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Received November 8, 2006
Accepted on June 19, 2007
BASIC RESEARCH: Basic Research |
,
,
*Institut für Vegetative Physiologie and *Institut für Vegetative Physiologie and
Medizinische Klinik–Kardiologie, Charité Universitätsmedizin Berlin, Berlin, Germany; and
Physiology Department, Yerevan State Medical University, Yerevan, Armenia
Medizinische Klinik–Kardiologie, Charité Universitätsmedizin Berlin, Berlin, Germany; and
Physiology Department, Yerevan State Medical University, Yerevan, Armenia
1 To whom correspondence should be addressed. E-mail: pontus.persson{at}charite.de.
| Abstract |
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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.
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