Acute kidney injury (AKI) refers to the rapid decline of renal function, typically resulting from toxic or ischemic insults due to chemotherapy, antibiotics, or infection-related shock. Notably, approximately one-third of patients undergoing cisplatin therapy develop AKI, predominantly due to the nephrotoxicity of cisplatin. Cisplatin, an anti-neoplastic agent used for various solid-organ cancers, has its use limited by nephrotoxicity, a significant adverse effect. Oxidative stress is a crucial mechanism underlying cisplatin-induced AKI, suggesting that antioxidants like vitamin D may mitigate these adverse effects. Stem cells, particularly bone marrow-derived mesenchymal stem cells (BM-MSCs), offer a promising therapeutic approach for renal repair. These undifferentiated cells possess considerable self-renewal and tissue generation capabilities. BM-MSCs can ameliorate renal functional deficits, tubular necrosis, and apoptosis while promoting tubular regeneration, likely through paracrine or endocrine mechanisms rather than direct engraftment.

AIM OF THE WORK:
The aim of the present work was to:
• Study the histological and immunohistochemical changes in a rat model of cisplatin – induced acute nephrotoxicity.
• Study the efficacy of BM -MSCs and alfacalcidol (ALFA) to treat cisplatin-induced acute nephrotoxicity in adult male albino rats.