In fact, the triad of symptoms, LMWP, hypercalciuria, and nephrocalcinosis, was present in almost all patients of Group I, indicating that the loss of ClC-5 function was the cause of clinical manifestations independently of allele heterogeneity, thus mimicking the picture shown in the ClC-5 KO mouse models. This evidence concerns the gene CLCN5 and nephrocalcinosis.