Hypercalciuria

Stephen W. Leslie 1, Hussain Sajjad 2

In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan.

2021 Sep 17.

Affiliations expand

PMID: 28846247

 

Bookshelf ID: NBK448183

 

Continuing Education Activity

Introduction

Etiology

Epidemiology

病理生理学    吸收性高钙尿症是最常见的过度尿钙排泄类型。大约 50% 的钙结石形成患者都有这种情况。胃肠道钙吸收增加会增加血清钙水平，同时降低血清维生素 D 和甲状旁腺激素水平。只有大约 20% 的摄入钙被吸收，通常发生在十二指肠。吸收性高钙尿症的维生素 D 依赖性版本可以通过其相对较高的血清维生素 D 水平来识别。[1] 肾钙泄漏 高钙尿症见于约 5% 至 10% 的所有高钙尿症结石形成者。它是由肾缺陷引起的，无论血清钙水平或膳食钙摄入量如何，都会导致尿液中钙的强制性流失。这通常伴有低钙血症和血清甲状旁腺激素 (PTH) 水平升高。在这种情况下，钙/肌酐比率往往很高（通常大于 0.20），并且与髓质海绵肾有关。[1]    从病理生理学的角度来看，肾磷酸盐泄漏性高钙尿症可能是最有趣的。肾功能不全会导致尿磷排泄过多，从而导致低磷血症。这会诱导肾脏中更高的维生素 D 活化，从而增加肠道磷酸盐的吸收，以纠正低血清磷酸盐。不幸的是，额外的维生素 D 也会增加肠道钙的吸收。吸收的额外钙最终通过尿液排出，导致高钙尿症。这种类型的高钙尿症依赖于维生素 D，对噻嗪类药物的反应相对较弱。诊断是根据血清磷酸盐低或正常低、高钙尿症、高尿磷酸盐和高血清维生素 D3 水平与正常血清钙和 PTH 水平的发现作出的[1]。虽然据报道它存在于所有高钙尿症患者中多达 20%，但我们的经验是，只有 5% 或更少的患者具有临床意义[11] [12]。吸收性高钙尿症仅占所有高钙尿症患者的约 3% 至 5%，并且几乎总是由甲状旁腺功能亢进引起。持续的、不适当的和过量的血清甲状旁腺激素会导致钙从骨骼中释放出来，导致骨质减少和高钙血症。最终，高钙血症克服了正常甲状旁腺激素减少尿钙排泄的作用，结果是高钙尿症（例如，类似于糖尿病患者尿液中的糖分溢出）。这解释了为什么甲状旁腺功能亢进症患者血清钙水平升高时高钙血症引起的高钙尿症比其他高钙血症患者少[1]。怀孕会增加所有三个孕期的高钙尿症，但这似乎不会增加新结石病的风险，因为肾结石抑制剂也会增加。有趣的是，骨矿物质密度与肾结石患者的高钙尿症呈负相关，但在没有肾结石的患者中则不然。[13]   在儿童中，反复腹痛和高钙尿症之间存在明显的联系。最近的一项研究将高钙尿症小儿肾结石患者与脂质代谢/转运相关蛋白的尿排泄增加联系起来。这表明脂质代谢异常可能在某种程度上与小儿高钙尿症和肾结石有关[1] [4]。

History and Physical

Evaluation

Treatment / Management

Differential Diagnosis

• Acute renal colic

• Hypervitaminosis D

• Hypophosphatemia

• Osteoporosis

• Pyelonephritis

• Rickets

• Sarcoidosis

• Uric acid stones

• Urinary tract infection

• Urolithiasis

Pearls and Other Issues

Enhancing Healthcare Team Outcomes

References

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 肾脏中的克洛托（ a ）klotho蛋白的肾脏分布。Klotho 在远曲小管 (DCT) 和连接小管 (CNT) 20 中与瞬时受体电位 Vallinoid 5 (TRPV5)、Na2+/Ca2+ 交换剂 (NCX1) 和钙结合蛋白-D28K 共表达。（ b ）klotho调节钙稳态的建议机制。PTH，甲状旁腺激素；FGF23，成纤维细胞生长因子。