Lithium-induced impairment of urine acidification.
The purpose of this study was to clarify the means by which lithium induced a disorder of urine acidification. Rats infused with hydrochloric acid (1 mEq/kg) developed acute metabolic acidosis (blood Ph = 7.32; bicarbonate, 18 mEq/liter) with a urine pH of approximately 5.85. The addition of lithium chloride (4 mEq/kg i.p) caused an increase in the urine pH (6.38) and a further decrease in blood bicarbonate (11.0 mEq/liter). During bicarbonate loading, lithium caused the urine PCO2 to fall significantly (urine minus blood PCO2 decreased from 25.3 +/-2.8 To 14.4 +/- 2.3 mm Hg) These changes were not seen following equimolar i.p. administration of sodium chloride. Similarly, lithium  administration depressed bicarbonate reabsorption by 11.1% (from 30.6 to 27.2muEq/ml of GFR) during alkali infusion, while saline caused only a 5% decrease (30.0 to 28.5muEq/ml of GFR). The combination of an increase in urine PCO2 in alkaline urine indicates that lithium produced a defect in distal nephron hydrogen ion secretion. The fall in bicarbonate reabsorption following lithium administration oculd be due to a mild hydrogen ion secretory defect located in the proximal tubule or a severe defect in the distal nephron.
D000137:Acid-Base Imbalance / Q000097:blood / Q000139:chemically induced / Q000652:urine*; D000138:Acidosis / Q000652:urine; D000141:Acidosis, Renal Tubular / Q000652:urine; D000818:Animals; D001639:Bicarbonates / Q000097:blood / Q000378:metabolism / Q000652:urine; D005919:Glomerular Filtration Rate; D006863:Hydrogen-Ion Concentration; D007687:Kidney Tubules, Proximal / Q000187:drug effects / Q000378:metabolism; D008094:Lithium / Q000494:pharmacology*; D008297:Male; D010710:Phosphates / Q000652:urine; D051381:Rats; D012965:Sodium Chloride / Q000494:pharmacology
D001639:Bicarbonates; D010710:Phosphates; D012965:Sodium Chloride; D008094:Lithium