Radiocontrast medium-induced declines in renal function: a role for oxygen free radicals

Abstract

Intrarenal injection of radiocontrast medium (RCM) results in transient vasoconstriction and a persistent decline in glomerular filtration rate (GFR). Adenosine modulates this vasoconstrictor response and is postulated to increase oxygen free radical (OFR) generation. We hypothesized that the persistent decline in (GFR that follows RCM administration results in an increased generation of OFR. We evaluated the effects of RCM injection on renal blood flow, inulin clearance, hypoxanthine, xanthine, and malondialdehyde concentrations in four groups of non-volume-expanded, pentobarbital sodium anesthetized dogs in the presence and absence of intravenous allopurinol, 25 mg/min (group 1), intrarenal superoxide dismutase (SOD), 400 U/min (group 2), heat-inactivated intrarenal SOD, 400 U/min (group 3), and simultaneous infusions of intrarenal SOD, 400 U/min, to one kidney and saline to the other (group 4). Both allopurinol and SOD significantly attenuated the fall in GFR after RCM administration over control. Malondialdehyde concentrations were attenuated over control in all treated groups, indicating a decrease in OFR generation. We conclude that intrarenal injection of RCM results in increased production of OFR. Inhibition of OFR production by allopurinol and increased OFR removal by SOD attenuates the effects of RCM on declines in GFR.

Risk of contrast-induced nephropathy in hospitalized patients with cirrhosis

“…Tubular toxicity is also thought to play a role in CIN through both direct nephrotoxicity and tubular obstruction. The generation of reactive oxygen species can cause toxic, ischemic, and immune-mediated direct nephrotoxicity [26][27][28] . Contrast dye increases urate excretion and leads to the deposition of Tamm-Horsfall proteins within the renal tubules, both of which can cause tubular obstruction [29][30][31] .…”

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“…Also, the osmotic pressure is elevated by infusion of contrast medium, which increases the amount of NaCl reaching the ascending limb of the loop of Henle, and increased sodium reabsorption accelerates renal oxygen consumption. This leads to renal medullary hypoxia and parenchymal injury due to accelerated production of free radicals by renal tubular epithelial cells 10. As contrast medium flows through the renal tubules, it gradually becomes highly concentrated, and toxicity of the agent itself can directly damage tubular epithelial cells 11, 12, 13.…”

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“…It certainly involves the interplay of multiples factors; however, little is known about the underlying cellular mechanisms 25 . Evidence suggests that free radicals have important role in the development of CIN associated with direct injury to the tubular epithelium [26][27][28] . Once the acidic environment typical of renal tubules propitiates the formation of free radicals is possible that alkalinization of urine may reduce the incidence of CIN.…”