Coe F L, Bushinsky D A
Am J Physiol. 1984 Jul;247(1 Pt 2):F1-13. doi: 10.1152/ajprenal.1984.247.1.F1.
The mechanisms responsible for hypercalciuria may involve intestinal calcium transport, renal tubule calcium reabsorption, and the regulation of bone mineral content. Both parathyroid hormone and 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) may alter urine calcium. For these reasons, understanding the pathogenesis of hypercalciuria in patients has proven to be difficult. We present here an analysis of pathways that regulate systemic calcium homeostasis and of the various mechanisms that have been proposed to explain normocalcemic hypercalciuria in humans. Available evidence seems to implicate disordered regulation of 1,25(OH)2D3 as a basis for at least one common form of hypercalciuria.
导致高钙尿症的机制可能涉及肠道钙转运、肾小管钙重吸收以及骨矿物质含量的调节。甲状旁腺激素和1,25 - 二羟维生素D3（1,25(OH)2D3）均可改变尿钙。由于这些原因，已证实了解患者高钙尿症的发病机制很困难。我们在此对调节全身钙稳态的途径以及已提出的用于解释人类正常血钙性高钙尿症的各种机制进行分析。现有证据似乎表明1,25(OH)2D3调节紊乱是至少一种常见形式的高钙尿症的基础。
