Contrast-associated nephropathy.

Contrast nephropathy can be defined as an acute impairment of renal function that follows exposure to radiocontrast materials and for which alternative explanations for renal impairment have been eliminated. Based on reported studies, the incidence of contrast associated nephropathy (CAN) varies from 0 to 22%. This wide variation can be traced to differences in study design and the criteria used to designate significant renal impairment. Irrespective of the exact incidence, 2 defined risk factors have been identified: preexisting renal disease and diabetes mellitus. Whereas preexisting renal insufficiency is the single most influential risk factor for CAN, when diabetes coexists the incidence approaches 100%. The clinical presentation of CAN is distinct, having a temporal relation between the performance of the contrast study in the high-risk patient and the onset of an increase in serum creatinine levels within the next 24 hours. Serum creatinine values greater than 50% of baseline or rising 1 mg/dl or more is diagnostic. The peak serum creatinine level occurs within 3 to 5 days of the contrast study and oliguria is associated in approximately 30% of the cases. Monitoring serum creatinine is the most useful clinical procedure in high-risk patients after angiography. At least 5 potential pathophysiologic mechanisms of CAN have been proposed: interference with renal perfusion, altered glomerular perm-selectivity, direct tubular injury, intraluminal obstruction, and immunologic mechanisms. Support for each mechanism, either singularly or in combination, can be found in published reports; however, none has achieved universal acceptance. The single most important clinical axiom regarding the prevention and management of CAN is, "Always use the least invasive diagnostic procedure available."(ABSTRACT TRUNCATED AT 250 WORDS)