A 35-year-old woman with type 1 distal RTA (urinary pH persistently >5.5 despite acidaemia) develops bilateral nephrolithiasis and nephrocalcinosis. Which biochemical mechanism directly links distal RTA to stone formation?
- A Impaired H+ secretion by alpha-intercalated cells leads to hypercalciuria and hypocitraturia, promoting calcium phosphate stone precipitation at alkaline urinary pH ✓
- B Systemic acidosis reduces renal tubular bicarbonate reabsorption, increasing urinary calcium excretion
- C Reduced urinary ammonium production concentrates calcium oxalate in tubular fluid
- D Impaired proximal tubular glucose reabsorption raises urinary oxalate concentrations
Explanation
In type 1 (distal) RTA, alpha-intercalated cells cannot secrete adequate H+ into collecting duct lumen. Systemic acidosis triggers bone buffering, releasing calcium and phosphate; hypercalciuria results. Simultaneously, proximal citrate reabsorption increases in acidosis, causing hypocitraturia (citrate normally inhibits calcium crystal nucleation). The alkaline urine (pH >6.0) favours calcium phosphate (hydroxyapatite) precipitation rather than calcium oxalate. This trifecta — hypercalciuria + hypocitraturia + alkaline urine — accounts for the nephrocalcinosis and nephrolithiasis characteristic of dRTA.
Reference: Harrison's Principles of Internal Medicine, 21st ed.
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