Arora Swati, Bhargava Arpit, Jasnosz Katherine, Clark Barbara
Division of Nephrology and Hypertension, Department of Medicine, Temple University School of Medicine, Pittsburgh, Pa., USA.
Case Rep Nephrol Urol. 2012 Jul;2(2):165-71. doi: 10.1159/000345278. Epub 2012 Nov 21.
We report a previously unrecognized complication of severe acute kidney injury (AKI) after the administration of pegfilgrastim with biopsy findings of mesangioproliferative glomerulonephritis (GN) and tubular necrosis. A 51-year-old white female with a history of breast cancer presented to the hospital with nausea, vomiting and dark urine 2 weeks after her third cycle of cyclophosphamide and docetaxel along with pegfilgrastim. She was found to have AKI with a serum creatinine (Cr) level of 6.9 mg/dl (baseline 0.7). At that time, her AKI was believed to be related to prior sepsis and/or daptomycin exposure that had occurred 5 weeks earlier. She was dialyzed for 6 weeks, after which her kidney function recovered to near baseline, but her urinalysis (UA) still showed 3.5 g protein/day and dysmorphic hematuria. Repeat blood cultures and serological workup (complement levels, hepatitis panel, ANA, ANCA and anti-GBM) were negative. She received her next cycle of chemotherapy with the same drugs. Two weeks later, she developed recurrent AKI with a Cr level of 6.7 mg/dl. A kidney biopsy showed mesangioproliferative GN, along with tubular epithelial damage and a rare electron-dense glomerular deposit. Pegfilgrastim was suspected as the inciting agent after exclusion of other causes. Her Cr improved to 1.4 mg/dl over the next 3 weeks, this time without dialysis. She had the next 2 cycles of chemotherapy without pegfilgrastim, with no further episodes of AKI. A literature review revealed a few cases of a possible association of filgrastim with mild self-limited acute GN. In conclusion, pegfilgrastim may cause GN with severe AKI. Milder cases may be missed and therefore routine monitoring of renal function and UA is important.
我们报告了一例在使用培非格司亭后出现的严重急性肾损伤(AKI)的先前未被认识的并发症,肾活检结果为系膜增生性肾小球肾炎(GN)和肾小管坏死。一名51岁有乳腺癌病史的白人女性,在接受环磷酰胺、多西他赛联合培非格司亭的第三个周期化疗2周后,因恶心、呕吐和深色尿入住医院。她被发现患有AKI,血清肌酐(Cr)水平为6.9mg/dl(基线值0.7)。当时,她的AKI被认为与5周前发生的先前败血症和/或达托霉素暴露有关。她接受了6周的透析,之后肾功能恢复至接近基线水平,但尿液分析(UA)仍显示每天有3.5g蛋白质和畸形血尿。重复血培养和血清学检查(补体水平、肝炎检测、抗核抗体、抗中性粒细胞胞浆抗体和抗肾小球基底膜抗体)均为阴性。她接受了下一周期相同药物的化疗。两周后,她再次出现AKI,Cr水平为6.7mg/dl。肾活检显示系膜增生性GN,伴有肾小管上皮损伤和罕见的电子致密性肾小球沉积物。在排除其他原因后,怀疑培非格司亭是致病因素。在接下来的3周内,她的Cr水平改善至1.4mg/dl,此次未进行透析。她在接下来的2个周期化疗中未使用培非格司亭,未再出现AKI发作。文献综述显示有几例可能与非格司亭相关的轻度自限性急性GN病例。总之,培非格司亭可能导致GN伴严重AKI。较轻的病例可能被漏诊,因此常规监测肾功能和UA很重要。