Idiopathic hypercalciuria (IH) mainly has two major hazards. On the one hand, it affects bone metabolism, easily leading to bone loss, osteoporosis, and increasing the risk of bone fracture. On the other hand, IH influences urinary system, mainly increasing the risk of kidney stones. The specific mechanism of osteoporosis caused by hypercalciuria is unclear. Existing studies have shown that the activation of RANKL/RANK/OPG pathway might be one of the main mechanisms of patients with IH causing osteoporosis. The lack of estrogen can cause increased urinary calcium and bone loss, which is one of the important etiology of hypercalciuria and osteoporosis. Bone loss in IH patients may be caused by increase of cell factors such as MCP-1. Research on genetic factors indicates several hypercalciuria and bone loss-associated genes, mainly including CTR gene, TRPV5 gene, and VDR gene. But the study of some genes exists different conclusions. Furthermore, the lack of estrogen can also influence the expression of TRPV5 gene. So genetic factors may become a research hotspot in the future. |