Mechanism of lithium-induced hypercalciuria in rats.

Publisher Website
Google Scholar
Abstract
Chronic administration of Li salts is associated with hypercalciuria in the rat. To study renal and extrarenal mechanisms of this phenomenon, balance and clearance techniques were used in rats pair-fed diets with or without Li2CO3 (0.5 meq/day per rat). Li induced hypercalcemia (mean .+-. SE: 5.40 .+-. 0.09 vs. 5.06 .+-. 0.05 meq/l) and hypercalciuria (Ca/creatinine = 0.28 .+-. 0.04 vs. 0.13 .+-. 0.03) only during feeding. When CaCO3 supplement to a Ca-deficient diet was abruptly withdrawn, hypercalciuria was abolished. Polyuria and polydipsia persisted. No significant changes in serum phosphate, urine phosphate, Na, pH or citrate were observed. Chronic parathyroidectomy (PTX) also abolished this effect. During clearance studies, fasting excretion of Ca was similar between treated and control animals. Superimposed acute PTX resulted in comparable changes, hence arguing against primary changes in renal Ca reabsorption or changes in parathyroid hormone effects on the renal tubule. Apparently, Li produces absorptive hypercalciuria by a mechanism dependent on intact parathyroid glands and adequate dietary Ca, but independent of urine Na, phosphate or pH. The active component of gut Ca transport may be involved, possibly via alterations of vitamin D metabolism.