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继发性甲状旁腺功能亢进在移植后急性肾小管坏死发生中的作用。

Role of secondary hyperparathyroidism in the development of post-transplant acute tubular necrosis.

作者信息

Torregrosa J V, Campistol J M, Fenollosa B, Montesinos M, Romar A, Martinez de Osaba M J

机构信息

Renal Transplant Unit, Hospital Clinic, University of Barcelona, Spain.

出版信息

Nephron. 1996;73(1):67-72. doi: 10.1159/000189002.

DOI:10.1159/000189002
PMID:8742960
Abstract

Post-transplant cure tubular necrosis (ATN) represents the most frequent cause of delayed graft function in the immediate post-transplant period. Several causes have been associated with the development of post-transplant ATN such as donor and recipient ages, cold-warm ischemia times, HLA mismatches, and postoperative hypotension. In the present study, we retrospectively evaluated the role of secondary hyperparathyroidism and high parathyroid hormone (PTHi) blood levels in the development of post-transplant ATN. One hundred patients submitted to cadaveric renal transplant between January 1992 and March 1993 in our unit were included. Twenty-seven patients (27%) developed post-transplant ATN and seventy-three (73%) did not. Post-transplant ATN was significantly associated with gender (p < 0.01), recipient age (p < 0.01), number of transplantations (p < 0.01), time on hemodialysis (p < 0.001), cold ischemic time (p < 0.05) and PTHi levels (p < 0.001). The bivariate and multivariate statistical analyses demonstrated that the development of post-transplant ATN was significantly more frequent in females; retransplanted patients, patients with a time on dialysis of more than 5 years, recipients over 60 years old, patients with a PTHi blood level higher than 240 pg/ml (4 times normal level) and a cold ischemia time of more than 18 h. Based on these results, we conclude that high PTHi blood levels in the renal transplant recipients represent a relevant factor in the development of post-transplant ATN. The administration of intravenous pulsed of 1,25(OH)2D3 and/or a calcium channel blocker in the perioperative period could be useful to decrease the incidence and severity of post-transplant ATN in these patients.

摘要

移植后急性肾小管坏死(ATN)是移植后即刻移植物功能延迟的最常见原因。移植后ATN的发生与多种因素有关,如供体和受体年龄、冷-热缺血时间、HLA错配以及术后低血压。在本研究中,我们回顾性评估了继发性甲状旁腺功能亢进和高甲状旁腺激素(PTHi)血水平在移植后ATN发生中的作用。纳入了1992年1月至1993年3月在我们单位接受尸体肾移植的100例患者。27例患者(27%)发生了移植后ATN,73例(73%)未发生。移植后ATN与性别(p < 0.01)、受体年龄(p < 0.01)、移植次数(p < 0.01)、血液透析时间(p < 0.001)、冷缺血时间(p < 0.05)和PTHi水平(p < 0.001)显著相关。双变量和多变量统计分析表明,移植后ATN在女性中发生的频率显著更高;再次移植的患者、透析时间超过5年的患者、60岁以上的受体、PTHi血水平高于240 pg/ml(正常水平的4倍)以及冷缺血时间超过18小时的患者。基于这些结果,我们得出结论,肾移植受者的高PTHi血水平是移植后ATN发生的一个相关因素。在围手术期静脉注射脉冲式1,25(OH)2D3和/或钙通道阻滞剂可能有助于降低这些患者移植后ATN的发生率和严重程度。

相似文献

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Nephron. 1996;73(1):67-72. doi: 10.1159/000189002.
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[Predisposing factors for the development of acute severe tubular necrosis in the immediate post-transplantation period].[移植后即刻发生急性严重肾小管坏死的易感因素]
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引用本文的文献

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Pre-Transplant Hyperparathyroidism and Graft or Patient Outcomes After Kidney Transplantation.移植前甲状旁腺功能亢进症与肾移植后移植物或患者结局。
Transpl Int. 2024 Feb 7;37:11916. doi: 10.3389/ti.2024.11916. eCollection 2024.
2
Successful treatment of early allograft dysfunction with cinacalcet in a patient with nephrocalcinosis caused by severe hyperparathyroidism: a case report.西那卡塞成功治疗严重甲状旁腺功能亢进所致肾钙质沉着症患者的早期移植肾功能障碍:一例报告
BMC Res Notes. 2017 Apr 8;10(1):153. doi: 10.1186/s13104-017-2477-0.
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Kidney allograft failure due to acute phosphate nephropathy associated with severe secondary hyperparathyroidism.
肾移植失败,原因是急性磷酸盐肾病伴严重继发性甲状旁腺功能亢进。
NDT Plus. 2011 Oct;4(5):324-6. doi: 10.1093/ndtplus/sfr078. Epub 2011 Jul 15.