THE RENAL EXCRETION OF CITRATE*

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Abstract
The effects of acidosis, alkalosis, acetazolamide and certain dicarboxylic acids of the Krebs cycle on the renal excretion of citric acid in the dog have been studied. Citrate clearances were increased by alkalosis and diminished by acidosis or acetazolamide. At normal or elevated plasma citrate concentrations the citrate clearances were less than the glomerular filtration rate (GFR) despite a superimposed metabolic alkalosis. The citrate clearances at normal plasma citrate levels became equal to the GFR following infusion of sodium malate, succinate or malonate. Renal utilization of citrate was inhibited by malate loading. These data are consistent with a renal mechanism of citrate involving filtration and reabsorption but not secretion. The reabsorption and subsequent utilization of citrate by the tubule cell appear to be competitively inhibited by the Krebs cycle substrates, malate and succinate, and also by malonate.