Renal Phosphate–Transporter Regulatory Proteins and Nephrolithiasis

Nephrolithiasis is a common disorder, and idiopathic hypercalciuria is the most frequent metabolic disorder associated with nephrolithiasis.1 Several studies have shown that subjects with idiopathic hypercalciuria have phosphaturia or renal phosphate leak. In fact, a study that measured the tubular maximal reabsorption of phosphate (TmP, or maximal renal phosphate threshold) normalized for the glomerular filtration rate (GFR) (the TmP/GFR value) in 207 subjects with calcium nephrolithiasis reported that 20% of persons with normal parathyroid function in whom stones formed have a decreased TmP/GFR value.2 The associated mild hypophosphatemia results in increased 1,25-dihydroxyvitamin D production, which causes increased intestinal phosphate and . . .