Department of Kidney Transplant Surgery and Urology, Sapporo City General Hospital, Sapporo, Japan.
Department of Renal and Genitourinary Surgery, Hokkaido University, Sapporo, Japan.
Nephron. 2023;147 Suppl 1:101-105. doi: 10.1159/000530340. Epub 2023 Mar 24.
Acute kidney injury (AKI) due to rhabdomyolysis occurs because of renal ischemia or acute tubular necrosis due to the deposition of myoglobin casts in the renal tubules. Donors with AKI due to rhabdomyolysis are not contraindication for transplantation. However, the dark red kidney raises concerns about renal hypofunction or primary nonfunction after transplantation. We report the case of a 34-year-old man with a 15-year history of hemodialysis for chronic renal failure due to congenital anomalies of the kidney and urinary tract. The patient received a renal allograft from a young woman who suffered cardiac death. The serum creatinine (sCre) level of the donor at the time of transport was 0.6 mg/dL, and renal ultrasonography revealed no abnormalities in renal morphology or blood flow. Her serum creatinine kinase level increased to 57,000 IU/L 58 h after femoral artery cannulation and sCre level worsened to 1.4 mg/dL, suggesting AKI due to rhabdomyolysis. However, since the urine output of the donor was maintained, the sCre elevation was thought to be nonproblematic. The allograft had a dark red appearance at the time of procurement. The perfusion of the isolated kidney was good, but the dark red color did not improve. A 0-h biopsy showed flattening of the renal tubular epithelium and absence of the brush border and myoglobin casts in 30% of the renal tubules. Rhabdomyolysis-related tubular damage was diagnosed. Hemodialysis was discontinued on postoperative day 14. Twenty-four days after the operation, the transplanted kidney function progressed favorably (sCre 1.18 mg/dL), and the patient was discharged. Protocol biopsy 1 month after transplantation showed disappearance of myoglobin casts and improvement in renal tubular epithelial damage. The patient's sCre level was approximately 1.0 mg/dL 24 months after transplantation, and he is doing well without complications.
横纹肌溶解症导致的急性肾损伤（AKI）是由于肾缺血或急性肾小管坏死，肌红蛋白管型在肾小管中沉积所致。横纹肌溶解症导致 AKI 的供者并非移植的禁忌证。然而，暗红色肾脏会让人担心移植后肾功能减退或原发性无功能。我们报告了 1 例 34 岁男性患者的病例，该患者因先天性肾和尿路畸形，15 年来一直接受血液透析治疗慢性肾衰竭。患者接受了一名年轻女性的肾移植，该女性死于心脏骤停。供者在运输时的血清肌酐（sCre）水平为 0.6mg/dL，肾脏超声检查显示肾脏形态或血流无异常。供者股动脉插管后 58 小时，血清肌酸激酶水平升高至 57000IU/L，sCre 水平恶化至 1.4mg/dL，提示横纹肌溶解症导致的 AKI。然而，由于供者的尿量保持不变，sCre 的升高被认为是无问题的。供肾在采集时呈暗红色外观。分离肾的灌注良好，但暗红色颜色没有改善。0 小时活检显示 30%的肾小管上皮扁平，刷状缘缺失，并且有肌红蛋白管型。诊断为与横纹肌溶解相关的肾小管损伤。术后第 14 天停止血液透析。术后 24 天，移植肾功能良好进展（sCre 为 1.18mg/dL），患者出院。移植后 1 个月的方案活检显示肌红蛋白管型消失，肾小管上皮损伤改善。移植后 24 个月，患者的 sCre 水平约为 1.0mg/dL，他状况良好，没有并发症。
