Renal tubular acidosis does not alter circulating values of calcitriol.

In 10 patients with renal tubular acidosis, seven with type I and three with Fanconi syndrome, simultaneous measurements of vitamin D metabolites and electrolytes were made. No marked abnormalities of calcidiol2, calcidiol3, 24,25(OH)2D, or calcitriol were found in these patients, whose mean serum HCO3 was 18 +/- 3 mM/L (SD). Further, no relationship between serum HCO3 and calcitriol could be found. These results suggest that either vitamin D deficiency may be required before any alterations in the production of calcitriol are seen, or that the effects of acidosis in animals may not be reflected in humans. Further, it appears less likely that the bone disease found in renal tubular acidosis is related to abnormalities in vitamin D metabolism resulting from systemic acidosis, but that bone disease is more likely related to the acidosis and hypercalcuria prevalent in this disorder.