The Relative Contributions of Tubular Reabsorption and Secretion to Urate Excretion in Lead Nephropathy

Abstract

Summary: Renal tubular reabsorption and secretion of urate have been separately assessed in patients with lead nephropathy by observation of the effect on renal disposition of urate of the drug pyrazinamide, which blocks active tubular secretion of urate. Tubular reabsorption of urate was found to be greater than expected for the degree of renal failure as reflected by the inulin clearance, whereas active tubular secretion of urate was within the range predicted from the plasma urate concentration. As the hypewricaemia of lead nephropathy has been shown to be renal in origin, these results suggest that it is mediated by excessive tubular reabsorption of urate. Though defective tubular secretion of urate has not been demonstrated, more extensive studies over a wide range of plasma urate concentrations would be needed to exclude an additional associated abnormality of the secretory process.