Adefovir-induced Fanconi syndrome associated with osteomalacia

Clinical and Molecular Hepatology

Yeo-Joo Kim¹  Hong-Soo Kim¹  Samel Park¹  Woo-Il Kim¹  Eun Young Lee¹  Dai-Hyun Cho¹  Sang Mi Lee²  Ji-Hye Lee³  Ji-Hee Kim⁴  Kyu-Sang Park⁴  Seung-Kuy Cha⁴ 

[1] Department of Internal Medicine, Soonchunhyang University Cheonan Hospital, Cheonan, Korea;Department of Nuclear Medicine, Soonchunhyang University Cheonan Hospital, Cheonan, Korea;Department of Pathology, Soonchunhyang University Cheonan Hospital, Cheonan, Korea;Department of Physiology, Yonsei University Wonju College of Medicine, Wonju, Korea;

关键词: Adefovir;    Fanconi syndrome;    Mitochondria;    Proximal tubules;    Osteomalacia;   

DOI  :  10.3350/cmh.2017.0009

来源: DOAJ

【 摘 要 】

Fanconi syndrome is a dysfunction of the proximal renal tubules that results in impaired reabsorption and increased urinary loss of phosphate and other solutes. The pathophysiology of drug-induced Fanconi syndrome is unclear. Here we report the case of a 36-year-old woman who presented with pain in multiple bones and proteinuria. She had a 7-year history of taking adefovir at 10 mg/day for chronic hepatitis B. Three years previously she had received surgery for a nontraumatic right femur neck fracture, after which she continued to complain of pain in multiple bones, and proteinuria, glycosuria, and phosphaturia were noted. The findings of a light-microscope examination of a renal biopsy sample were normal, but mitochondrial damage of the proximal tubules was evident in electron microscopy. Western blot analysis revealed that the level of serum fibroblast growth factor 23 (FGF23) was lower than in normal controls. After 2 months of treatment, hypophosphatemia and proximal tubular dysfunction were reversed, and serum FGF23 had normalized. This case suggests that direct mitochondrial damage in proximal tubules can cause drug-induced Fanconi syndrome associated with osteomalacia.

【 授权许可】

Unknown