Inoshita H, Gohda T, Io H, Kaneko K, Hamada C, Horikoshi S, Tomino Y
Division of Nephrology, Department of Internal Medicine, Juntendo University School of Medicine, Tokyo, Japan.
Clin Nephrol. 2008 Jan;69(1):58-62. doi: 10.5414/cnp69058.
Peritoneal calcification is one of the complications of peritoneal dialysis (PD). It can become serious, leading to severe abdominal pain and even death. Possible mediators of peritoneal calcification in PD patients are assumed to include acetate buffer, overdosage of vitamin D, repeated peritonitis, hypertonic dialysate, calciphylaxis and secondary hyperparathyroidism (SHPT). However, the mechanism and treatment of peritoneal calcification are controversial. Few reports have appeared on improvement of peritoneal calcification after parathyroidectomy (PTX) for SHPT of long duration. We report herein the case of a 48-year-old man on dialysis for 17 years including PD for 14 years. In 1989, he was admitted to hospital because of end-stage renal disease (ESRD), and started treatment with PD. Abdominal computed tomography (CT) first showed peritoneal calcification in August 2002. Peritoneal calcification did not improve despite conventional treatment including discontinuation of PD, control of calcium phosphate product to less than 55 mg2/dl2, removal of the peritoneal catheter and empirical prednisolone (PSL) usage. The intact parathyroid hormone (i-PTH) level was increased over 1,000 pg/ml and extra-osseous calcification occurred. Total PTX was performed in November 2004. Postoperatively, the i-PTH level decreased immediately and calcium phosphate product was maintained in the reference range. Abdominal CT after PTX showed improvement of peritoneal calcification in September 2005. It appeared that PTX could be used to treat patients with persistent peritoneal calcification not responding to conventional treatment. It was postulated that SHPT might play a crucial role in accelerating peritoneal calcification in PD patients.
腹膜钙化是腹膜透析（PD）的并发症之一。它可能会变得严重，导致剧烈腹痛甚至死亡。PD患者腹膜钙化的可能介导因素被认为包括醋酸盐缓冲液、维生素D过量、反复腹膜炎、高渗透析液、钙化防御和继发性甲状旁腺功能亢进（SHPT）。然而，腹膜钙化的机制和治疗存在争议。关于长期SHPT患者甲状旁腺切除术后（PTX）腹膜钙化改善的报道很少。我们在此报告一例48岁男性，透析17年，其中PD治疗14年。1989年，他因终末期肾病（ESRD）入院，并开始接受PD治疗。2002年8月腹部计算机断层扫描（CT）首次显示腹膜钙化。尽管采取了包括停止PD、将钙磷乘积控制在55mg²/dl²以下、拔除腹膜导管和经验性使用泼尼松龙（PSL）在内的常规治疗，腹膜钙化仍未改善。完整甲状旁腺激素（i-PTH）水平升高超过1000pg/ml，且出现了骨外钙化。2004年11月进行了全甲状旁腺切除术。术后，i-PTH水平立即下降，钙磷乘积维持在参考范围内。PTX后2005年9月的腹部CT显示腹膜钙化有所改善。看来PTX可用于治疗对常规治疗无反应的持续性腹膜钙化患者。据推测，SHPT可能在加速PD患者腹膜钙化中起关键作用。
