Abstract
A 46-year-old white woman has been followed in this nephrology clinic since 1995 due to recurrent nephroli-thiasis and medullary nephrocalcinosis resulting from renal tubular acidosis (urinary pH of 8 in the context of systemic normal anion gap acidosis; serum potassium at lower limit, and 24-hour urine with normocalciuria but no detectable citrate) due to Sjogren’s syndrome (SS). During follow-up, her adherence to alkali therapy had been suboptimal due to gastric intolerance to Shohl’s solution, potassium citrate, and sodium bicarbonate. As consequence, she had progression in her nephrocal-cinosis and passed several urinary calculi (biochemical analysis showed them to be composed of calcium phos-phate and calcium oxalate). Currently, she presents nor-mal estimated GFR (MDRD, 82 mL/min/1.73 m
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