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Title: Hypoaldosteronism  
Author: World Heritage Encyclopedia
Language: English
Subject: Renal tubular acidosis, Hyperaldosteronism, Aldosterone, Trans-tubular potassium gradient, List of MeSH codes (C19)
Publisher: World Heritage Encyclopedia


Classification and external resources
Specialty Endocrinology
ICD-10 E27.4
DiseasesDB 20960
MeSH D006994

In medicine (endocrinology), hypoaldosteronism refers to decreased levels of the hormone aldosterone.

Isolated hypoaldosteronism is the condition of having lowered aldosterone without corresponding changes in cortisol.[1] (The two hormones are both produced by the adrenals.)


  • Causes 1
  • Treatment 2
  • Effects 3
  • See also 4
  • References 5


There are several causes for this condition, including primary adrenal insufficiency, congenital adrenal hyperplasia, and medications (certain diuretics, NSAIDs, and ACE inhibitors).

  1. Primary adrenal insufficiency
  2. Congenital adrenal hyperplasia (21 and 11β but not 17)
  3. Aldosterone synthase deficiency
  • Hyporeninemic hypoaldosteronism (due to decreased angiotensin 2 production as well as intra-adrenal dysfunction)[2]
  1. Renal dysfunction-most commonly diabetic nephropathy
  2. ACE inhibitors
  3. NSAIDs
  4. Cyclosporine



This condition may result in hyperkalemia, when it is sometimes termed 'type 4 renal tubular acidosis' even though it doesn't actually cause acidosis. It can also cause urinary sodium wasting, leading to volume depletion and hypotension.

Na+ is lost in the urine. K+ is retained, and the plasma K+ rises.

When adrenal insufficiency develops rapidly, the amount of Na+ lost from the extracellular fluid exceeds the amount excreted in the urine, indicating that Na+ also must be entering cells. When the posterior pituitary is intact, salt loss exceeds water loss, and the plasma Na+ falls. However, the plasma volume also is reduced, resulting in hypotension, circulatory insufficiency, and, eventually, fatal shock. These changes can be prevented to a degree by increasing the dietary NaCl intake. Rats survive indefinitely on extra salt alone, but in dogs and most humans, the amount of supplementary salt needed is so large that it is almost impossible to prevent eventual collapse and death unless mineralocorticoid treatment is also instituted.

See also


  1. ^ Becker, Kenneth L. (2001). Principles and practice of endocrinology and metabolism. Lippincott Williams & Wilkins. pp. 785–.  
  2. ^ a b DeFronzo RA (1980). "Hyperkalemia and hyporeninemic hypoaldosteronism". Kidney Int. 17 (1): 118–34.  
  3. ^ Sebastian A, Schambelan M, Sutton JM (1984). "Amelioration of hyperchloremic acidosis with furosemide therapy in patients with chronic renal insufficiency and type 4 renal tubular acidosis". Am. J. Nephrol. 4 (5): 287–300.  
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