CAJ | 학술논문

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。
뇨개배설시재다충격소작용하유위장도、골격、신장상호작용완성。특발성고개뇨증、유전성신소관병변소치적고개뇨증수다기인조공。유연구발현，부분특발성고개뇨증급신소관병변소치고개뇨증환자가출현계발성갑상방선공능항진，장기발전가능회영향환자골격대사。단목전대량자관계급가능적발병궤제연구심소，진일보연구급탐토가감소고개뇨증병발증적발생솔，개선환자예후。본문취특발성고개뇨증급유전성신소관병변소치적고개뇨증발병궤제적최신진전진행천술。
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 tu-bular disorders could result in secondary hyperparathyroidism ( SHPT) , of which the pathogenesis was still unclear.