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

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


Contrast nephropathy is a generally reversible form of acute kidney injury (AKI) that occurs soon after the administration of radiocontrast media [1-11]. Although AKI is reversible in most cases, its development may be associated with adverse outcomes. (See "Kidney and patient outcomes after acute kidney injury in adults".)

This topic reviews the pathogenesis, clinical characteristics, and diagnosis of iodinated radiocontrast media-induced nephropathy. The epidemiology of contrast nephropathy, 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 "Evaluation of acute kidney injury among hospitalized adult patients" and "Diagnostic approach to adult patients with subacute kidney injury in an outpatient setting" and "Etiology and diagnosis of prerenal disease and acute tubular necrosis in acute kidney injury in adults".)


The best data related to the pathogenesis of contrast nephropathy are 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 effects of viscosity and by alterations in nitric oxide, endothelin, and/or adenosine, and that ATN is a direct result of the cytotoxic effects of the contrast agents on tubular cells [12-20]. Tubular cell injury may be exacerbated by renal vasoconstriction [12,13,18].

Compared with other types of ATN (such as ischemic), contrast nephropathy is usually characterized by relatively rapid recovery of renal function (see 'Clinical features' below). 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. One possibility is that the degree of tubular necrosis is much less severe than seen in other settings. It is also possible that the decline in glomerular filtration rate (GFR) is due to functional changes in tubule epithelial cells rather than necrosis. This phenomenon may be at least in part due to redistribution of membrane transport proteins from the basolateral to the luminal membrane [21].

In addition, it is possible that prerenal factors or intratubular obstruction contribute to the pathogenesis. This possibility is suggested by the observation that the fractional sodium excretion (FENa) may be <1 percent in patients with contrast nephropathy, which is characteristic of prerenal physiology [22]. (See "Fractional excretion of sodium, urea, and other molecules in acute kidney injury (acute renal failure)", section on 'Fractional excretion of sodium in acute kidney injury' and 'Clinical features' below.)

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Literature review current through: Nov 2017. | This topic last updated: Jun 16, 2017.
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