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Contrast nephropathy is the third most common cause of hospital-acquired renal insufficiency. While its exact pathogenesis is unclear, patients with existing renal disease are now known to be at increased risk for developing this complication. Identification of these patients by determination of serum creatinine levels may enable avoidance of contrast exposure or initiation of suitable therapy to minimize this complication if exposure to contrast is unavoidable.

The prospective study involved 50 patients without known renal masses or previous renal surgery who received intravascular contrast medium for various radiologic procedures and subsequently underwent unenhanced computed tomography (CT) of the kidneys 22-26 hours later. In 42 patients, cortical readings did not exceed 50 HU and corticomedullary attenuation differences (CMADs) did not exceed 10 HU. In seven patients (intermediate group), there was persistent cortical enhancement (mean attenuation, 58.3-84.8 HU; CMAD, 10.3-40.3 HU), but there was no significant rise in levels of blood urea nitrogen or serum creatinine. A single patient had contrast nephropathy and exhibited a mean cortical attenuation of 141.6 HU and a mean CMAD of 85.8 HU on the 24-hour CT scan. The authors have seen two additional cases of contrast nephropathy presaged by mean cortical attenuations of 162 and 209 HU on the 24-hour CT scan. One of these patients had been in the intermediate group in the prospective study. A cortical attenuation of 55-110 HU on a 24-hour postcontrast scan may help identify a group of patients with subclinical renal impairment who are at high risk of nephropathy on subsequent exposure to contrast medium, while cortical attenuations in excess of 140 HU seem to be an early indicator of contrast nephropathy.

—Dr Tannenbaum raises two interesting questions. First, was this patient's renal failure a consequence of obstructive jaundice, unrelated to the administration of angiographic contrast, and second, would mannitol be suitable prophylaxis against renal failure in this clinical setting. Renal failure has been described following uncomplicated biliary obstruction, 1 although the authors gave no details of the patient's degree of hydration or the severity of azotemia. Renal failure does not commonly occur with biliary obstruction alone, but develops after major surgery, 2-5 possibly as a result of endotoxemia resulting from handling the bowel. 6,7 Although obstructive jaundice was clearly a risk factor for renal failure in the patient under discussion, it seems unlikely to be the sole cause, particularly as renal failure resolved despite persisting severe hyperbilirubinemia. The temporal relationship of cholangiography and azotemia suggests contrast nephropathy. As Tannenbaum points out, Dawson demonstrated the efficacy of mannitol prophylaxis in jaundiced rats

The paper by Marenzi et al. ([1][1]) in JACC: Cardiovascular Interventions on prevention of contrast-induced nephropathy (CIN) using furosemide with matched hydration deals with a pertinent and pervasive problem. In this randomized trial of 170 patients who received contrast media during coronary