Aliskiren alleviates doxorubicin-induced nephrotoxicity by inhibiting oxidative stress and podocyte injury (original) (raw)

Doxorubicin (DXR) is widely used for cancer therapy but is known to cause nephrotoxicity, characterized by proteinuria and hypoalbuminemia, due to mechanisms involving oxidative stress and overactivity of the renin-angiotensin system (RAS). Preliminary studies have shown that while angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) provide some renal protection, they may inadvertently increase plasma renin activity. Aliskiren (ALK), a direct renin inhibitor, is hypothesized to mitigate DXR-induced nephrotoxicity more effectively by reducing renin activity from the outset of the RAS cascade. Experimental results indicate that ALK significantly improves renal function parameters and reduces oxidative stress markers in DXR-treated subjects.