ROLE OF MONTELUKAST IN DICLOFENAC-INDUCED KIDNEY INJURY

Objectives: Diclofenac is the main trigger of nephrotoxicity and acute kidney injury (AKI) because it causes oxidative stress. Therefore, the aim of this study is to evaluate kidney injury biomarkers in diclofenac-induced AKI in rats. Methods: Eighteen Sprague-Dawley Male rats were used and randomly divided into three groups. Group 1 (n = 6): Rats treated with 0.5 % sodium carboxyl methylcellulose (PO) for 7 days. Group 2 (n = 6): Rats treated with single injection of Diclofenac (100 mg/kg, i.p). Group 3 (n = 6): Montelukast (20mg/kg, oral) for 7 days then at 7th day rats injected single dose of Diclofenac (100 mg/kg, i.p). Serum creatinine, Blood urea, Proteinuria, Creatinine clearance (CrCl), neutrophil gelatinase associated lipocalin (NGAL), kidney injury molecules (KIM-1) were estimated in three groups. Results: Diclofenac (100 mg/kg, i.p) caused substantial AKI by significantly reducing CrCl and raising blood urea and serum creatinine. Plasma levels of KIM-1 and NGAL were considerably higher than the other kidney biomarkers, with high sensitivity and specificity for AKI. Conclusion: In diclofenac-induced AKI, KIM-1 level is more accurate, sensitive, and specific than the other renal biomarkers. For high-risk individuals, estimating KIM-1 and NGAL levels should be considered cornerstones of early AKI detection. Additionally, Montelukast demonstrated a protective effect in a diclofenac-induced renal damage model in rats.