Radiocontrastinduced Nephrotoxicity

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Radiocontrast-induced nephropathy is a leading cause of hospital-acquired acute renal failure (ARF) with an incidence ranging from 2 to 10% depending on the population's risk factors. Risk factors include preexistent volume depletion, age, underlying chronic renal insufficiency, diabetes mellitus, proteinuria, and the amount of the radiocontrast dye used. The pathogenesis of ARF in this setting is probably related to decreased renal blood flow and medullary ischemia resulting from an imbalance of vasodilative and vasoconstrictive factors [ 14]. Radiocontrast agents may also be directly toxic to the renal tubule epithelium. This form of ARF is somewhat unique because preexisting risk factors can be identified and the timing and dose of dye can be controlled. Measures which have been proposed to prevent or reduce the severity of contrast-induced nephrotoxicity include volume expansion and the administration of furose-mide, mannitol, calcium channel blockers, dopamine, atrial natriuretic peptide, and theophylline [2],

The protective effect of jurosemide in preventing contrast-induced ARF may be related to medullary renal vasodilation, reduction of the oxygen demand imposed by active sodium reabsorption, release of vasodilators, prostaglandins, and a reduction of the intratubular concentration of contrast media. The infusion of hypertonic mannitol may be protective by causing renal vasodilatation, inducing an osmotic diuresis, and increased atrial natriuretic peptide release and as a free oxygen radical scavenger. In some experimental animal models both mannitol and furosemide have attenuated contrast-induced renal dysfunction. In contrast, three randomized controlled studies in humans have shown that mannitol has either no effect or is deleterious in diabetic patients with renal insufficiency [7]. Similarly, two randomized prospective studies have shown that furosemide may increase the incidence of radiocontrast-induced ARF in uremic diabetic patients [7]. In a randomized trial of the efficacy of 0.45% saline alone compared with saline plus either furosemide or mannitol, saline alone was superior to the other two regimens in preventing contrast-induced nephrotoxicity [23], Thus, the use of mannitol and/or furosemide remains controversial in preventing contrast media induced ARF.

In patients at risk for developing this complication, intravenous saline should be given before and after the administration of contrast agents. When the patient also has congestive heart failure or renal insufficiency, the use of furosemide may be indicated. In nondiabetic patients with normal renal function there is no need to use mannitol or furosemide to prevent contrast-induced nephrotoxicity.

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