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Rhabdomyolysis-induced acute kidney injury in a patient with undifferentiated connective tissue disease: A case report and literature review rhabdomyolysis-induced AKI in a patient with UCTD

机译:横纹肌溶解症致未分化结缔组织病患者的急性肾损伤:一例病例报告和文献综述UCTD患者横纹肌溶解症所致的AKI

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Rationale: 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. Patient concerns: 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. Diagnosis: The patient was diagnosed with rhabdomyolysis -induced AKI secondary to UCTD. Interventions: The patient was successfully treated with intravenous methylprednisolone with other supportive treatment. Outcomes: A fter 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. Lessons: 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.
机译:理由:急性肾损伤(AKI)占住院人数的8%至16%,并且可使医院死亡率增加四倍,给健康经济带来了沉重负担。急性肾损伤(AKI)主要是由于脱水,休克,感染,败血症,心脏病或肾毒性药物的副作用引起的。横纹肌溶解症患者中约10%至60%会发展为AKI,而10%的AKI可归因于横纹肌溶解症。然而,以前从未报道过横纹肌溶解诱导的继发于未分化结缔组织病(UCTD)的AKI。病人担忧:我们报告了一位UCTD的50岁男性,表现出黑褐色尿液,上肢肿胀和浮肿以及尿量减少。诊断:该患者被诊断为横纹肌溶解引起的继发于UCTD的AKI。干预措施:该患者已成功接受静脉内甲基强的松龙及其他支持治疗。结果:入院后开始服用木炭片,碳酸氢钠和静脉注射液的三天后,患者的血清肌酐从145.0μmol/ L轻度变化至156.0μmol/ L,但尿量从1000 mL / 24 h增加到2400 mL / 24 h,他的肌酸激酶(CK)和肌红蛋白分别从474 IU / L上升到962 IU / L和从641.5ng / mL上升到1599 ng / mL。然后,我们尝试通过给予糖皮质激素来凭经验启动UCTD治疗。每天服用40 mg甲基强的松龙后,第二天血清肌酐水平降至97μmol/ L,在1周内CK降至85 IU / L,在10天内肌红蛋白降至65.05 ng / mL。每天给予4 mg维持剂量时,患者肌酐或CK水平未见异常。经验教训:关于横纹肌溶解引起的AKI与UCTD之间的关联的报道很少,其机制仍不清楚。临床医生应意识到UCTD是横纹肌溶解引起的AKI的可能原因。

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