Distal nephron function in patients receiving chronic lithium therapy.
Renal tubular function was studied in 14 patients chronically treated with lithium for affective disorders. Patients were separated into two groups according to the duration of lithium therapy: long-term (35 +/- 7.0 months) and short-term (4.8 +/- 0.8 months). At comparable urine lithium concentrations, patients on long-term therapy had a lower maximal urine osmolality (Umax) and free water reabsorption (TcH2O) than did patients on short-term therapy. The latter group achieved a Umax above 800 mOsm kg H2O. In contrast, both groups of patients failed to increase the urine-blood (U-B) Pco2 gradient normally during acute sodium bicarbonate loading. This low U-B Pco2 was observed at comparable urine bicarbonate concentrations between both groups of patients and controls, and thus was associated with a higher urine pH in patients. These findings indicate that the inability of these patients to achieve a normal U-B Pco2 in a maximally alkaline urine was the result of decreased distal hydrogen ion secretion rather than inability to raise urine bicarbonate concentrations as a result of a concentrating defect. Bicarbonate reabsorptive capacity was normal in our lithium-treated subjects. Both groups of patients achieved a normal U-B Pco2 gradient in response to sodium phosphate loading. They also were able to achieve a minimal urine pH and a maximal acid excretion similar to those of controls in response to a 3-day ammonium chloride loading test. Our data demonstrate that chronic lithium therapy is associated with a mild distal acidification defect disclosed only by the finding of a low U-B Pco2 gradient during sodium bicarbonate loading. This peculiar defect can be found in short-term lithium-treated patients in whom the concentrating capacity is relatively well preserved.
D000643:Ammonium Chloride / Q000494:pharmacology; D001639:Bicarbonates / Q000494:pharmacology / Q000652:urine; D002245:Carbon Dioxide / Q000652:urine; D005919:Glomerular Filtration Rate; D006801:Humans; D006863:Hydrogen-Ion Concentration; D007684:Kidney Tubules / Q000502:physiology*; D007686:Kidney Tubules, Distal / Q000502:physiology*; D008094:Lithium / Q000494:pharmacology* / Q000627:therapeutic use*; D009994:Osmolar Concentration; D017693:Sodium Bicarbonate; D014867:Water / Q000502:physiology; D014868:Water Deprivation
D001639:Bicarbonates; D000643:Ammonium Chloride; D014867:Water; D002245:Carbon Dioxide; D017693:Sodium Bicarbonate; D008094:Lithium