ArticlePhysiological reports2014
Effects of chronic lithium administration on renal acid excretion in humans and rats.
Article in Physiological reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 24 citations in OpenAlex.
- Lithium-induced hypokalemic periodic paralysis: A rare and life-threatening complication in bipolar disorder management.Indian journal of psychiatry · 2026Article
- Assessment of the biological efficacy of gold Nannochloropsis oculata nano-extract against lithium-induced toxicity in rats.Scientific reports · 2026Article
- Carbamazepine-induced Hyperammonemia and Asterixis in Young Adults.Indian journal of psychological medicine · 2025Article
- New Advances in the Pharmacology and Toxicology of Lithium: A Neurobiologically Oriented Overview.Pharmacological reviews · 2024Review
- Lithium-induced apoptotic cell death is not accompanied by a noticeable inflammatory response in the kidney.Frontiers in physiology · 2024Article
- Mechanistic insights into the primary and secondary alterations of renal ion and water transport in the distal nephron.Journal of internal medicine · 2023Review
- Regulation of Rhcg, an ammonia transporter, by aldosterone in the kidney.The Journal of endocrinology · 2021Article
- Identification ofJournal of the American Society of Nephrology : JASN · 2019Article
- Thyroid dysfunction and kidney disease: An update.Reviews in endocrine & metabolic disorders · 2017Review
- Recent advances in understanding renal ammonia metabolism and transport.Current opinion in nephrology and hypertension · 2016Review
- NBCe1 expression is required for normal renal ammonia metabolism.American journal of physiology. Renal physiology · 2015Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
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, lithium-treated 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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.