Abstract
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 (U(max)) and free water reabsorption (T(c)H2O) than did patients on short-term therapy. The latter group achieved a U(max) 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 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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 477-485 |
| Number of pages | 9 |
| Journal | Unknown Journal |
| Volume | 21 |
| Issue number | 3 |
| DOIs | |
| State | Published - Jan 1 1982 |
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ASJC Scopus subject areas
- Nephrology
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Distal nephron function in patients receiving chronic lithium therapy. / Batlle, D.; Gaviria, M.; Grupp, M.; Arruda, J. A.; Wynn, J.; Kurtzman, N. A.
In: Unknown Journal, Vol. 21, No. 3, 01.01.1982, p. 477-485.Research output: Contribution to journal › Article
TY - JOUR
T1 - Distal nephron function in patients receiving chronic lithium therapy
AU - Batlle, D.
AU - Gaviria, M.
AU - Grupp, M.
AU - Arruda, J. A.
AU - Wynn, J.
AU - Kurtzman, N. A.
PY - 1982/1/1
Y1 - 1982/1/1
N2 - 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 (U(max)) and free water reabsorption (T(c)H2O) than did patients on short-term therapy. The latter group achieved a U(max) 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 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.
AB - 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 (U(max)) and free water reabsorption (T(c)H2O) than did patients on short-term therapy. The latter group achieved a U(max) 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 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.
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U2 - 10.1038/ki.1982.49
DO - 10.1038/ki.1982.49
M3 - Article
C2 - 6283233
AN - SCOPUS:0020085759
VL - 21
SP - 477
EP - 485
JO - Free Radical Biology and Medicine
JF - Free Radical Biology and Medicine
SN - 0891-5849
IS - 3
ER -