ICU · Renal / acid-base
Renal Tubular Acidoses (Types I, II, IV) — The Hyperchloraemic Acidoses
Also known as Renal tubular acidosis · RTA · Type 1 RTA · Distal RTA · Type 2 RTA · Proximal RTA · Type 4 RTA · Hypoaldosteronism · Fanconi syndrome · Non-anion-gap metabolic acidosis · Hyperchloraemic acidosis · Nephrocalcinosis · Fludrocortisone
The renal tubular acidoses (RTA) are a group of disorders of the renal acid-base handling that produce a non-anion-gap (the hyperchloraemic) metabolic acidosis from the impaired renal acid excretion (the bicarbonate reabsorption or the acid secretion). The three types: the Type 1 (the distal) — the impaired distal H-plus secretion; the urine pH stays HIGH (over 5.5) despite the acidosis; the HYPOkalaemia; the causes the autoimmune (the Sjogren), the amphotericin B, the lithium; the nephrocalcinosis and the stones; the treatment the bicarbonate plus the potassium. The Type 2 (the proximal) — the impaired proximal bicarbonate reabsorption; the urine pH high then low; the HYPOkalaemia; the Fanconi syndrome, the myeloma, the ifosfamide, the tenofovir, the acetazolamide; the treatment the bicarbonate plus the potassium. The Type 4 — the hypoaldosteronism (or the aldosterone resistance); the urine pH LOW (under 5.5); the HYPERkalaemia (the key discriminator); the diabetes, the Addison, the ACEi, the ARB, the K-sparing diuretics; typically in mild-to-moderate CKD; the treatment the low-dose fludrocortisone and the treat the hyperkalaemia.
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A 42-year-old woman with known Sjögren syndrome presents with proximal muscle weakness and recurrent left flank pain. ABG: pH 7.28, HCO₃ 14, K⁺ 2.9. A non-contrast CT shows bilateral medullary nephrocalcinosis. Urine pH on a catheterised specimen is 6.2.[13]
The three numbers that decide the next hour are the anion gap (normal here — this is a hyperchloraemic acidosis), the potassium (low — Type 1 or 2, or a gut loss), and the urine pH (persistently above 5.5 — the kidney cannot acidify). Hold those three values and the rest of the topic slots into place.[13][18]
References19ShowHide
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- [11]Hall AM, Bass P, Unwin RJ Drug-induced renal Fanconi syndrome QJM, 2014.PMID 24368854
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- [17]Rehman MZ, Melamed M, Harris A, et al. Urinary Ammonium in Clinical Medicine: Direct Measurement and the Urine Anion Gap as a Surrogate Marker During Metabolic Acidosis Adv Kidney Dis Health, 2023.PMID 36868734
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- [19]Unsal Y, Baltu D, Gulhan B, et al. Calcineurin inhibitor-related hyperkalemia is caused by hyporeninemic hypoaldosteronism and fludrocortisone is an effective treatment: Report of a case series and review of the literature Pediatr Transplant, 2024.PMID 38767038
- [20]Geldermann N, Dzimiera J, Fischer H, Christ M Acute hyperkalaemia in emergency care: evidence-based approaches Emerg Med J, 2026.PMID 41506858