Kakani Elijah, Sloan David, Sawaya B Peter, El-Husseini Amr, Malluche Hartmut H, Rao Madhumathi
Division of Nephrology, Bone and Mineral Metabolism, University of Kentucky, Lexington, KY, USA.
Division of Endocrine Surgery, University of Kentucky, Lexington, KY, USA.
Semin Dial. 2019 Nov;32(6):541-552. doi: 10.1111/sdi.12833. Epub 2019 Jul 16.
Parathyroidectomy (PTX) remains an important intervention for dialysis patients with poorly controlled secondary hyperparathyroidism (SHPT), though there are only retrospective and observational data that show a mortality benefit to this procedure. Potential consequences that we seek to avoid after PTX include persistent or recurrent hyperparathyroidism, and parathyroid insufficiency. There is considerable subjectivity in defining and diagnosing these conditions, given that we poorly understand the optimal PTH targets (particularly post PTX) needed to maintain bone and vascular health. While lowering PTH after PTX decreases bone turnover, long-term changes in bone activity have been poorly explored. High turnover bone disease, usually present at the time a PTX is considered, often swings to a state of low turnover in the setting of sufficiently low PTH levels. It remains unclear if all low bone turnover equate with disease. However, such changes in bone turnover appear to predispose to vascular calcification, with positive calcium balance after PTX being a potential contributor. We know little of how the post-PTX state resets calcium balance, how calcium and VDRA requirements change or what kind of adjustments are needed to avoid calcium loading. The current consensus cautions against excessive reduction of PTH although there is insufficient evidence-based guidance regarding the management of chronic kidney disease - mineral bone disease (CKD-MBD) parameters in the post-PTX state. This article aims to compile existing research, provide an overview of current practice with regard to PTX and post-PTX chronic management. It highlights gaps and controversies and aims to re-orient the focus to clinically relevant contemporary priorities in CKD-MBD management after PTX.
甲状旁腺切除术（PTX）仍然是对继发性甲状旁腺功能亢进症（SHPT）控制不佳的透析患者的一项重要干预措施，尽管仅有回顾性和观察性数据表明该手术对降低死亡率有益。我们试图在PTX后避免的潜在后果包括持续性或复发性甲状旁腺功能亢进以及甲状旁腺功能减退。鉴于我们对维持骨骼和血管健康所需的最佳甲状旁腺激素（PTH）目标（尤其是PTX后）了解不足，在定义和诊断这些病症时存在相当大的主观性。虽然PTX后降低PTH可减少骨转换，但对骨活性的长期变化研究甚少。高转换型骨病通常在考虑进行PTX时就已存在，在PTH水平足够低的情况下，往往会转变为低转换状态。目前尚不清楚所有的低骨转换是否都等同于疾病。然而，这种骨转换的变化似乎易导致血管钙化，PTX后的正钙平衡可能是一个促成因素。我们对PTX后的状态如何重置钙平衡、钙和维生素D受体激动剂（VDRA）的需求如何变化，或者需要进行何种调整以避免钙负荷增加知之甚少。目前的共识告诫不要过度降低PTH，尽管对于PTX后状态下慢性肾脏病 - 矿物质和骨异常（CKD - MBD）参数的管理，缺乏足够的循证指南。本文旨在汇总现有研究，概述PTX及PTX后慢性管理的当前实践。它突出了差距和争议，并旨在将重点重新转向PTX后CKD - MBD管理中与临床相关的当代优先事项。
