Sawyer M H, Webb D E, Balow J E, Straus S E
Medical Virology Section, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland.
Am J Med. 1988 Jun;84(6):1067-71. doi: 10.1016/0002-9343(88)90313-0.
Four patients with a chronic fatigue syndrome experienced five episodes of acute renal insufficiency associated with high-dose (500 mg/m2) intravenous acyclovir administered intravenously as one-hour infusions. Nephrotoxicity developed despite precautions to avoid volume contraction. Examination of the urinary sediment of three patients by polarizing microscopy showed birefringent needle-shaped crystals within leukocytes. In the most severely affected patient, a serum creatinine concentration of 8.6 mg/dl developed and the patient underwent percutaneous renal biopsy that revealed foci of interstitial inflammation without tubular necrosis. Urine, blood, and renal tissue levels of acyclovir were high. One patient was rechallenged with low-dose intravenous acyclovir and the four patients later received oral acyclovir, all without adverse effect. The combined data from these patients support crystalluria and obstructive nephropathy as a mechanism of acyclovir-induced renal failure in humans. This experience emphasizes the importance of maintaining adequate hydration during high-dose acyclovir therapy.
4例慢性疲劳综合征患者在接受大剂量（500mg/m²）静脉注射阿昔洛韦（静脉滴注1小时）治疗期间发生了5次急性肾功能不全。尽管采取了预防措施以避免血容量减少，但仍出现了肾毒性。通过偏振显微镜检查3例患者的尿沉渣，发现白细胞内有双折射针状晶体。在受影响最严重的患者中，血清肌酐浓度升至8.6mg/dl，该患者接受了经皮肾活检，结果显示存在间质炎症灶但无肾小管坏死。阿昔洛韦的尿液、血液和肾组织水平均很高。1例患者再次接受小剂量静脉注射阿昔洛韦治疗，另外4例患者随后接受口服阿昔洛韦治疗，均未出现不良反应。这些患者的综合数据支持结晶尿和梗阻性肾病是阿昔洛韦诱导人类肾衰竭的一种机制。这一经验强调了在大剂量阿昔洛韦治疗期间维持充足水化的重要性。
