Is pyruvate carboxylase involved in the renal tubular reabsorption of bicarbonate?

Abstract

The co-existence of a hereditary defect of pyruvate carboxylase activity along with proximal renal tubular acidosis in several patients prompted the following theories: (1) Some of the bicarbonate which is normally reabsorbed from the glomerular filtrate is trapped in the mitochondria by pyruvate carboxylase in the conversion of pyruvate to oxaloacetate. The subsequent conversion of oxaloacetate to phosphoenol pyruvate releases CO2 in the cytosol. (2) The trapping of HCO-3 by pyruvate (or other carboxylases) provides an important route for the recovery of filtered HCO-3. (3) The process of trapping HCO-3 from the glomerular filtrate followed by release of CO2 in the cytosol contributes to the apparently high RQ of kidney, since the CO2 does not originate from a metabolic fuel. (4) Lactate and possibly other fuels are actively taken up by the kidney and are used as energy sources. Diversion of lactate for gluconeogenesis may contribute to the "excess substrate uptake" phenomenon. (5) It is possible that some of the glucose which is synthesized in the cortex is used for glycolysis in the medulla. Conversely, lactate produced in the medulla may be available to the cortex for bicarbonate trapping and thus for gluconeogenesis.