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This Article Full Text Full Text (PDF) All Versions of this Article: 297/1/F106    most recent 00126.2009v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Google Scholar Articles by Cho, K.-h. Articles by Vaziri, N. D. PubMed PubMed Citation Articles by Cho, K.-h. Articles by Vaziri, N. D.

Niacin ameliorates oxidative stress, inflammation, proteinuria, and hypertension in rats with chronic renal failure

¹Division of Nephrology and Hypertension, University of California, Irvine, California; ²Department of Internal Medicine, Yeungnam University, Daegu, Korea; and ³Renal Service, Hospital Universitario, Universidad del Zulia and Centro de Investigaciones Biomédicas (IVIC-Zuli), Maracaibo, Venezuela

Submitted 4 March 2009 ; accepted in final form 28 April 2009

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, nephrectomized [chronic kidney disease (CKD)] rats were randomly assigned to niacin-treated (50 mg·kg^–1·day^–1 in the drinking water for 12 wk) and untreated groups. Sham-operated rats served as controls. The untreated CKD rats exhibited azotemia, hypertension, hypertriglyceridemia, proteinuria, glomerulosclerosis, tubulointerstitial damage, upregulation of MCP-1, plasminogen activator inhibitor-1 (PAI-1), transforming growth factor (TGF)-β, cyclooxygenase (COX)-1, COX-2, and NAD(P)H oxidase (NOX-4, gp91^phox, p47^phox and p22^phox subunits) and activation of NF-B (IB phosphorylation). Niacin administration reduced MCP-1, PAI-1, TGF-β, p47^phox, p22^phox, COX-1, and NF-B activation, ameliorated hypertension, proteinuria, glomerulosclerosis, and tubulointerstitial 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 upregulation of oxidative and inflammatory systems in the remnant kidney.

malnutrition; glomerulosclerosis; fibrosis; TGF; CTGF; NAD(P)H oxidase; cyclooxygenase; NF-B; lipid disorder; atherosclerosis

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