Renal regulation of acid-base balance in malnourished man

Abstract

Renal excretion of acid in adult patients with moderate to severe protein malnutrition was studied before and after protein repletion. In malnourished patients steady-state blood pH and bicarbonate concentration values were found to be within normal limits, but total renal acid excretion during the malnourished state averaged only 16.4 mEq in twenty-four hours (2.6 mEq of titratable acid and 13.8 mEq of ammonium). Following a standard dose of ammonium chloride there was a striking decrease in blood pH and plasma bicarbonate concentrations. Total renal acid excretion rose only to 44.2 mEq per twenty-four hours (6.7 mEq of titratable acid and 37.5 mEq of ammonium) on the fifth day of ammonium chloride administration. After two to three months of protein repletion the total acid excretion increased over twofold (8.6 mEq of titratable acid and 27.3 of ammonium). On the fifth day of ammonium chloride administration titratable acid excretion increased to 27.3 mEq per twenty-four hours, ammonium excretion to 61.9 mEq per twenty-four hours. The decreased excretion of titratable acid during malnutrition was associated with a reduced rate of urinary phosphate excretion. Infusion of phosphate during the malnourished state resulted in a marked increase in titratable acid production. The baseline excretion of ammonium was much higher in the protein-repleted state. In addition greater increases in ammonium excretion were observed after protein repletion, following ammonium chloride administration, despite the presence of a lesser degree of metabolic acidosis than in the malnourished state. These studies thus provide evidence for a decreased renal excretion of acid in patients with protein malnutrition, due largely to a decreased generation of titratable acid which in turn is related to a decreased urinary excretion of phosphate in malnourished patients. The impaired adaptation in ammonia production in the malnourished state may relate to decreased ammonia production due to either decreased substrate delivery or decreased renal gluconeogenesis.