In a study in mice scientists found that medicines usually used to treat angina and high blood pressure prevented much of the long-term damage to the kidney and cardiovascular system caused by acute kidney injury (AKI).
Experts hope the findings will pave the way for improved treatment of AKI – a common illness that occurs in approximately 20 per cent of emergency hospital admissions in the UK.
The condition is usually caused by other illnesses that reduce blood flow to the kidney, or due to toxicity arising from some medicines.
Kidney damage
AKI must be treated quickly to prevent death. Even if the kidneys recover, AKI can cause long lasting damage to the kidneys and the cardiovascular system.
Of those who survive an episode of AKI, 30 per cent are left with chronic kidney disease (CKD). The remaining 70 per cent that recover full kidney function are at an almost 30-fold increased risk of developing CKD.
A team from the University of Edinburgh found that patients with AKI had increased blood levels of endothelin – a protein that activates inflammation and causes blood vessels to constrict. Endothelin levels remained high long after kidney function had recovered.
Mouse study
After finding the same increase in endothelin in mice with AKI, experts treated the animals with medicines that block the endothelin system. The medicines – normally used to treat angina and high blood pressure – work by stopping the production of endothelin or by shutting off endothelin receptors in cells.
The mice were monitored over a four-week period after AKI. Those that were treated with the endothelin-blocking medicines had lower blood pressure, less inflammation and reduced scarring in the kidney.
Their blood vessels were more relaxed and kidney function was also improved, compared with untreated mice.
The study is published in Science Translational Medicine. It was funded by the Medical Research Council and the British Heart Foundation.