Abstract

To discover whether the increase in urinary excretion of Tamm-Horsfall protein (THP) is mediated by oxygen free radicals generated after injection of contrast medium, the authors tested the hypothesis that inhibition of oxygen free radical production after injection of sodium methylglucamine diatrizoate or iothalamate sodium diminishes urinary THP excretion. In three groups of dogs, kidneys received continuous infusions of either superoxide dismutase (SOD) and normal saline (six dogs), heat-inactivated SOD and normal saline (six dogs), or normal saline alone (four dogs). Urinary THP excretion, glomerular filtration rate, renal blood flow, mean arterial pressure, and renal venous malondialdehyde concentrations were measured before and after administration of contrast medium to each kidney. During the postcontrast period, SOD significantly attenuated the increase in urinary THP excretion, accompanied by an attenuated increase in renal venous malondialdehyde concentration. Heat-inactivated SOD did not attenuate renal hemodynamics or urinary THP excretion. The use of another contrast medium, iothalamate sodium, similarly increased urinary THP excretion. These results show that intrarenal administration of contrast medium induces a transient increase in urinary THP mediated in part by oxygen free radical damage to the kidney. Thus, THP may be a marker of renal tubular injury after injection of contrast medium.

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