特发性高钙尿与骨质疏松的研究进展

特发性高钙尿症(idiopathic hypercalciuria,IH)主要有两大危害,一则影响骨代谢,容易引起骨量减少、骨质疏松,增加骨折风险;二则影响泌尿系统,主要表现为增加患肾结石风险。高钙尿引起骨质疏松及肾结石的具体机制尚不明确。现有的研究表明核因子κB受体活化因子配体(RANKL)/核因子κB受体活化因子(RANK)/护骨素(OPG)通路激活可能是IH患者引起骨质疏松的主要机制之一。雌激素缺乏会引起尿钙升高、骨量减少,是高钙尿及骨质疏松的重要病因。高钙尿症还可能通过单核细胞趋化因子-1(MCP-1)等细胞因子的增加从而引起骨量减少。对遗传因素的研究中发现了许多与高钙尿及骨量减少相关联的基因,主要包括降钙素受体基因、瞬时感受器电位阳离子通道香草精受体5基因、维生素D受体基因。但对上述一些基因型与骨质疏松的研究存在不同的结论,而雌激素缺乏还可通过影响瞬时感受器电位阳离子通道香草精受体5基因的表达起作用,因此遗传因素可能成为未来研究的热点。

Research progress of the relationship between idiopathic hypercalciuria and osteoporosis

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.