Contrast-induced Nephropathy in Coronary Intervention

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US Cardiology, 2007;4(1):66-8

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Contrast-induced nephropathy (CIN) in the actual essence of the term refers to renal damage induced by a contrast medium. The ultimate clinical manifestation of CIN is renal failure requiring dialysis, and this article will concentrate on CIN as a clinical outcome. However, transient rises in serum creatinine have been frequently used as a surrogate marker that is suggested to predict renal failure, and these transient rises are usually also termed CIN. The definition and the pitfalls of this surrogate marker will also be part of this review, but in order to maintain a clear nomenclature the focus will be on CIN as a clinical outcome in coronary intervention. This article will also discuss the effectiveness of proposed strategies for prophylaxis of CIN.

Incidence of Actual Renal Failure in Coronary Intervention

The incidence of renal failure requiring dialysis following coronary intervention is very low, amounting to 0.1–0.5%.1,2 The incidence is higher in risk patients, i.e. patients with pre-existing chronic kidney disease, increasing to 1% in high-risk patients and up to 13% in very high-risk patients.3 What needs to be appreciated, however, is that not all cases of renal failure requiring dialysis after coronary intervention are actually caused by the administered contrast medium. In fact, there are several other possible causes for such an event, e.g. atheroemboli or other procedural-related causes, as well as procedure-unrelated progress of disease in risk patients. Still, renal failure requiring dialysis is a serious complication after percutaneous coronary intervention (PCI) associated with a significantly poorer prognosis for the respective patient, which is to be avoided as much as possible.

Pathophysiology of Contrast-induced Nephropathy

The pathophysiology of CIN is not completely understood, but it is certain to involve the interplay of multiple factors leading to hypoxia of the outer medulla.4 Several characteristics of contrast media (CM) have been suggested as possible causes of CIN, e.g. osmolality, direct tubular cytotoxicity, and, more recently, viscosity.
The role of one of these factors, osmolality, may have been over-interpreted. A widespread explanation for the development of CIN is that hyperosmotic CM cause diuresis, which activates tubuloglomerular feedback and subsequently compromises renal blood flow and glomerular filtration. However, this theory is not a likely explanation for CIN, as pioneering experiments with retrograde perfusion of the tubule have already shown that osmolality has no effect on tubuloglomerular feedback.4

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