URINARY CITRATE, BONE-RESORPTION AND INTESTINAL ALKALI ABSORPTION IN STONE FORMERS WITH FASTING HYPERCALCIURIA

Reduced citrate in urine and increased fasting excretion of calcium ar e abnormalities frequently reported in stone forming (SF) patients. In creased dietary acid (or reduced alkali) introduction or absorption ma y be a potential cause of both these pathological findings. To test th is hypothesis, we studied 64 SF patients {32 with fasting hypercalciur ia (FH) and 32 without FH (NFH)}. After a basal evaluation for nephrol ithiasis, while on a 500 mg calcium diet, they were evaluated for: (1) daily intestinal alkali absorption (IAA), by urinary electrolyte excr etion; (2) basal concentrations of PTH, calcitonin (CT) and 1,25(OH)2- VitD; (3) oral calcium load for evaluation of changes in calcium and h ydroxyproline urinary excretions;' (4) intestinal calcium absorption ( 18 patients), with double curve analysis (stable Sr as tracer); and (5 ) changes in citrate excretion after an alkali load (50 mEq of a mixtu re of calcium gluconate, lactate and carbonate) in 10 patients. The re sults demonstrated: (1) FH stone formers had reduced citrate excretion and lower mean IAA levels than NFH stone formers; (2) FH stone former s also had higher bone resorption levels with lower PTH and higher CT levels; (3) IAA levels were related to both citrate excretion and bone turnover indices; and (4) the increases in citrate excretion after or al alkali load were strictly related to basal IAA values (index of alk ali absorption and/or generation after oral load), demonstrating that a different absorptive capacity of alkali rather than a different diet ary content may underlie these metabolic abnormalities.