Renal complications associated with contrast media

Abstract

The use of iodinated contrast media (CM) is associated with a risk of renal insufficiency. However, the definition of renal insufficiency varies. Contrast media impair the renal medullary flow and exert a direct toxic effect on renal tubular cells. The ensuing renal insufficiency results from haemodynamic disturbances and tubular cell injury. Under normal conditions, the renal medulla—in which the loop of Henle and the vasa recta follow a deep, ‘hairpin’-like course and achieve urinary concentration/ dilution—is a region of low blood flow and low pO2. Extracellular volume depletion contributes to further reduce blood flow to the deeper portion of the outer medulla. Contrast media markedly diminish renal medulla perfusion and oxygenation. The thick ascending limb (TAL) of the loop of Henle is particularly affected by hypoxic stress. Contrast media-induced nephrotoxicity (CIN) stems from a combination of erythrocyte sludge in the vasa recta, renal vasoconstriction and toxicity to tubular epithelial cells, especially in the TAL. Ageing, dehydration and chronic renal insufficiency, especially diabetic nephropathy, are three conditions under which CM most commonly induce renal insufficiency, with an increased risk in the case of concomitant treatment with nephrotoxic medications. The prevention of CIN follows from these intricate pathophysiological mechanisms. It is based on reducing CM osmolality, opposing medullary vasoconstriction and hypoxic stress with pharmacological agents and, above all, increasing the renal medullary flow by intravenous infusion of saline.