A 30-year-old woman with SLE presents with serum bicarbonate 14 mEq/L, urine pH 6.8 (inappropriately high), serum potassium 3.0 mEq/L, urine anion gap positive (+12), and normal anion gap metabolic acidosis. Serum creatinine 1.0. What type of renal tubular acidosis (RTA) does she have and what is its mechanism?
- A Type 2 (proximal RTA) — failure of HCO3- reabsorption in proximal tubule
- B Type 1 (distal RTA) — failure of H+ secretion in distal nephron ✓
- C Type 4 (hyperkalemic RTA) — aldosterone deficiency/resistance
- D Type 3 (mixed RTA) — deficiency of carbonic anhydrase II
Explanation
Type 1 (distal) RTA is characterized by: inability to acidify urine below pH 5.5 (urine pH inappropriately high >5.5 despite systemic acidosis), positive urine anion gap (impaired NH4+ excretion in distal nephron), hypokalemia (due to compensatory aldosterone-driven K+ wasting), and normal anion gap metabolic acidosis. It is commonly associated with SLE (due to interstitial nephritis and Sjögren's overlap). Mechanism: failure of alpha-intercalated cells' H+-ATPase in collecting duct. Type 2 proximal RTA has low urine pH during systemic acidosis as distal acidification is intact. Type 4 RTA causes hyperkalemia.
Reference: Harrison's Principles of Internal Medicine, 21st ed.
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Written and medically reviewed by the StethoPrep medical team.