Renogrit protects against folic acid-induced kidney damage in rat model of acute renal failure by regulating serum creatinine and urea levels.

Abstract

Renogrit, a polyherbal formulation, is used for managing chronic kidney conditions. This investigation explored the protective effects of Renogrit against folic acid-induced acute renal failure in Sprague-Dawley rat model. Phytochemical investigation of Renogrit was performed using High-Performance Thin-Layer Chromatography (HPTLC) and Ultra-High-Performance Liquid Chromatography (UHPLC). Rats were treated with incremental doses of Renogrit (10-300 mg/kg, b.i.d.) for 21 days before inducing acute nephrotoxicity using folic acid. Nephroprotective activity of Renogrit was assessed by evaluating urea nitrogen in serum (BUN) and in urine (UUN), serum and urinary creatinine, BUN clearance, creatinine clearance, and estimated glomerular filtration rate. Biomarkers of renal tubular injury, namely kidney injury molecule-1 (KIM-1) and N-acetyl-β-D-glucosidase (NAG), serum electrolyte (Na, K, Cl) levels, liver enzyme (AST), relative kidney weight and renal-histopathological anomalies were also assessed. HPTLC and UHPLC revealed the presence of gallic acid, bergenin, quercetin, methyl gallate, and boeravinone B. In folic acid-induced conditions, Renogrit significantly protected renal function, including BUN and serum creatinine levels, suggesting enhanced filtration and excretory function, prophylactically. Renogrit normalized urinary creatinine and decreased urinary KIM-1 levels, indicating reduced tubular injury post folic acid induction. Histopathological findings in Renogrit treated animals corroborated these biochemical outcomes as evidenced by reduced tubular degeneration, Bowman's space enlargement, and tubular dilatation. Renogrit treatment did not affect serum electrolytes or liver enzymes, demonstrating preclinical safety with respect to the evaluated parameters. Collectively, these findings revealed that Renogrit offers a promising therapeutic strategy for managing acute renal injury, with protecting renal function and reno-structural integrity under nephrotoxic stress.