Adefovir-induced Fanconi syndrome associated with osteomalacia.
- Author:
Samel PARK
1
;
Woo Il KIM
;
Dai Hyun CHO
;
Yeo Joo KIM
;
Hong Soo KIM
;
Ji Hee KIM
;
Seung Kuy CHA
;
Kyu Sang PARK
;
Ji Hye LEE
;
Sang Mi LEE
;
Eun Young LEE
Author Information
- Publication Type:Case Report
- Keywords: Adefovir; Fanconi syndrome; Mitochondria; Proximal tubules; Osteomalacia
- MeSH: Adult; Biopsy; Blotting, Western; Fanconi Syndrome*; Female; Femoral Neck Fractures; Fibroblast Growth Factors; Glycosuria; Hepatitis B, Chronic; Humans; Hypophosphatemia; Hypophosphatemia, Familial; Kidney Tubules, Proximal; Microscopy, Electron; Mitochondria; Osteomalacia*; Proteinuria
- From:Clinical and Molecular Hepatology 2018;24(3):339-344
- CountryRepublic of Korea
- Language:English
- Abstract: 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.
