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Editorial Review
Lights and shadows on the pathogenesis of contrast-induced nephropathy: state of the art
University of Parma, Internal Medicine and Nephrology, Parma, Italy
For reprints and correspondence: Giorgio Savazzi, University of Parma, Internal Medicine and Nephrology, Parma, Italy. Email: giorgio.savazzi@unipr.it
Keywords: adenosine; contrast-induced nephropathy; endothelial dysfunction; endothelins; intrarenal vascular resistances; low-osmolar and iso-osmolar contrast media
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Introduction |
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A recent report has suggested that contrast media-induced nephropathy (CMIN) is the third highest cause of hospital-acquired acute renal failure [1]. In nearly half of these patients, CMIN occurred during cardiac diagnostic or interventional procedures such as percutaneous coronary intervention. However, considering the amount of contrast media (CM) used today in extracardiac diagnostic procedures, the incidence of nephropathy still remains relatively low. This low incidence may be attributed to the introduction and use of nonionic, low- or iso-osmolal compounds, to the use of smaller volumes of CM and to an increasing awareness of patients who may be at risk for impairment of renal function. The latter is especially true in patients with pre-existing renal failure, diabetes, or both.
Understandably, the reason a number of patients develop acute renal failure following a cardiac procedure is the necessity to perform these procedures in the presence of pre-existing, and often non-modifiable,
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Haemodynamic alterations and tubuloglomerular feedback |
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Endothelial dysfunction |
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Vasoactive mediators |
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Haemorheological factors |
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Free radicals and reperfusion damage |
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Tubular toxicity and immunological mechanisms |
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Physicochemical characteristics of different contrast media |
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Clinical perspectives on the prevention of contrast-induced nephropathy |
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Conclusions |
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