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Pathogenesis, clinical features, and diagnosis of contrast-induced nephropathy

Author
Michael R Rudnick, MD
Section Editor
Paul M Palevsky, MD
Deputy Editor
Alice M Sheridan, MD

INTRODUCTION

Contrast nephropathy is a generally reversible form of acute kidney injury (AKI) that occurs soon after the administration of radiocontrast media [1-11]. Important issues that remain unresolved include its pathogenesis and relative efficacies of various prophylactic strategies.

A review of the pathogenesis, clinical characteristics, and diagnosis of iodinated radiocontrast media-induced nephropathy is presented here. Preventive strategies for reducing the risk of contrast nephrotoxicity and a discussion of acute tubular necrosis (ATN), the most common cause of AKI developing in hospitalized patients, are presented separately. (See "Prevention of contrast-induced nephropathy" and "Etiology and diagnosis of prerenal disease and acute tubular necrosis in acute kidney injury (acute renal failure)".)

PATHOGENESIS

Overview — The best data related to the pathogenesis of contrast nephropathy come from animal models. Studies show evidence of acute tubular necrosis (ATN), but the mechanism by which ATN occurs is not well understood [12-14]. The two major theories are that ATN is caused by renal vasoconstriction resulting in medullary hypoxia, possibly mediated by alterations in nitric oxide, endothelin, and/or adenosine, and that ATN is a direct result of the cytotoxic effects of the contrast agents [12-20].

However, unlike other types of ATN, contrast nephropathy is usually characterized by relatively rapid recovery of renal function. If ATN contributes to contrast nephropathy, it is not clear why recovery occurs relatively quickly (ie, within a few days), compared with a longer duration (ie, one to three weeks), as with ATN due to other causes. There are at least two possibilities to explain the short duration of ATN:

The degree of tubular necrosis is much less severe than seen in other settings.

                 

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Literature review current through: Nov 2016. | This topic last updated: Wed Feb 03 00:00:00 GMT+00:00 2016.
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