Effects of chronic lithium administration on renal acid excretion in humans and rats

Weiner, I. David, Leader, John P., Bedford, Jennifer J., Verlander, Jill W., Ellis, Gaye, Kalita, Priyakshi, Vos, Frederiek, de Jong, Sylvia and Walker, Robert J. (2014) Effects of chronic lithium administration on renal acid excretion in humans and rats. Physiological Reserach, 2 12: e12242.1-e12242.15. doi:10.14814/phy2.12242

Author Weiner, I. David
Leader, John P.
Bedford, Jennifer J.
Verlander, Jill W.
Ellis, Gaye
Kalita, Priyakshi
Vos, Frederiek
de Jong, Sylvia
Walker, Robert J.
Title Effects of chronic lithium administration on renal acid excretion in humans and rats
Journal name Physiological Reserach   Check publisher's open access policy
ISSN 2051-817X
Publication date 2014-12-11
Sub-type Article (original research)
DOI 10.14814/phy2.12242
Open Access Status DOI
Volume 2
Issue 12
Start page e12242.1
End page e12242.15
Total pages 15
Place of publication Oxford, United Kingdom
Publisher John Wiley & Sons
Language eng
Formatted abstract
Lithium therapy’s most common side effects affecting the kidney are nephrogenic diabetes insipidus (NDI) and chronic kidney disease. Lithium may also induce a distal renal tubular acidosis. This study investigated the effect of chronic lithium exposure on renal acid–base homeostasis, with emphasis on ammonia and citrate excretion. We compared 11 individuals on long-term lithium therapy with six healthy individuals. Under basal conditions, lithiumtreated individuals excreted significantly more urinary ammonia than did control subjects. Following an acute acid load, urinary ammonia excretion increased approximately twofold above basal rates in both lithium-treated and control humans. There were no significant differences between lithium treated and control subjects in urinary pH or urinary citrate excretion. To elucidate possible mechanisms, rats were randomized to diets containing lithium or regular diet for 6 months. Similar to humans, basal ammonia excretion was significantly higher in lithium-treated rats; in addition, urinary citrate excretion was also significantly greater. There were no differences in urinary pH. Expression of the critical ammonia transporter, Rhesus C Glycoprotein (Rhcg), was substantially greater in lithium-treated rats than in control rats. We conclude that chronic lithium exposure increases renal ammonia excretion through mechanisms independent of urinary pH and likely to involve increased collecting duct ammonia secretion via the ammonia transporter, Rhcg.
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collection: UQ Centre for Clinical Research Publications
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Created: Tue, 03 Nov 2015, 00:03:16 EST by Priyakshi Kalita-de Croft on behalf of UQ Centre for Clinical Research