The kidney is responsible for retaining essential proteins and removing waste products from the blood stream. Injury to the kidney results in loss of kidney filter function, which if not treated promptly, can induce kidney failure.
In this issue of the Journal of Clinical Investigation, Anna Greka and colleagues at Massachusetts General Hospital determined that mice lacking the ion channel TRPC5 were protected from losing kidney filter function following kidney injury. In the absence of TRPC5, kidney podocytes did not undergo any cytoskeletal remodeling, which kept the filtration barrier in tact. Furthermore, the authors demonstrated that pharmacological inhibition of TRPC5 protects animals from protein loss in the urine following kidney injury.
This study indicates that activation of ion channel TRPC5 following kidney injury promotes loss of kidney filter function, and inhibition of this ion channel may have therapeutic potential.
Pooled analysis shows finerenone reduces all-cause mortality but not cardiovascular death