Significant reduction of renal mass causes progressive deterioration of renal function and structure which is mediated by systemic and glomerular hypertension, hyperfiltration, oxidative stress, inflammation and dyslipidemia. Niacin is known to improve lipid metabolism and exert antioxidant/anti-inflammatory actions. Therefore, we considered that niacin supplementation may attenuate oxidative stress, inflammation and tissue injury in the remnant kidney. To this end, 5/6 nephrectomized (CKD), rats were randomly assigned to niacin-treated (50 mg/Kg/day in drinking water for 12 weeks) and untreated groups. Sham-operated rats served as controls. The untreated CKD rats exhibited azotemia, hypertension, hypertriglyceridemia, proteinuria, glomerulosclerosis, tubulo-interstitial damage, up-regulations of MCP-1, PAI-1, TGF, COX-1, COX-2 and NAD(P)H oxidase (NOX-4, gp91^phox, p47^phox and p22^phox subunits) and activation of NFB (IKB phosphorylation). Niacin administration reduced MCP-1, PAI-1, TGF, p47^phox, p22^phox , COX-1, and NFB activation, ameliorated hypertension, proteinuria, glomerulosclerosis and tubulo-interstitial injury. Although niacin lowered serum creatinine and raised creatinine clearance, the differences did not reach statistical significance. Thus, niacin supplementation helps to attenuate histological injury and mitigate up-regulation of oxidative and inflammatory systems in the remnant kidney.