CAJ | 학술논문

目的：分析阿昔洛韦致急性肾损伤的临床表现和病理特征，探讨其可能的发病机制。方法：对6例使用阿昔洛韦后急性肾损害患者的临床资料、实验室检查和肾活检病理资料进行回顾性分析。结果：出现腰痛5例，出现少尿1例，尿液检查均可见不同程度的蛋白尿，血尿2例及白细胞尿2例，血肌酐平均236.67±77.60μmol/L， NAG酶、视黄醇结合蛋白、溶菌酶、微球蛋白等明显升高；肾活检病理示：急性肾小管坏死5例，予以还原型谷胱甘肽治疗3.0±0.89天后肾功能恢复正常；急性间质性肾炎1例，予以小、中剂量泼尼松20~30mg/d治疗，所有患者均未行血液透析治疗。结论：阿昔洛韦所致肾脏损伤临床表现缺乏特异性，以腰痛及肾功能减退为主，可能由于干扰肾小管上皮细胞代谢而导致急性肾损伤。
목적：분석아석락위치급성신손상적림상표현화병리특정，탐토기가능적발병궤제。방법：대6례사용아석락위후급성신손해환자적림상자료、실험실검사화신활검병리자료진행회고성분석。결과：출현요통5례，출현소뇨1례，뇨액검사균가견불동정도적단백뇨，혈뇨2례급백세포뇨2례，혈기항평균236.67±77.60μmol/L， NAG매、시황순결합단백、용균매、미구단백등명현승고；신활검병리시：급성신소관배사5례，여이환원형곡광감태치료3.0±0.89천후신공능회복정상；급성간질성신염1례，여이소、중제량발니송20~30mg/d치료，소유환자균미행혈액투석치료。결론：아석락위소치신장손상림상표현결핍특이성，이요통급신공능감퇴위주，가능유우간우신소관상피세포대사이도치급성신손상。
Objective: To investigate the clinical and pathological manifestations of acute kidney injury(AKI) follow-ing infusion of acyclovir and to discuss its pathogenesis. Method: Six patients who had suffered acyclovir-induced acute kidney injury were enrolled in this restrospective study in our department, their clinical manifestations ,laboratory examina-tions, pathological change, therapy and prognosis were analysed. Results: lumbodynia appeared in 5 patients while only 1 patients encountered olyguria. Urine examinations revealed proteinuria in 6, anemia in 2 and leucocyturia in 2 patients, blood analysis showed the average creatinine reached 236.67±147.60umol/L, and renal tubular damage markers (NAG en-zyme, lysozyme, urinary β 2 microglobulin, Cystatin C etc.) increased obviously. Renal biopsy showed that the histological diagnosis of acute interstitial nephritides(AIN) in 1 patients(17.7%) and acute tubular necrosis(ATN)in 5(83.3%). Pred-nisone(20-30mg/d) was delivered to 1 patient (AIN), the other patients were treated with reduced glutathione. No patient re-ceived renal replacement therapy and the renal function returned to normal 3.0±0.89 days later. Conclusion:The histologi-cal change of acyclovir-induced AKI revealed ATN, while the clinical features showed lumbodynia and renal insufficiency lacking of specificity. Renal fuction was fully restored after a short period of time through symptomatic and reduced glu-tathione therapy, most probably because acyclovir might have caused AKI through interrupting the metabolism of epithelial cells of renal tubules.