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Pathophysiology of primary distal renal tubular acidosis.

Functional indices of distal acidification were assessed in five unrelated children with primary distal renal tubular acidosis. All patients were unable to lower urinary pH below 6.0 both during ammonium chloride-induced acidosis or after acute i.v. administration of furosemide. In these patients the urine minus blood Pco2 gradient failed to increase normally during acute sodium bicarbonate loading (mean +/- SEM: 5.8 +/- 2.0 mmHg), or after neutral phosphate administration (13 +/- 2.7 mmHg), despite adequate urinary concentrations or bicarbonate (72.2 +/- 14.6 mmol/L) and phosphate (25 +/- 2.3 mmol/L), respectively. They also failed to decrease urine pH below 5.5 with sodium sulfate (7.17 +/- 0.08), but urinary potassium excretion increased significantly. These results strongly suggest that the mechanism responsible for defective distal acidification is a failure of hydrogen ion secretion ("secretory' defect) and not an inability to establish a steep hydrogen ion gradient, as it was formerly believed.

Acidosis, Renal Tubular↗
PubMed1985

Hypokalemic periodic paralysis secondary to renal tubular acidosis.

A 62-year-old woman with distal renal tubular acidosis (RTA) and hypokalemic muscle paralysis is described. As neither the history nor the clinical examination can differentiate between hypokalemic paralysis caused by RTA and that of familial hypokalemic paralysis, and because the emergency as well as prophylactic treatment of the two disorders are quite different, a simple differential diagnostic workup is emphasized.

Acidosis↗