• Elif Ari, Yusuf Yilmaz, Alla Elden Kedrah, Yesim Alahdab, Fulya Cakalagaoglu, Hakki Arikan, Hüseyin Kocak, Beyza Macunluoglu, Aydin Atakan, Arzu Kahveci, Ebru Asicioglu, Serhan Tuglular, and Cetin Ozener.
• Department of Nephrology, Marmara University School of Medicine, Istanbul, Turkey.
• Am. J. Nephrol. 2011 Jan 1; 33 (3): 269-76.

Background/AimsContrast-induced nephropathy (CIN) remains a leading cause of iatrogenic acute renal failure. Terlipressin, a long-acting analog of vasopressin, may improve renal function. This study aimed to investigate the possible protective effect of terlipressin against the development of experimental CIN in rats.MethodsWistar albino rats (n = 32) were allocated randomly into four equal groups of 8 each, i.e. control, terlipressin, contrast media (CM), and terlipressin plus contrast media (TCM). CIN was induced by intravenous administration of indomethacin (10 mg/kg), N-nitro L-arginine methyl ester (L-NAME, 10 mg/kg, twice at 15 and 30 min), and high-osmolar contrast media meglumine amidotrizoate 60%. Renal function parameters, kidney histology, and tubular expression of vascular endothelial growth factor (VEGF) were determined.ResultsMean serum creatinine levels were decreased (p < 0.05) and creatinine clearance (p < 0.05) increased in the TCM group compared with the CM group. Notably, rats in the TCM group displayed less tubular necrosis (p < 0.05), medullary congestion (p < 0.05), and a reduced tubular expression of VEGF (p < 0.05) compared with the CM group.ConclusionThese results demonstrate that terlipressin can inhibit the development of CIN.Copyright © 2011 S. Karger AG, Basel.

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