Helmholtz Gemeinschaft

Search
Browse
Statistics
Feeds

Viscosity of contrast media perturbs renal hemodynamics

Item Type:Article
Title:Viscosity of contrast media perturbs renal hemodynamics
Creators Name:Seeliger, E., Flemming, B., Wronski, T., Ladwig, M., Arakelyan, K., Godes, M., Moeckel, M. and Persson, P.B.
Abstract:Contrast-induced nephropathy is a common cause of acute renal failure, and the mechanisms underlying this injury are not completely understood. We sought to determine how physicochemical properties of contrast media may contribute to kidney damage in rats. We administered contrast media of equivalent iodine concentrations but differing physiocochemical properties: the high-osmolality iopromide was compared to the high-viscosity iodixanol. In addition, the non-iodinated substances mannitol (equivalent osmolality to iopromide) and dextran (equivalent viscosity to iodixanol) were also studied. Both types of contrast media transiently increased renal and hindquarter blood flow. The high-osmolality agents iopromide and mannitol markedly increased urine production whereas iodixanol, which caused less diuresis, significantly enhanced urine viscosity. Only the high-viscosity agents iodixanol and dextran decreased renal medullary blood flux, erythrocyte concentration, and pO2. Moreover, iodixanol prolonged the tubuloglomerular feedback response and increased plasma creatinine levels to a greater extent than iopromide or dextran. Therefore, the viscosity of contrast media may play a significant role in contrast-induced nephropathy.
Keywords:Contrast Media, Hemodynamics, Hindlimb, Iohexol, Osmolar Concentration, Regional Blood Flow, Renal Circulation, Triiodobenzoic Acids, Urination, Viscosity, Animals, Rats
Source:Journal of the American Society of Nephrology
ISSN:1046-6673
Publisher:American Society of Nephrology
Volume:18
Number:11
Page Range:2912-2920
Date:November 2007
Official Publication:https://doi.org/10.1681/ASN.2006111216
PubMed:View item in PubMed

Repository Staff Only: item control page

Open Access
MDC Library