Clin Nephrol. 2024 Feb;101(2):93-98. doi: 10.5414/CN110925.
A sporadic occurrence of Fanconi syndrome associated with adefovir dipivoxil (ADV) has been reported, particularly when confirmed by renal biopsy. This study presents the case of a 53-year-old man who had been taking ADV 10 mg daily for 10 years to treat chronic hepatitis B (CHB) and subsequently developed Fanconi syndrome. The clinical manifestations included hypophosphatemic osteomalacia, glucosuria, renal tubular acidosis, low-molecular-weight proteinuria, and renal insufficiency. Renal biopsy revealed significant injury to proximal tubular epithelial cells, including vacuolar degeneration and regeneration of tubular epithelial cells. The ultrastructural pathology indicated severe morphological abnormalities of mitochondria, such as densely packed and enlarged mitochondria, with loss, blunting, and disordered arrangement of cristae. Following discontinuation of ADV and supplementation with oral phosphate, hypophosphatemia, glucosuria, and proteinuria were resolved. These findings support the previous hypothesis that ADV-induced nephrotoxicity may involve mitochondrial injury.
散发性与阿德福韦酯（ADV）相关的 Fanconi 综合征已有报道，特别是经肾活检证实时。本研究报告了一例 53 岁男性患者，他因慢性乙型肝炎（CHB）而每日服用 ADV 10mg，10 年后出现 Fanconi 综合征。临床表现包括低磷性骨软化症、糖尿、肾小管性酸中毒、低分子量蛋白尿和肾功能不全。肾活检显示近端肾小管上皮细胞损伤明显，包括空泡变性和肾小管上皮细胞再生。超微结构病理学显示线粒体严重形态异常，如线粒体致密堆积和增大，嵴丢失、变钝和排列紊乱。停用 ADV 并口服补充磷酸盐后，低磷血症、糖尿和蛋白尿得到缓解。这些发现支持 ADV 诱导的肾毒性可能涉及线粒体损伤的先前假说。
