Hyporeninemic Hypoaldosteronism Clinical Presentation

  • Author: James H Sondheimer, MD, FACP; Chief Editor: Vecihi Batuman, MD, FACP, FASN   more...
 
Updated: May 10, 2012
 

History

Renal tubular acidosis (RTA) type IV generally is asymptomatic unless severe hyperkalemia leads to muscle weakness or life-threatening arrhythmia (see Hyperkalemia).[4] Acidosis usually is mild and asymptomatic. The condition is usually discovered during routine laboratory evaluations.

Because several commonly used drugs may unmask RTA type IV, hyperkalemia commonly is discovered during follow-up testing of a patient started on one of those agents. These drugs include medications affecting the renin-angiotensin-aldosterone axis (see Causes). Hyperkalemia with moderate doses of such agents may suggest a forme fruste of RTA type IV.

If the patient is newly discovered to have hyperkalemia and mild-to-moderate renal failure, focus the history on the causes of renal disease. In particular, consider long-term analgesic use, exposure to lead (industrial or from moonshine liquor), and obstructive symptoms. Other illnesses (eg, diabetes, sickle cell anemia, and systemic lupus erythematosus [SLE]) would likely have become apparent earlier.

Other important historical data consist of dietary intake (including pica, fad diets, and use of salt substitutes) and current use of medications (ie, over-the-counter [OTC] and prescription drugs).

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Physical Examination

The underlying renal disease and any associated illnesses (eg, SLE or sickle cell disease) dominate the physical findings. Except for arrhythmia and muscle weakness in severe cases, hyperkalemia produces no physical signs.

Mild acidosis may be present, but associated physical signs (eg, Kussmaul respiration) usually are absent. However, some cases of symptomatic acidosis with dyspnea have been described. Patients demonstrate no signs of adrenal insufficiency, because glucocorticoid excretion is intact by definition. Patients usually are hypertensive, in association with their underlying renal disease. Assessment of patient volume status is important because therapy commonly includes the use of diuretics.

Adrenal insufficiency is part of the differential diagnosis and manifests with findings (such as fever, orthostatic changes, hyperpigmentation, and signs of illnesses [eg, SLE]) that, when resulting in treatment with long-term corticosteroids, can lead to secondary hypoadrenalism.

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Contributor Information and Disclosures
Author

James H Sondheimer, MD, FACP  Associate Professor of Medicine, Wayne State University School of Medicine; Medical Director of Hemodialysis, Harper University Hospital at Detroit Medical Center; Medical Director, DaVita Greenview Dialysis (Southfield)

James H Sondheimer, MD, FACP is a member of the following medical societies: American College of Physicians and American Society of Nephrology

Disclosure: Nothing to disclose.

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.

Additional Contributors

The author would like to thank Dr Jaideep Hingorani for his many helpful comments and suggestions.

Additional Contributors

Donald A Feinfeld, MD, FACP, FASN Consulting Staff, Division of Nephrology & Hypertension, Beth Israel Medical Center

Donald A Feinfeld, MD, FACP, FASN is a member of the following medical societies: American Academy of Clinical Toxicology, American Society of Hypertension, American Society of Nephrology, and National Kidney Foundation

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

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 Heart Association, American Society of Nephrology, and Royal College of Physicians

Disclosure: Nothing to disclose.

References
  1. Hoskote SS, Joshi SR, Ghosh AK. Disorders of potassium homeostasis: pathophysiology and management. J Assoc Physicians India. Sep 2008;56:685-93. [Medline].

  2. Karet FE. Mechanisms in hyperkalemic renal tubular acidosis. J Am Soc Nephrol. Feb 2009;20(2):251-4. [Medline].

  3. Schambelan M, Sebastian A, Biglieri EG. Prevalence, pathogenesis, and functional significance of aldosterone deficiency in hyperkalemic patients with chronic renal insufficiency. Kidney Int. Jan 1980;17(1):89-101. [Medline].

  4. Lehnhardt A, Kemper MJ. Pathogenesis, diagnosis and management of hyperkalemia. Pediatr Nephrol. Mar 2011;26(3):377-84. [Medline]. [Full Text].

  5. Düsing R, Sellers F. ACE inhibitors, angiotensin receptor blockers and direct renin inhibitors in combination: a review of their role after the ONTARGET trial. Curr Med Res Opin. Sep 2009;25(9):2287-301. [Medline].

  6. Estacio RO. Renin-angiotensin-aldosterone system blockade in diabetes: role of direct renin inhibitors. Postgrad Med. May 2009;121(3):33-44. [Medline]. [Full Text].

  7. Doulton TW, Macgregor GA. Combination renin-angiotensin system blockade with the renin inhibitor aliskiren in hypertension. J Renin Angiotensin Aldosterone Syst. Jul 17 2009;[Medline].

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