Morning Rounds · Renal Tubular Disorders
Renal Tubular Acidosis — Comparison
Feature
Type I (Distal)
Type II (Proximal)
Type IV
Normal AG acidosis
Defect
H⁺ secretion
(collecting duct)
HCO₃⁻ reabsorption
(proximal tubule)
Aldosterone deficiency
/ resistance
All three are NAGMA
Serum K⁺
↓ Low
↓ Low
↑ High
Key distinguishing point
Urine pH
> 5.5 (cannot acidify)
Variable / <5.5 possible
≤5.5
Type I: always >5.5
Stones / NCC
Yes (nephrocalcinosis)
Rare
No
Classic Type I feature
Treatment
Oral NaHCO₃
or K-citrate
Large doses NaHCO₃
+ K supplementation
Fludrocortisone
or loop diuretic
Treat cause + alkali
Causes
Sjögren, SLE,
amphotericin B,
lithium
Fanconi (Wilson,
cystinosis, tenofovir,
multiple myeloma)
DM, hyporeninism,
ACEi/ARB,
heparin, CKD
No Type III in
current classification
(obsolete)
All three RTA types produce a normal anion gap metabolic acidosis (NAGMA) . The serum potassium is the pivotal differentiator: low in Types I and II, high in Type IV. Urine pH >5.5 in the face of systemic acidosis is pathognomonic of Type I — the distal tubule cannot secrete H⁺.
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