Patients with FGF23-mediated renal phosphate wasting usually also show low UCa/Crea values due to diminished 1,25 vitamin D synthesis, whereas most patients with primary renal tubular phosphate wasting show hypercalciuria due to elevated 1,25(OH)2D synthesis (e.g., HHRH, IIH, cystinosis, Dent disease), which can be associated with nephrocalcinosis/nephrolithiasis (Table 1). This evidence concerns the gene FGF23 and Hypercalciuria.