Homozygous loss-of-function mutations of the SLC34A1 gene have been reported to cause vitamin D-resistant hypophosphatemic rickets, associated with renal Fanconi syndrome, elevated serum 1,25(OH)2D (stimulated by hypophosphatemia), and subsequent hypercalciuria (40, 41) due to enhanced intestinal calcium absorption (42, 43). This evidence concerns the gene SLC34A1 and Dent disease.