Department of Internal Medicine, Onze Lieve Vrouwe Gasthuis, Amsterdam, The Netherlands.
The pathophysiology of renal tubular acidosis is slowly being unraveled, which has implications for the traditional classification of the condition. Nonetheless, the diagnosis of renal tubular acidosis is still easy to establish, and identification of the specific pathophysiological subtype is relatively straightforward. The diagnostic information required usually includes only urinary pH and sodium, potassium, and chloride concentrations and serum potassium level.
Calcium stone (renal) formation in patients with hyperuricosuria has been ascribed to the urate-induced crystallization of calcium oxalate. Citrate (0.5mM), added to synthetic medium metastably supersaturated with respect to calcium oxalate, was shown to inhibit heterogeneous nucleation of calcium oxalate by monosodium urate (2 mg/mL). Long-term trial with potassium citrate (60 to 80 mEq/day) was therefore undertaken to determine whether induced hypercitraturia would prevent calcium oxalate stone formation in 19 patients with hyperuricosuria.