Ga. Porter, CONTRAST-ASSOCIATED NEPHROPATHY - PRESENTATION, PATHOPHYSIOLOGY AND MANAGEMENT, Mineral and electrolyte metabolism, 20(4), 1994, pp. 232-243
Contrast-associated nephropathy, a significant rise in serum creatinin
e 1-5 days following intervascular contrast injection, remains one of
the most serious complications of contrast imaging. The reported incid
ence varies widely; in consecutive random cases ranges from 2 to 7%, b
ut it can increase 5- to 10-fold in high risk patients with serum crea
tinine > 1.5 mg/dl. Postulated mechanisms of renal damage include vaso
constriction and direct tubular cell injury. The usual clinical presen
tation is an asymptomatic increase in serum creatinine without oliguri
a. Residual loss of renal function occurs in principle in patients wit
h preexisting renal impairment. Aggressive prestudy hydration along wi
th selective use of low osmolar contrast media can significantly reduc
e the risk of contrast nephropathy for patients with either chronic re
nal failure or diabetic nephropathy.