Renal tubular acidosis causes

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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.

	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.	Autoimmune disorders Medications Ifosfamide Amphotericin B Lithium carbonate Ibuprofen Hypercalciuric conditions Hyperparathyroidism 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) 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 Renal transplant rejection Wilson disease
Type 4	Congenital hypoaldosteronism 21-hydroxylase deficiency Isolated hypoaldosteronism Pseudohypoaldosteronism type 2 Primary adrenal insufficiency Pseudohypoaldosteronism type 1	Angiotensin inhibitors, such as ACE inhibitors Angiotensin II receptor blockers Direct renin inhibitors Antibiotics, trimethoprim, and pentamidine Potassium-sparing diuretics Spironolactone Eplerenone Amiloride Triamterene