Sawada Anri, Kawanishi Kunio, Morikawa Shohei, Nakano Toshihiro, Kodama Mio, Mitobe Mitihiro, Taneda Sekiko, Koike Junki, Ohara Mamiko, Nagashima Yoji, Nitta Kosaku, Mochizuki Takahiro
Department of Surgical Pathology, Tokyo Women's Medical University, 8-1 Kawadacho, Shinjuku, Tokyo, 162-8666, Japan.
Department of Medicine Kidney Center, Tokyo Women's Medical University, Tokyo, Japan.
BMC Nephrol. 2018 Mar 27;19(1):72. doi: 10.1186/s12882-018-0845-1.
Vancomycin is the first-line antibiotic for methicillin-resistant Staphylococcus aureus and coagulase-negative strains. The risk of vancomycin-induced acute kidney injury increases with plasma vancomycin levels. Vancomycin-induced acute kidney injury is histologically characterized by acute interstitial nephritis and/or acute tubular necrosis. However, only 12 biopsy-proven cases of vancomycin-induced acute kidney injury have been reported so far, as renal biopsy is rarely performed for such cases. Current recommendations for the prevention or treatment of vancomycin-induced acute kidney injury are drug monitoring of plasma vancomycin levels using trough level and drug withdrawal. Oral prednisone and high-flux haemodialysis have led to the successful recovery of renal function in some biopsy-proven cases.
We present the case of a 41-year-old man with type 1 diabetes mellitus, who developed vancomycin-induced acute kidney injury during treatment for Fournier gangrene. His serum creatinine level increased to 1020.1 μmol/L from a baseline of 79.6 μmol/L, and his plasma trough level of vancomycin peaked at 80.48 μg/mL. Vancomycin discontinuation and frequent haemodialysis with high-flux membrane were immediately performed following diagnosis. Renal biopsy showed acute tubular necrosis and focal acute interstitial nephritis, mainly in the medullary rays (medullary ray injury). There was no sign of glomerulonephritis, but mild diabetic changes were detected. He was discharged without continuing haemodialysis (serum creatinine level, 145.0 μmol/L) 49 days after initial vancomycin administration.
This case suggests that frequent haemodialysis and renal biopsy could be useful for the treatment and assessment of vancomycin-induced acute kidney injury, particularly in high-risk cases or patients with other renal disorders.
万古霉素是耐甲氧西林金黄色葡萄球菌和凝固酶阴性菌株的一线抗生素。万古霉素诱导的急性肾损伤风险随血浆万古霉素水平升高而增加。万古霉素诱导的急性肾损伤在组织学上的特征是急性间质性肾炎和/或急性肾小管坏死。然而,迄今为止,仅有12例经活检证实的万古霉素诱导的急性肾损伤病例报道,因为此类病例很少进行肾活检。目前预防或治疗万古霉素诱导的急性肾损伤的建议是通过谷浓度监测血浆万古霉素水平并停药。口服泼尼松和高通量血液透析已使一些经活检证实的病例肾功能成功恢复。
我们报告了一名41岁1型糖尿病男性患者,其在治疗福尼尔坏疽期间发生了万古霉素诱导的急性肾损伤。他的血清肌酐水平从基线的79.6 μmol/L升至1020.1 μmol/L,其血浆万古霉素谷浓度峰值达到80.48 μg/mL。诊断后立即停用万古霉素并使用高通量膜进行频繁血液透析。肾活检显示急性肾小管坏死和局灶性急性间质性肾炎,主要位于髓放线(髓放线损伤)。没有肾小球肾炎的迹象,但检测到轻度糖尿病改变。在首次给予万古霉素49天后,他出院时无需继续血液透析(血清肌酐水平为145.0 μmol/L)。
该病例表明,频繁血液透析和肾活检可能有助于万古霉素诱导的急性肾损伤的治疗和评估,特别是在高危病例或患有其他肾脏疾病的患者中。