Renal Excretion of Ammonium in Renal Tubular Acidosis

Abstract

In 10 patients with distal renal tubular acidosis (distal RTA), 8 with multiple tubular dysfunction, and 15 with primary hyperparathyroidism including 8 of skeletal syndrome, the rates of ammonium excretion without the influence of any medications were determined in respective specimens of 24-hour urine. In the majority of the patients with either distal RTA, multiple tubular dysfunction, or skeletal syndrome of primary hyperparathyroidism, the rates of ammonium excretion corrected for creatinine clearance were significantly higher than conceivable in reference to the urinary pH levels. The rates of increase in ammonium excretion tended to be higher in the cases with than in those without metabolic acidosis and/or hypokalemia. Metabolic acidosis attributable to RTA was observed in all cases with skeletal syndrome but in none without this syndrome among the patients with primary hyperparathyroidism. It is concluded that in the patients with RTA, proximal and distal alike, urinary excretion of ammonium is generally increased. This may well be attributed to the increased renal ammonium production in response to acidosis and/or potassium deficiency. The greater secretion of parathyroid hormone in cases with skeletal syndrome than in cases with other syndromes of primary hyperparathyroidism is regarded accounting for the higher incidence of RTA in the former than in the latter.ammonium excretion; renal tubular acidosis; hyperparathyroidism