Correspondence

Renal Tubular Acidosis

N Engl J Med 1996; 335:675August 29, 1996

Article

To the Editor:

The Image in Clinical Medicine of Drs. Kwan and Marsh (April 25 issue)1 shows an excellent radiographic example of type 1 (distal) renal tubular acidosis with nephrocalcinosis, but there are some irregularities in the accompanying clinical description. Although the stones passed by this patient were composed mainly of calcium oxalate, most patients with type 1 renal tubular acidosis produce calcium phosphate (brushite) calculi. The patient's plasma bicarbonate concentration was in the low range of normal, so the diagnosis was more likely to be incomplete type 1 renal tubular acidosis.

Despite the absence of systemic acidosis requiring alkalization therapy in such patients, specific medical therapy should be instituted to address intermittent stone passage as well as to prevent worsening of nephrocalcinosis. The most important factor causing calculi formation in patients with type 1 renal tubular acidosis is hypocitraturia, which is due to either a primary defect in citrate transport or intracellular acidosis in the distal tubular cells that prevents citrate excretion into the urine. Citrate is a major inhibitor of stone formation. The pronounced hypocitraturia in type 1 renal tubular acidosis requires therapy with oral citrate preparations at doses of 60 to 90 meq per day. The potassium salt is recommended because serum potassium levels in patients with type 1 renal tubular acidosis, which are already depressed, can drop even further during alkali therapy. The addition of this regimen to a generous fluid intake is more likely to reduce calculi formation than high fluid intake alone.

J. Stuart Wolf, Jr., M.D.
Washington University School of Medicine, St. Louis, MO 63110

1 References