Lithium Nephropathy Medication

  • Author: Eleanor Lederer, MD; Chief Editor: Vecihi Batuman, MD, FACP, FASN   more...
 
Updated: Jan 12, 2012
 

Medication Summary

Diuretics and NSAIDs are used in the treatment of stable lithium-induced nephrogenic diabetes insipidus.[23]

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Diuretics

Class Summary

Decrease extracellular fluid and promote proximal tubular resorption that is not ADH dependent. Ultimately, less free water is transmitted to distal collecting tubules, which is where the urine-concentrating defect is located; therefore, the polyuria decreases. However, extracellular fluid depletion can also increase the risk of lithium intoxication by enhancing lithium reabsorption at the proximal tubule. Diuretics have a gradual onset of action and are less useful in an acute setting.

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Amiloride (Midamor)

 

Prevents uptake of lithium by epithelial cells. Has less potential for lithium toxicity because has a weak natriuretic effect and is less likely to increase lithium level by causing volume contraction. Has the advantage of being potassium-sparing; hypokalemia itself may potentiate a defect in concentrating ability. Also induces less extracellular fluid contraction than thiazides.

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Hydrochlorothiazide (Esidrix)

 

Thiazides may require potassium supplementation; more often associated with lithium toxicity. Inhibits reabsorption of sodium in distal tubules, causing increased excretion of sodium and water as well as potassium and hydrogen ions. Equivalent dosages of other thiazide preparations may be used. Use same dose range effective for treating hypertension.

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Nonsteroidal Anti-inflammatory Drugs

Class Summary

Have an antiprostaglandin effect in rats. Inhibiting prostaglandin increases cAMP in the collecting tubules, which promotes water resorption (see Pathophysiology). NSAIDs also inhibit the production of prostaglandin that regulates glomerular blood flow and therefore decreases the GFR and urine flow to the distal tubules. Physicians do not recommend long-term NSAID therapy.

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Indomethacin (Indocin, Indochron ER)

 

Rapidly absorbed; metabolism occurs in liver by demethylation, deacetylation, and glucuronide conjugation. Inhibits prostaglandin synthesis. One case report exists of IV ketorolac used in acutely ill patient failing to respond to indomethacin.

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Contributor Information and Disclosures
Author

Eleanor Lederer, MD  Professor of Medicine, Chief, Nephrology Division, Director, Nephrology Training Program, Director, Metabolic Stone Clinic, Kidney Disease Program, University of Louisville School of Medicine; Consulting Staff, Louisville Veterans Affairs Hospital

Eleanor Lederer, MD is a member of the following medical societies: American Association for the Advancement of Science, American Federation for Medical Research, American Society for Biochemistry and Molecular Biology, American Society for Bone and Mineral Research, American Society of Nephrology, American Society of Transplantation, International Society of Nephrology, Kentucky Medical Association, National Kidney Foundation, and Phi Beta Kappa

Disclosure: Dept of Veterans Affairs Grant/research funds Research

Coauthor(s)

Clifford C Dacso, MD, MPH, MBA  John S Dunn Sr Research Chair, The Methodist Hospital Research Institute; Distinguished Research Professor, University of Houston

Clifford C Dacso, MD, MPH, MBA is a member of the following medical societies: American College of Physicians, American Medical Association, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Mark DT Tran, MD  Staff Physician, Department of Internal Medicine, Baylor College of Medicine

Mark DT Tran, MD is a member of the following medical societies: American Academy of Family Physicians

Disclosure: Nothing to disclose.

Specialty Editor Board

Anil Kumar Mandal, MD  Clinical Professor, Department of Internal Medicine, Division of Nephrology, University of Florida School of Medicine

Anil Kumar Mandal, MD is a member of the following medical societies: American College of Clinical Pharmacology, American College of Physicians, American Society of Nephrology, and Central Society for Clinical Research

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

George R Aronoff, MD  Director, Professor, Departments of Internal Medicine and Pharmacology, Section of Nephrology, Kidney Disease Program, University of Louisville School of Medicine

George R Aronoff, MD is a member of the following medical societies: American Federation for Medical Research, American Society of Nephrology, Kentucky Medical Association, and National Kidney Foundation

Disclosure: Nothing to disclose.

Rebecca J Schmidt, DO, FACP, FASN  Professor of Medicine, Section Chief, Department of Medicine, Section of Nephrology, West Virginia University School of Medicine

Rebecca J Schmidt, DO, FACP, FASN is a member of the following medical societies: American College of Physicians, American Medical Association, American Society of Nephrology, International Society of Nephrology, National Kidney Foundation, Renal Physicians Association, and West Virginia State Medical Association

Disclosure: Renal Ventures Ownership interest Other

Chief Editor

Vecihi Batuman, MD, FACP, FASN  Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Medicine Service, Southeast Louisiana Veterans Health Care System

Vecihi Batuman, MD, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, and International Society of Nephrology

Disclosure: Nothing to disclose.

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