Mai Hongxia, Zhao Yuliang, Salerno Stephen, Li Yi, Yang Letian, Fu Ping
Division of Nephrology, Kidney Research Institute, West China Hospital of Sichuan University, Chengdu, China.
Department of Biostatistics, University of Michigan, Ann Arbor, MI.
Medicine (Baltimore). 2019 Jul;98(30):e16492. doi: 10.1097/MD.0000000000016492.
Acute kidney injury (AKI) accounts for 8% to 16% of hospital admissions and can quadruple hospital mortality, placing a serious burden on the health economy. Acute kidney injury (AKI) is mainly caused by dehydration, shock, infection, sepsis, heart disease, or as a side-effect of nephrotoxic drugs. About 10% to 60% of patients with rhabdomyolysis develop AKI, and 10% of AKI is attributable to rhabdomyolysis. However, rhabdomyolysis-induced AKI secondary to undifferentiated connective tissue disease (UCTD) has rarely been reported before.
We report the case of a 50-year-old male of UCTD presented with dark brown urine, swelling and edema of the upper limbs, and decreased urine output.
The patient was diagnosed with rhabdomyolysis-induced AKI secondary to UCTD.
The patient was successfully treated with intravenous methylprednisolone with other supportive treatment.
After 3 days of initiating treatment of medicinal charcoal tablets, sodium bicarbonate and intravenous fluids upon admission, the patient's serum creatinine changed mildly from 145.0 μmol/L to 156.0 μmol/L, but the urinary output increased from 1000 mL/24 h to 2400 mL/24 h, with his creatine kinase (CK) and myoglobin rose from 474 IU/L to 962 IU/L and from 641.5ng/mL to 1599 ng/mL, respectively. We then tried to empirically initiate UCTD therapy by giving corticosteroids. After the administration of the 40 mg of methylprednisolone daily, the serum creatinine level dropped to 97 μmol/L the second day, CK decreased to 85 IU/L within 1 week and myoglobin decreased to 65.05 ng/mL within 10 days. When maintenance dose of 4 mg daily was given, the patient showed no abnormalities in creatinine or CK levels.
There have been few reports on the association between rhabdomyolysis-induced AKI and UCTD and its mechanism remains unclear. Clinicians should be aware of UCTD as a possible cause to rhabdomyolysis-induced AKI.
急性肾损伤（AKI）占住院患者的8%至16%，可使医院死亡率增加四倍，给卫生经济带来沉重负担。急性肾损伤主要由脱水、休克、感染、脓毒症、心脏病或作为肾毒性药物的副作用引起。约10%至60%的横纹肌溶解症患者会发生急性肾损伤，且10%的急性肾损伤归因于横纹肌溶解症。然而，以前很少报道未分化结缔组织病（UCTD）继发的横纹肌溶解症所致急性肾损伤。
我们报告了一例50岁的未分化结缔组织病男性患者，其出现深棕色尿液、上肢肿胀和水肿以及尿量减少。
该患者被诊断为未分化结缔组织病继发的横纹肌溶解症所致急性肾损伤。
患者接受静脉注射甲泼尼龙及其他支持治疗，治疗成功。
入院后给予药用炭片、碳酸氢钠和静脉输液治疗3天后，患者血清肌酐从145.0μmol/L轻度变化至156.0μmol/L，但尿量从1000ml/24小时增加至2400ml/24小时，其肌酸激酶（CK）和肌红蛋白分别从474IU/L升至962IU/L以及从641.5ng/ml升至1599ng/ml。然后我们尝试通过给予皮质类固醇经验性启动未分化结缔组织病治疗。在每日给予40mg甲泼尼龙后，第二天血清肌酐水平降至97μmol/L，1周内CK降至85IU/L，10天内肌红蛋白降至65.05ng/ml。当给予每日4mg的维持剂量时，患者肌酐或CK水平无异常。
关于横纹肌溶解症所致急性肾损伤与未分化结缔组织病之间的关联报道较少，其机制仍不清楚。临床医生应意识到未分化结缔组织病可能是横纹肌溶解症所致急性肾损伤的一个原因。
