高钙尿症病因学研究进展  

Progress of pathogenesis ofhypercalciuria

作　　者：全婷婷[1] 王鸥[1] 邢小平[1] 

机构地区：[1]中国医学科学院北京协和医学院北京协和医院内分泌科卫生部内分泌重点实验室,北京100730

出　　处：《中华骨质疏松和骨矿盐疾病杂志》2015年第2期174-180,共7页Chinese Journal Of Osteoporosis And Bone Mineral Research

基　　金：国家自然科学基金青年基金(81100559);国家自然科学基金面上项目(81270873)

摘　　要：尿钙排泄是在多种激素作用下由胃肠道、骨骼、肾脏相互作用完成。特发性高钙尿症、遗传性肾小管病变所致的高钙尿症受多基因调控。有研究发现,部分特发性高钙尿症及肾小管病变所致高钙尿症患者可出现继发性甲状旁腺功能亢进,长期发展可能会影响患者骨骼代谢。但目前对两者关系及可能的发病机制研究甚少,进一步研究及探讨可减少高钙尿症并发症的发生率,改善患者预后。本文就特发性高钙尿症及遗传性肾小管病变所致的高钙尿症发病机制的最新进展进行阐述。The excretion of urinary calcium is controlled by a complex interplay between the gastrointestinal tract, bone and kidney. The whole process is orchestrated by multiple hormones. Hypercalciuria caused by idiopathic hy- percalciuria （IH） and hereditary renal tubular disorders is believed to be a polygenic trait. In this review, we demonstrate the latest progress of pathogenesis of these diseases. Researchers also found that IH or hypercalciuria caused by renal tubular disorders could result in secondary hyperparathyroidism （SHPT） , of which the pathogenesis was still unclear.

关 键 词：遗传性肾小管病变 特发性高钙尿症 继发性甲状旁腺功能亢进症 

分 类 号：R681[医药卫生—骨科学]