Center for Pediatric and Adolescent Medicine Heidelberg, University of Heidelberg, INF 430, Heidelberg, Germany.
Nephrol Dial Transplant. 2010 Aug;25(8):2590-5. doi: 10.1093/ndt/gfq074. Epub 2010 Feb 24.
Hyperparathyroidism (HPT) is an essential contributor to bone disease and cardiovascular calcifications in children with chronic kidney disease (CKD). Pharmacological and dietary interventions are of limited efficacy; calcimimetics are not yet recommended in children. Parathyroidectomy (PTX) is ultimately performed if HPT becomes refractory to conservative measures; the long-term results and the impact of subsequent kidney transplantation (NTX), however, have not yet been evaluated.
We analyzed the postsurgical course of 18 paediatric CKD patients with refractory HPT who underwent PTX and autotransplantation of tissue fragments. PTX was successful in all but one patient with an ectopic fifth gland; median follow-up time was 8.3 (range 2.8-19) years.
Parathyroid hormone (PTH) dropped within 1 year after PTX from 1030 +/- 108 to 98 +/- 18 pg/ml, CaP from 59.5 +/- 3 to 49 +/- 2 mg(2)/dl(2). Oral calcium supply transiently increased from 18.7 +/- 4.2 to 24.1 +/- 4.8 mg/kg/day within the first 6 months (all P < 0.05). Haemoglobin increased from 10.7 +/- 0.4 to 11.5 +/- 0.3 g/dl (P < 0.01), despite similar erythropoietin dose and ferritin levels. In patients on long-term dialysis, CaP increased again after 18 months; three patients required a second PTX after 3.8, 12 and 12.3 years. Twelve patients underwent NTX 1.8 (0.3-3.8) years after PTX, which decreased mean PTH and Ca*P into the target range throughout the entire post-NTX observation period. Postoperative complications included one transient recurrent nerve palsy, one hypocalcaemic seizure and a case of haemopericardium. At present, no patient has clinical signs of bone disease.
PTX accomplishes long-term control of HPT and calcium-phosphate metabolism in children with CKD and following PTX and may thus mitigate uraemic bone and cardiovascular disease. This has to be taken into account if alternative long-term therapy with calcimimetics (with as yet unknown effects on longitudinal growth and pubertal development) is considered.
甲状旁腺功能亢进症(HPT)是慢性肾脏病(CKD)儿童骨病和心血管钙化的重要病因。药物和饮食干预的疗效有限;钙敏感受体激动剂尚未推荐用于儿童。如果 HPT 对保守治疗无反应,则最终进行甲状旁腺切除术(PTX);然而,其长期结果和随后肾移植(NTX)的影响尚未得到评估。
我们分析了 18 例接受 PTX 和组织碎片自体移植的难治性 HPT 儿童 CKD 患者的术后病程。除 1 例异位第五腺外,所有患者的 PTX 均成功;中位随访时间为 8.3(2.8-19)年。
PTX 后 1 年内甲状旁腺激素(PTH)从 1030±108 降至 98±18 pg/ml,钙磷乘积从 59.5±3 降至 49±2 mg2/dl2。口服钙供应在最初 6 个月内从 18.7±4.2 增加至 24.1±4.8 mg/kg/天(均 P<0.05)。血红蛋白从 10.7±0.4 增加至 11.5±0.3 g/dl(P<0.01),尽管红细胞生成素剂量和铁蛋白水平相似。在长期透析的患者中,18 个月后钙磷乘积再次增加;3 例患者在 3.8、12 和 12.3 年后再次进行 PTX。12 例患者在 PTX 后 1.8(0.3-3.8)年接受 NTX,整个 NTX 观察期间,平均 PTH 和钙磷乘积均降至目标范围。术后并发症包括一过性喉返神经麻痹 1 例、低钙血症性癫痫发作 1 例和心包积血 1 例。目前,无患者出现骨病临床症状。
PTX 可长期控制 CKD 儿童的 HPT 和钙磷代谢,且在 PTX 后,可减轻尿毒症性骨病和心血管疾病。如果考虑替代的长期钙敏感受体激动剂治疗(对纵向生长和青春期发育的影响尚不清楚),则需要考虑这一点。