Renal tubular acidosis causes: Difference between revisions
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__NOTOC__ | __NOTOC__ | ||
{{Renal tubular acidosis}} | {{Renal tubular acidosis}} | ||
{{CMG}} ; {{AE}} {{ADG}} | |||
{{CMG}} ; {{AE}} {{ADG}} {{JSS}} {{SAH}} | |||
==Ovevriew== | ==Ovevriew== | ||
Primary causes of renal tubular acidosis include genetic [[mutations]] causing defects in the kidney [[anion]] exchanger [kAE1] in [[Distal convoluted tubule|distal]] tubule intercalated cells and [[congenital adrenal hyperplasia]]. Secondary causes include medications and [[Autoimmune disease|autoimmune]] diseases. | |||
==Causes== | ==Causes== | ||
The following table summarizes the common primary and secondary causes of [[renal tubular acidosis]].<ref name="pmid23235953">{{cite journal |vauthors=Haque SK, Ariceta G, Batlle D |title=Proximal renal tubular acidosis: a not so rare disorder of multiple etiologies |journal=Nephrol. Dial. Transplant. |volume=27 |issue=12 |pages=4273–87 |date=December 2012 |pmid=23235953 |pmc=3616759 |doi=10.1093/ndt/gfs493 |url=}}</ref><ref name="pmid23114896">{{cite journal |vauthors=Batlle D, Haque SK |title=Genetic causes and mechanisms of distal renal tubular acidosis |journal=Nephrol. Dial. Transplant. |volume=27 |issue=10 |pages=3691–704 |date=October 2012 |pmid=23114896 |doi=10.1093/ndt/gfs442 |url=}}</ref><ref name="pmid21170890">{{cite journal |vauthors=Alper SL |title=Familial renal tubular acidosis |journal=J. Nephrol. |volume=23 Suppl 16 |issue= |pages=S57–76 |date=2010 |pmid=21170890 |doi= |url=}}</ref> | |||
{| class="wikitable" | {| class="wikitable" | ||
! | ! | ||
!Primary Causes | !Primary Causes | ||
!Secondary Causes | !Secondary Causes | ||
|- | |- | ||
|Type 1 | |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. | |||
| | | | ||
* [[Autoimmune disorders]] | |||
* Medications | |||
** [[Ifosfamide]] | |||
** [[Amphotericin B]] | |||
** [[Lithium carbonate]] | |||
** [[Ibuprofen]] | |||
* [[Hypercalciuric]] conditions | |||
** [[Hyperparathyroidism]] | |||
** [[Vitamin D -- adverse effects|Vitamin D intoxication]] | |||
** [[Sarcoidosis]] | |||
** [[Idiopathic hypercalciuria]] | |||
* Others | |||
|- | |- | ||
|Type 2 | |||
| | | | ||
* [[Recessive]] | |||
** Proximal tubule cell sodium bicarbonate co-transporter (NBCe1) defect | |||
** Carbonic anhydrase type 2 deficiency | |||
* [[Cystinosis]] | |||
* [[Tyrosinemia]] | |||
* Hereditary fructose intolerance | |||
* [[Galactosemia]] | |||
* [[Glycogen storage disease type I|Glycogen storage disease]] (type I) | |||
* [[Lowe syndrome]] | |||
| | | | ||
| | * M-protein disorders | ||
| | ** [[Amyloidosis]] | ||
** [[Multiple myeloma]] | |||
* Medications | |||
** [[Ifosfamide]] | |||
** [[Tenofovir]] | |||
** [[Acetazolamide]] | |||
** [[Topiramate]] | |||
** [[Aminoglycosides]] | |||
* Heavy metals | |||
** [[Lead]] | |||
** [[Cadmium]] | |||
** [[Mercury]] | |||
** [[Copper]] | |||
* Other | |||
** [[Medullary sponge kidney]] | |||
** [[Obstructive uropathy]] | |||
** [[Kidney transplantation|Renal transplant rejection]] | |||
** [[Wilson's disease|Wilson disease]] | |||
|- | |- | ||
|Type 4 | |||
| | | | ||
* [[Congenital adrenal hyperplasia|Congenital hypoaldosteronism]] | |||
** [[21-hydroxylase deficiency]] | |||
** [[Isolated hypoaldosteronism]] | |||
* [[Pseudohypoaldosteronism|Pseudohypoaldosteronism type 2]] | |||
* [[Primary adrenal insufficiency]] | |||
* [[Pseudohypoaldosteronism|Pseudohypoaldosteronism type 1]] | |||
| | | | ||
| | * Angiotensin inhibitors, such as | ||
| | ** [[ACE inhibitor|ACE inhibitors]] | ||
** [[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}} | ||
Latest revision as of 13:35, 1 August 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] Jogeet Singh Sekhon, M.D. [3] Syed Ahsan Hussain, M.D.[4]
Ovevriew
Primary causes of renal tubular acidosis include genetic mutations causing defects in the kidney anion exchanger [kAE1] in distal tubule intercalated cells and congenital adrenal hyperplasia. Secondary causes include medications and autoimmune diseases.
Causes
The following table summarizes the common primary and secondary causes of renal tubular acidosis.[1][2][3]
| Primary Causes | Secondary Causes | |
|---|---|---|
| Type 1 | ||
| Type 2 |
|
|
| Type 4 |
|
References
- ↑ Haque SK, Ariceta G, Batlle D (December 2012). "Proximal renal tubular acidosis: a not so rare disorder of multiple etiologies". Nephrol. Dial. Transplant. 27 (12): 4273–87. doi:10.1093/ndt/gfs493. PMC 3616759. PMID 23235953.
- ↑ Batlle D, Haque SK (October 2012). "Genetic causes and mechanisms of distal renal tubular acidosis". Nephrol. Dial. Transplant. 27 (10): 3691–704. doi:10.1093/ndt/gfs442. PMID 23114896.
- ↑ Alper SL (2010). "Familial renal tubular acidosis". J. Nephrol. 23 Suppl 16: S57–76. PMID 21170890.