Nephroprotective effect of lercanidipine against gentamicin-induced kidney damage

Gentamicin, an aminoglycoside antibiotic, induces nephrotoxicity mainly through oxidative stress. This study evaluated the nephroprotective potential of lercanidipine, a calcium-channel blocker, against gentamicin-induced renal injury in rats. Adult Sprague-Dawley rats were randomly divided into four groups: control, lercanidipine (3 mg/kg/day, p.o.), gentamicin (50 mg/kg/day, i.m.), and a combination group pretreated with lercanidipine for 5 days followed by concurrent gentamicin for 5 days. Serum urea, creatinine, sodium (Na⁺), and potassium (K⁺) were determined, and kidney homogenates were analyzed for malondialdehyde (MDA), glutathione (GSH), and superoxide dismutase (SOD). Gentamicin treatment produced marked renal dysfunction, with elevated serum urea and creatinine, increased Na ⁺ by 29%, and decreased K ⁺ by 27.5% relative to control, accompanied by a 37% reduction in urine volume. Co-treatment with lercanidipine restored electrolyte balance, lowering Na ⁺ by 20% and raising K ⁺ by 27% compared with gentamicin alone, while increasing urine volume by 42%. Lercanidipine also markedly attenuated oxidative stress, reducing MDA by about 65% and increasing SOD and GSH activities by approximately 183% and 140%, respectively, relative to gentamicin alone. These findings demonstrate that lercanidipine significantly protects against gentamicin-induced nephrotoxicity by improving renal function, restoring electrolyte homeostasis, and enhancing the antioxidant defence system.