Aladrén Regidor M J
Hospital Ernest Lluch, Calatayud, Spain.
Clin Nephrol. 2009 Feb;71(2):207-13. doi: 10.5414/cnp71207.
Management of secondary hyperparathyroidism (SHPT) in chronic kidney disease patients on hemodialysis (HD) can be challenging. Conventional treatments can lead to hypercalcemia and hyperphosphatemia, both of which are associated with vascular and soft tissue calcification and increased risk of cardiovascular disease. We report the effect of treatment with the Type II calcimimetic cinacalcet on vascular calcification in a HD patient with SHPT. A 40-year-old male with a 24-year history of kidney failure secondary to mesangial proliferative glomerulonephritis, commenced HD in October 2004 following chronic graft dysfunction. The patient was admitted to hospital with renal insufficiency and metabolic abnormalities. An anatomopathological study showed calcium (Ca) deposits in the alveolar septa, bronchial wall and pulmonary arterioles. Parathyroid methoxy isobutyl isonitrile (MIBI) scintigraphy revealed multiglandular parathyroid disease and an ectopic gland behind the sternal notch. Serum intact parathyroid hormone (iPTH) was repeatedly found to be > or = 2,500 pg/ml, and was accompanied by significant abnormalities in phosphorus (P) and Ca metabolism which were difficult to control. The patient was initially treated with sevelamer, low dose calcium carbonate, a low P and reduced protein diet and high doses of intravenous erythropoietin. In addition, he received HD with a high efficiency membrane for 4.5 hours, 4-times weekly. Treatment with cinacalcet was initiated at 30 mg/day and adjusted to achieve National Kidney Foundation Kidney Disease Outcomes Quality Initiative targets for iPTH, P, Ca and Ca-P product. One year following cinacalcet treatment, a chest x-ray showed a moderate reduction in Ca deposits, a bone X-ray showed a significant reduction in vascular calcifications, and parathyroid MIBI scintigraphy showed a disappearance of ectopic focus and minimal remains of glands. Significant reductions in calcemia were controlled by concomitant modifications to oral Ca supplementation, Ca concentration in the dialysis liquid, and administration of paricalcitriol. In the second year of treatment, iPTH was maintained within the target range, with moderate rises in P and stabilization of serum Ca. An echocardiogram showed an improvement in left ventricular hypertrophy. Chest and hand X-rays showed a progressive reduction in calcifications. Radiology showed an improvement in bone morphology, with reduced trabeculation and better cortical definition in the phalanx bones. In conclusion, the changes in iPTH, P and Ca associated with cinacalcet treatment were accompanied by reduced vascular and soft tissue calcification in this patient. There were no cardiovascular events and the patient experienced a marked improvement in quality of life.
对接受血液透析（HD）的慢性肾病患者的继发性甲状旁腺功能亢进症（SHPT）进行管理可能具有挑战性。传统治疗方法可能导致高钙血症和高磷血症，这两者均与血管和软组织钙化以及心血管疾病风险增加相关。我们报告了使用II型拟钙剂西那卡塞治疗一名患有SHPT的HD患者的血管钙化的效果。一名40岁男性，有24年系膜增生性肾小球肾炎继发肾衰竭病史，于2004年10月因慢性移植功能障碍开始接受HD治疗。该患者因肾功能不全和代谢异常入院。解剖病理学研究显示在肺泡间隔、支气管壁和肺小动脉中有钙（Ca）沉积。甲状旁腺甲氧基异丁基异腈（MIBI）闪烁扫描显示多腺体甲状旁腺疾病以及胸骨切迹后方有一个异位腺体。血清完整甲状旁腺激素（iPTH）多次被发现≥2500 pg/ml，并伴有磷（P）和Ca代谢的显著异常，难以控制。该患者最初接受司维拉姆、低剂量碳酸钙、低P和低蛋白饮食以及高剂量静脉注射促红细胞生成素治疗。此外，他每周接受4次、每次4.5小时的高效膜HD治疗。西那卡塞治疗从30 mg/天开始，并进行调整以达到美国国立肾脏基金会肾脏病预后质量倡议（NKF-KDOQI）关于iPTH、P、Ca和Ca-P乘积的目标。西那卡塞治疗1年后，胸部X线显示Ca沉积适度减少；骨骼X线显示血管钙化显著减少；甲状旁腺MIBI闪烁扫描显示异位灶消失且腺体残留极少。通过同时调整口服Ca补充剂、透析液中的Ca浓度以及给予帕立骨化醇，控制了血钙的显著降低。在治疗的第二年，iPTH维持在目标范围内，P适度升高且血清Ca稳定。超声心动图显示左心室肥厚有所改善。胸部和手部X线显示钙化逐渐减少。放射学检查显示骨形态有所改善，指骨小梁减少且皮质清晰度更好。总之，该患者西那卡塞治疗相关的iPTH、P和Ca变化伴随着血管和软组织钙化减少。未发生心血管事件，患者生活质量显著改善。
