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Hyperchloremic Acidosis Clinical Presentation

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

History

Metabolic acidosis, per se, has no specific symptoms and signs, unless it is extremely severe or of acute onset; however, it can produce symptoms and signs from changes in pulmonary, cardiovascular, neurologic, and musculoskeletal function.

General

If the acidosis is marked and/or of acute onset, the patient may report headache, lack of energy, nausea, and vomiting.

Neurologic

Neurologic abnormalities such as mental confusion progressing to stupor, when observed, are not usually secondary to the acidosis but are the cause of the acidosis itself.

In general, neurologic abnormalities are less common in persons with metabolic acidosis than in persons with respiratory acidosis.

Pulmonary

An increase in minute ventilation of up to 4- to- 8-fold may occur in persons with respiratory compensation.

Persistent tachypnea or hyperpnea (affecting the depth more than the rate of ventilation) may be the only clinical clue to an underlying acidotic state. This type of tachypnea/hyperpnea characteristically persists in sleep or interferes with sleep.

Cardiovascular

Effects on the cardiovascular system include direct impairment of myocardial contraction (especially at a pH < 7.2), tachycardia, and increased risk of ventricular fibrillation or heart failure with pulmonary edema. Patients may report dyspnea upon exertion or, in severe cases, at rest.

In advanced stages, overt cardiovascular collapse may occur from impaired catecholamine release.

Musculoskeletal

Chronic acidemia, as is observed in RTA, can lead to a variety of skeletal problems. This is probably due in part to the release of calcium and phosphate during bone buffering of the excess protons. Decreased tubular absorption of calcium secondary to acidemia, especially in dRTA, leads to a negative calcium balance.

Clinical consequences include osteomalacia (leading to impaired growth in children), osteitis fibrosa (from secondary hyperparathyroidism), rickets (in children), and osteomalacia or osteopenia (in adults).

Genitourinary

An important complication of chronic renal tubular acidosis (mainly distal, type I) is nephrocalcinosis and urolithiasis. A number of pathophysiological alterations contribute to stone formation:

  • Buffering of the chronic acid load by the bone, causing bone dissolution and promoting hypercalciuria
  • Diminution of renal tubular calcium reabsorption, further aggravating the hypercalciuria
  • Hypocitraturia because of avid citrate reabsorption by the PCT
  • High urinary pH, causing insolubility of calcium phosphate and promoting its precipitation

In contrast, stone disease is rare with type II RTA because of the difference in its pathogenesis. Since the fall in plasma HCO3- is nonprogressive, after the renal HCO3 threshold is reached (transport maximum not exceeded), there is complete absorption of luminal HCO3. At this point, the urine pH is acid, since urine is devoid of HCO3- and there is no defect in distal proton secretion. The daily acid load is thus excreted by the collecting duct, obviating the need for bone buffering. Also, citrate usually escapes proximal reabsorption (along with other solutes) and promotes calcium phosphate solubility.

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Physical Examination

Pulmonary

An increase in minute ventilation of up to 4- to- 8-fold may occur in persons with respiratory compensation.

Tachypnea or hyperpnea (affecting the depth more than the rate of ventilation) may be the only clinical clue to an underlying acidotic state.

Musculoskeletal

Chronic acidemia, as is observed in RTA, can lead to a variety of skeletal problems. This is probably due in part to the release of calcium and phosphate during bone buffering of the excess protons. Decreased tubular absorption of calcium secondary to acidemia, especially in dRTA, leads to a negative calcium balance.

Clinical consequences include osteomalacia (leading to impaired growth in children), osteitis fibrosa (from secondary hyperparathyroidism), rickets (in children), and osteomalacia or osteopenia (in adults).

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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
  1. Liborio AB, Daher EF, de Castro MC. Characterization of acid-base status in maintenance hemodialysis: physicochemical approach. J Artif Organs. 2008. 11(3):156-9. [Medline].

  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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