Renal tubular acidosis epidemiology and demographics: Difference between revisions

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Revision as of 16:40, 29 May 2018

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

The estimated annual incidence of distal renal tubular acidosis is 10 in 100,000 population.
Proximal renal tubular acidosis is a r

@@ Line 21: / Line 21: @@
 ===Race===
 * There is racial predilection for renal tubular acidosis.
-::
-; •
-; •
-: There is no sex predominance in DRTA or in Type 4 RTA.
-; •
-: DRTA may be inherited as an autosomal dominant or recessive trait.
-:; ○
-:: Autosomal recessive DRTA often presents in infancy, whereas autosomal dominant DRTA may not present until adolescence or young adulthood.
-:; ○
-:: Mutations in the genes encoding carbonic anhydrase II, kidney anion exchanger 1 (kAE1), and subunits of the renal proton pump (H+‐ATPase) have been identified in patients with DRTA.
-; •
-: DRTA is almost always permanent.
-; •
-: Isolated PRTA is more common in males.
-; •
-: Isolated PRTA may be transient.
-; •
-: Genetically transmitted PRTAs include autosomal dominant and recessive forms.
-; •
-: PRTA (with ocular abnormalities) may be caused by inactivating mutations in the Na/HCO3 cotransporter gene (SLC4A4).
-; •
-: PRTA may also be associated with other genetically transmitted disorders, such as osteopetrosis with carbonic anhydrase II deficiency.
-; •
-: Inherited defects leading to Type 4 RTA are due to aldosterone deficiency or resistance.
-:; ○
-:: Congenital adrenal hyperplasia with salt wasting
-:; ○
-:: Isolated hypoaldosteronism
-:; ○
-:: Pseudohypoaldosteronism (defect at the aldosterone receptor level)
 ==References==
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