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一名透析患者肿瘤性钙化逆转导致甲状旁腺激素非依赖性严重高钙血症的突然发作。

Sudden onset of parathyroid hormone-independent severe hypercalcemia from reversal of tumoral calcinosis in a dialysis patient.

作者信息

Kamar Fareed B, Mann Bikaramjit, Kline Gregory

机构信息

Department of Medicine, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada.

Department of Critical Care Medicine, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada.

出版信息

BMC Nephrol. 2016 Sep 29;17(1):137. doi: 10.1186/s12882-016-0355-y.

Abstract

BACKGROUND

Tumoral calcinosis is a rare manifestation of extraskeletal calcification, featuring large calcified cystic masses in the periarticular regions of large joints. In chronic kidney disease (CKD), this disorder is thought to evolve through a chronically elevated calcium-phosphorus solubility product leading to calcium precipitation in soft tissue. Treating tumoral calcinosis in these patients involves interventions to lower the calcium-phosphorus product such as reduction in vitamin D therapy and intensive hemodialysis regimens.

CASE PRESENTATION

We report the case of a 54-year old woman with polycystic kidney disease on peritoneal dialysis with widespread tumoral calcinosis in the context of hypercalcemic tertiary hyperparathyroidism who had been on long-term alfacalcidol therapy. After withdrawal of the vitamin D analogue and initiation of daily hemodialysis, there was rapid dissolution of her tumoral calcium deposits with the abrupt onset of parathyroid hormone (PTH)-independent transient hypercalcemia that resolved once the soft tissue deposits disappeared.

CONCLUSIONS

Resorption of soft tissue calcific deposits may result in transient parathyroid hormone (PTH)-independent hypercalcemia. In CKD patients, this hypercalcemia causes a decrease in the PTH level, distinguishing it from tertiary hyperparathyroidism, though PTH may not be totally suppressed, the way it is seen in PTH-independent hypercalcemia in non-CKD patients.

摘要

背景

肿瘤性钙化是一种罕见的骨骼外钙化表现,其特征是大关节周围区域出现大的钙化囊性肿块。在慢性肾脏病(CKD)中,这种疾病被认为是通过钙磷溶解度乘积长期升高导致钙在软组织中沉淀而发展的。治疗这些患者的肿瘤性钙化需要采取降低钙磷乘积的干预措施,如减少维生素D治疗和强化血液透析方案。

病例报告

我们报告了一例54岁患有多囊肾病且正在进行腹膜透析的女性病例,该患者在高钙血症性三发性甲状旁腺功能亢进的情况下出现广泛的肿瘤性钙化,长期接受阿法骨化醇治疗。停用维生素D类似物并开始每日血液透析后,她的肿瘤性钙沉积物迅速溶解,同时突然出现与甲状旁腺激素(PTH)无关的短暂高钙血症,一旦软组织沉积物消失,高钙血症即消退。

结论

软组织钙化沉积物的吸收可能导致与甲状旁腺激素(PTH)无关的短暂高钙血症。在CKD患者中,这种高钙血症导致PTH水平降低,这使其有别于三发性甲状旁腺功能亢进,尽管PTH可能不会像非CKD患者中与PTH无关的高钙血症那样被完全抑制。

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