lithium-chloride and maleic-acid

Lithium, administered to patients of bipolar disorders, is mainly excreted into urine, and tubular reabsorption at the proximal tubule is involved in the renal handling of lithium. In this study, we examined the renal excretion of lithium in rats with Fanconi syndrome, characterized by defects of transports of various compounds at the proximal tubules, induced by maleic acid. After maleic acid was intravenously injected, mannitol and lithium chloride were infused in turn. Using samples of plasma and bladder urine during the mannitol infusion, renal parameters were determined. Pharmacokinetic parameters of lithium were obtained using samples during the lithium chloride infusion. Maleic acid decreased creatinine clearance and increased the fractional excretion of glucose and phosphate, suggesting the induction of Fanconi syndrome. In rats with Fanconi syndrome, plasma concentration of lithium was increased, and its renal clearance was decreased. No effect on the fractional excretion of lithium was exhibited. This study represents that the tubular reabsorption of lithium was impaired to the same degree with glomerular filtration in rats with experimental Fanconi syndrome and that the dysfunction of the tubular reabsorption of glucose and phosphate was more severe. It is possible that Fanconi syndrome inhibited the reabsorption of lithium at the proximal tubule and facilitated the reabsorption of lithium from the loop of Henle to the collecting duct.

Topics: Animals; Antimanic Agents; Creatinine; Disease Models, Animal; Fanconi Syndrome; Glucose; Injections, Intravenous; Kidney Tubules, Proximal; Lithium Chloride; Male; Maleates; Phosphates; Rats; Rats, Wistar

A state of renal tubular acidosis has been produced in rats by the administration of sodium maleate or acetazolamide (proximal tubular acidosis) and of lithium chloride of amiloride (distal tubular acidosis). During progressive alkaline diuresis, delta PCO2 (urine minus blood PCO2) increases significantly in rats presenting proximal tubular acidosis. Delta PCO2 is significantly depressed in rats presenting distal tubular acidosis. In well defined conditions of bicarbonate or phosphate excretion, delta PCO2 is a valuable index of distal ion secretion.

Topics: Acetazolamide; Acidosis, Renal Tubular; Amiloride; Animals; Carbon Dioxide; Chlorides; Disease Models, Animal; Lithium; Lithium Chloride; Maleates; Partial Pressure; Rats