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Hyperchloremic Acidosis Medication

  • Author: Sai-Ching Jim Yeung, MD, PhD, FACP; Chief Editor: Romesh Khardori, MD, PhD, FACP  more...
 
Updated: Aug 04, 2016
 

Medication Summary

The goals of pharmacotherapy are to correct the acidosis, to reduce morbidity, and to prevent complications. Alkalinizing agents, electrolytes, diuretics, mineralocorticoids, and vitamin D supplements can be used against acidosis.

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Alkalinizing Agents

Class Summary

These are used as gastric, systemic, and urinary alkalinizers and have been used in the treatment of acidosis resulting from metabolic and respiratory causes, including diarrhea, kidney disturbances, shock, and diabetic coma.

Sodium bicarbonate

 

Sodium bicarbonate is indicated for the treatment of metabolic acidosis. It increases renal clearance of acidic drugs.

Sodium citrate (Cytra-2, Oracit, Modified Shohl solution)

 

Sodium citrate treats metabolic acidosis and is used as an alkalinizing agent when long-term maintenance of alkaline urine is desirable.

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Electrolytes

Class Summary

Electrolytes are used to correct disturbances in fluid and electrolyte homoeostasis or acid-base balance and to reestablish the osmotic equilibrium of specific ions.

Potassium chloride (Klor-Con, Micro-K, Epiklor)

 

Potassium chloride is essential for the transmission of nerve impulses, the contraction of cardiac muscle, the maintenance of intracellular tonicity, skeletal and smooth muscle function, and the maintenance of normal renal function.

Gradual potassium depletion occurs via renal excretion, through GI loss, or because of low intake. Depletion usually results from diuretic therapy, primary or secondary hyperaldosteronism, diabetic ketoacidosis, severe diarrhea (if associated with vomiting), or inadequate replacement during prolonged parenteral nutrition.

Potassium depletion sufficient to cause a 1-mEq/L decrease in serum potassium requires the loss of approximately 100-200 mEq of potassium from total body stores.

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Diuretics, Loop

Class Summary

Diuretics are used to overcome fluid overload. They increase the distal delivery of sodium by rendering the collecting tubule impermeable to chloride and increase the exchange of sodium for hydrogen and potassium.

Furosemide (Lasix)

 

This agent increases water excretion by interfering with the chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in the ascending loop of Henle and distal renal tubule. The dose must be individualized to patient.

Bumetanide (Bumex, Burinex)

 

Bumetanide increases the excretion of water by interfering with the chloride-binding cotransport system, which, in turn, inhibits sodium, potassium, and chloride reabsorption in the ascending loop of Henle. These effects increase urinary excretion of sodium, chloride, and water, resulting in profound diuresis. Renal vasodilation occurs following administration, renal vascular resistance decreases, and renal blood flow is enhanced. Bumetanide is roughly four times as potent as furosemide on a milligram basis. Depending on the response, administer bumetanide at small dose increments (0.5-5 mg) until desired diuresis occurs.

Torsemide (Demadex)

 

Torsemide acts from within the lumen of the thick ascending portion of the loop of Henle, where it inhibits the sodium, potassium, and chloride carrier system. It increases urinary excretion of sodium, chloride, and water, but does not significantly alter the glomerular filtration rate, renal plasma flow, or acid-base balance. Torsemide is roughly twice as potent as furosemide on a milligram basis. Depending on the response, administer furosemide at small dose increments (10-100 mg) until desired diuresis occurs.

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Mineralocorticoids

Class Summary

Mineralocorticoids may be useful for aldosterone deficiency. Combine mineralocorticoid therapy with sodium loading and diuretics to prevent heart failure.

Fludrocortisone

 

Fludrocortisone promotes increased sodium reabsorption and potassium loss in renal distal tubules.

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Vitamin D Supplements

Class Summary

Vitamin D is a fat-soluble vitamin that promotes the absorption of calcium and phosphorus in the small intestine. It also promotes renal tubule phosphate resorption.

Calcitriol (Calcijex, Rocaltrol)

 

This is the active form of vitamin D. It is used in pRTA as multitherapy with large quantities of alkali and potassium supplementation.

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Contributor Information and Disclosures
Author

Sai-Ching Jim Yeung, MD, PhD, FACP Professor of Medicine, Department of Emergency Medicine, Department of Endocrine Neoplasia and Hormonal Disorders, The University of Texas MD Anderson Cancer Center

Sai-Ching Jim Yeung, MD, PhD, FACP is a member of the following medical societies: American Association for Cancer Research, American College of Physicians, American Medical Association, American Thyroid Association, Endocrine Society

Disclosure: Nothing to disclose.

Coauthor(s)

Mahendra Agraharkar, MD, MBBS, FACP FASN, Clinical Associate Professor of Medicine, Baylor College of Medicine; President and CEO, Space City Associates of Nephrology

Mahendra Agraharkar, MD, MBBS, FACP is a member of the following medical societies: American College of Physicians, American Society of Nephrology, National Kidney Foundation

Disclosure: Received ownership interest/medical directorship from South Shore DaVita Dialysis Center for other; Received ownership/medical directorship from Space City Dialysis /American Renal Associates for same; Received ownership interest from US Renal Care for other.

Nicholas J Sarlis, MD, PhD, FACP Vice President, Head of Medical Affairs, Incyte Corporation

Nicholas J Sarlis, MD, PhD, FACP is a member of the following medical societies: American Association for the Advancement of Science, American Association for Cancer Research, American Association of Clinical Endocrinologists, American College of Physicians, American Federation for Medical Research, American Head and Neck Society, American Medical Association, American Society for Radiation Oncology, American Thyroid Association, Endocrine Society, New York Academy of Sciences, Royal Society of Medicine, Association for Psychological Science, American College of Endocrinology, European Society for Medical Oncology, American Society of Clinical Oncology

Disclosure: Received salary from Incyte Corporation for employment; Received ownership interest from Sanofi-Aventis for previous employment; Received ownership interest/ stock & stock option (incl. rsu) holder from Incyte Corporation for employment.

Mark T Fahlen, MD Private Practice, Mark T Fahlen, MD, Inc

Mark T Fahlen, MD is a member of the following medical societies: American College of Physicians, Renal Physicians Association

Disclosure: Nothing to disclose.

Kanwarpreet Baweja, MD Fellow in Nephrology, University of Texas Health Science Center

Kanwarpreet Baweja, MD is a member of the following medical societies: American Medical Association, American Society of Nephrology, National Kidney Foundation, Medical Council of India

Disclosure: Nothing to disclose.

Chief Editor

Romesh Khardori, MD, PhD, FACP Professor of Endocrinology, Director of Training Program, Division of Endocrinology, Diabetes and Metabolism, Strelitz Diabetes and Endocrine Disorders Institute, Department of Internal Medicine, Eastern Virginia Medical School

Romesh Khardori, MD, PhD, FACP is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Physicians, American Diabetes Association, Endocrine Society

Disclosure: Nothing to disclose.

Acknowledgements

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

Christie P Thomas, MBBS, FRCP, FASN, FAHA Professor, Department of Internal Medicine, Division of Nephrology, Medical Director, Kidney and Kidney/Pancreas Transplant Program, University of Iowa Hospitals and Clinics

Christie P Thomas, MBBS, FRCP, FASN, FAHA is a member of the following medical societies: American College of Physicians, American Federation for Medical Research, American Heart Association, American Society of Nephrology, American Society of Transplantation, American Thoracic Society, International Society of Nephrology, and Royal College of Physicians

Disclosure: Genzyme Grant/research funds Other

References
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  2. Davenport A. Potential adverse effects of replacing high volume hemofiltration exchanges on electrolyte balance and acid-base status using the current commercially available replacement solutions in patients with acute renal failure. Int J Artif Organs. 2008 Jan. 31(1):3-5. [Medline].

  3. Blake-Palmer KG, Karet FE. Cellular physiology of the renal H+ATPase. Curr Opin Nephrol Hypertens. 2009 Jun 24. [Medline].

  4. Basic DT, Hadzi-Djokic J, Ignjatovic I. The history of urinary diversion. Acta Chir Iugosl. 2007. 54(4):9-17. [Medline].

  5. Toyonaga Y, Kikura M. Hyperchloremic acidosis is associated with acute kidney injury after abdominal surgery. Nephrology (Carlton). 2016 Jun 16. [Medline].

  6. Grünfeld JP, Rossier BC. Lithium nephrotoxicity revisited. Nat Rev Nephrol. 2009 May. 5(5):270-6. [Medline].

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