of four weeks after AKI. Those who were treated with the endothelin blocking drugs had lower blood pressure, less inflammation and less scarring in the kidneys.
Their blood vessels were more relaxed and kidney function was also improved, compared to untreated mice.
Dr. Bean Dhaun, Clinical Lecturer and Honorary Consultant Nephrologist at the University of Edinburgh Cardiovascular Science Centre, said: “ARI is a harmful disease, particularly in the elderly and even with recovery, it can have a long-term impact on a person’s health. Our study shows that blocking the endothelin system prevents long-term damage from IRA in mice. As these drugs are already available for use in humans, hopefully we can move quickly to see if the same beneficial effects are seen in our patients.
Professor James Leiper, Associate Medical Director at the British Heart Foundation, said: “Impaired kidney function resulting from acute kidney injury can also increase the risk of developing and dying from heart and circulatory diseases. It is therefore essential to find ways to reduce this. . ” risk.
This promising research suggests that widely available drugs could help combat the impact of acute kidney injury before it causes damage and other complications. While more studies will be needed to demonstrate whether this treatment is safe and effective for patients, this initial research is an encouraging first step.
Reference: “Endothelin Blockade Prevents Long-Term Cardiovascular and Renal Sequelae of Acute Kidney Injury in Mice” by Alicja Czopek, Rebecca Moorhouse, Peter J. Gallacher, Dan Pugh, Jessica R. Ivy, Tariq E. Farrah , Emily Godden, Robert W. Hunter, David J. Webb, Pierre-Louis Tharaux, David C. Kluth, James W. Dear, Matthew A. Bailey and Neeraj Dhaun, December 14, 2022, Science Translational Medicine.
DOI: 10.1126/scitranslmed.abf5074
The study was published on December 14, 2022 in the journal Science Translational Medicine. It was funded by the Medical Research Council and the British Heart Foundation.
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