背景:急性肾损伤(AKI)占住院人数的8%至16%,并且可以使医院死亡率翻两番,给卫生经济带来沉重负担。急性肾损伤(AKI)主要由脱水引起,震惊,感染,脓毒症,心脏病,或作为肾毒性药物的副作用。约10%至60%的横纹肌溶解症患者发生AKI,10%的AKI可归因于横纹肌溶解。然而,以前很少报道横纹肌溶解症引起的继发于未分化结缔组织病(UCTD)的AKI。
方法:我们报告了一名50岁的UCTD男性,表现为深棕色尿液,上肢肿胀和水肿,尿量减少。
方法:患者被诊断为横纹肌溶解症引起的UCTD继发AKI。
方法:患者成功接受静脉注射甲基强的松龙和其他支持治疗。
结果:开始药用炭片治疗3天后,入院时的碳酸氢钠和静脉输液,患者的血清肌酐从145.0μmol/L轻度变化至156.0μmol/L,但尿量从1000毫升/24小时增加到2400毫升/24小时,他的肌酸激酶(CK)和肌红蛋白从474IU/L上升到962IU/L,从641.5ng/mL上升到1599ng/mL,分别。然后,我们尝试通过给予皮质类固醇来经验性地开始UCTD治疗。每天服用40毫克甲基强的松龙后,第二天血清肌酐降到97μmol/L,CK在1周内降至85IU/L,肌红蛋白在10天内降至65.05ng/mL。当每天给予4毫克的维持剂量时,患者的肌酐或CK水平未见异常.
结论:关于横纹肌溶解症诱导的AKI与UCTD之间的关系及其机制的报道尚不清楚。临床医生应该意识到UCTD是横纹肌溶解引起的AKI的可能原因。
BACKGROUND: 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.
METHODS: 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.
METHODS: The patient was diagnosed with rhabdomyolysis-induced AKI secondary to UCTD.
METHODS: The patient was successfully treated with intravenous methylprednisolone with other supportive treatment.
RESULTS: 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.
CONCLUSIONS: 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.