Renal tubular acidosis causes: Difference between revisions

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|Type 4
|Type 4
|
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* Congenital hypoaldosteronism (21-hydroxylase deficiency and isolated hypoaldosteronism)
* [[Congenital adrenal hyperplasia|Congenital hypoaldosteronism]]
* Pseudohypoaldosteronism type 2 (Gordon's syndrome)
** [[21-hydroxylase deficiency]]
* Primary adrenal insufficiency
** [[Isolated hypoaldosteronism]]
* Pseudohypoaldosteronism type 1
* [[Pseudohypoaldosteronism|Pseudohypoaldosteronism type 2]]
* [[Primary adrenal insufficiency]]
* [[Pseudohypoaldosteronism|Pseudohypoaldosteronism type 1]]
|
|
* Angiotensin inhibitors, such as ACE inhibitors, angiotensin II receptor blockers, and direct renin inhibitors
* Angiotensin inhibitors, such as
* Antibiotics, trimethoprim, and pentamidine
** [[ACE inhibitor|ACE inhibitors]]
* Potassium-sparing diuretics, such as spironolactone, eplerenone, amiloride, and triamterene
** [[Angiotensin II receptor antagonist|Angiotensin II receptor blockers]]
** Direct renin inhibitors
* [[Antibiotics]], [[trimethoprim]], and [[pentamidine]]
* Potassium-sparing diuretics
** [[Spironolactone]]
** [[Eplerenone]]
** [[Amiloride]]
** [[Triamterene]]
|}
|}


==References==
==References==
{{reflist|2}}
{{reflist|2}}

Revision as of 17:30, 14 May 2018

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Ovevriew

Causes

Primary Causes Secondary Causes
Type 1
  • Idiopathic
  • Familial
    • Autosomal dominant
      • Mainly due to mutations causing defects in the kidney anion exchanger [kAE1] in distal tubule intercalated cells.
  • Autosomal recessive
    • Mainly due to mutations causing defects in V-ATPase in distal tubule intercalated cells.
Type 2
Type 4

References