Primary hyperparathyroidism, presenting with acute kidney injury in the first trimester of pregnancy; a case report

E. Zakharova, E. Pashkova, D. Levikov, Aza Tseloeva, R. Kuznetsov, O. Ignatchenko, I. Lebedinsky, A. Evsikov, V.R. Gadzhiev, Dmitry Eremin, S. Sorokoletov, E. Rodionov, D. Grekov
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Abstract

Primary hyperparathyroidism (PHPT) is the leading cause of hypercalcemia. Total serum calcium level >3.5 mmol/L is associated with a high risk of a hypercalcemic crisis, manifesting with nausea, vomiting, dehydration, myalgia’s, abdominal pain, acute pancreatitis, acute kidney injury (AKI), cardiac rhythm disorders and disturbances of consciousness. We report here a case of PHPT, manifested with hypercalcemic crisis during pregnancy. A 30-year-old woman in the first trimester of pregnancy admitted complaining on loss of appetite, nausea, vomiting, lower abdomen pain, weakness, and leg pain during the last 10 days. She had a history of two uncomplicated pregnancies, and two episodes of renal colic, her kidney function was normal 2 weeks prior to admission. Work-up showed hypochloremia, hypokalemia, hyponatremia, total serum calcium was 5.34 mmol/L, and serum creatinine 226 µmol/L, and she underwent urgent hemodialysis (HD). Her parathyroid hormone (PTH) was 948 pg/mL, and imaging revealed missed miscarriage 9-10 weeks, soft tissue mass 30x20x33mm near the lower pole of the left lobe of the thyroid gland, small stones in renal calices, and polysegmental pneumonia. She received antibiotics, calcimimetics, and every-day hemodiafiltration (HDF), and underwent vacuum aspiration of uterine cavity and surgical removal of the parathyroidoma. Her PTH shortly returned to the reference level, and serum creatinine dropped to 140 µmol/L after kidney replacement therapy (KRT) secession. Pathology confirmed the diagnosis of parathyroid adenoma. PHPT should be included in the diagnostic algorithm of AKI in pregnancy along with vomiting of pregnant, sepsis, pre-eclampsia and other causes. Successful management of PHPT complications in pregnancy demands multidisciplinary team.
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原发性甲状旁腺功能亢进,在妊娠早期表现为急性肾损伤;病例报告
原发性甲状旁腺功能亢进(PHPT)是导致高钙血症的主要原因。血清总钙水平bb0 3.5 mmol/L与高钙血症危重的高风险相关,表现为恶心、呕吐、脱水、肌痛、腹痛、急性胰腺炎、急性肾损伤(AKI)、心律失常和意识障碍。我们在这里报告一个PHPT的情况下,表现为高钙危机在怀孕期间。一名30岁的怀孕前三个月的妇女承认在过去的10天里抱怨食欲不振,恶心,呕吐,下腹疼痛,虚弱和腿部疼痛。患者有两次无并发症妊娠史,两次肾绞痛发作,入院前2周肾功能正常。检查显示低氯血症、低钾血症、低钠血症,血清总钙5.34 mmol/L,血清肌酐226µmol/L,行紧急血液透析(HD)。患者甲状旁腺激素948 pg/mL,影像学示9-10周漏产,甲状腺左叶下极附近软组织肿块30x20x33mm,肾肾盂小结石,多节段性肺炎。给予抗生素、钙化剂、每日血液滤过(HDF)、子宫腔真空抽吸及手术切除甲状旁腺瘤。她的PTH很快恢复到参考水平,肾替代治疗(KRT)结束后血清肌酐降至140µmol/L。病理证实为甲状旁腺瘤。妊娠期AKI的诊断算法中应包括PHPT与妊娠呕吐、败血症、先兆子痫等原因。妊娠期PHPT并发症的成功管理需要多学科的团队。
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