Clin Mol Hepatol.  2018 Sep;24(3):339-344. 10.3350/cmh.2017.0009.

Adefovir-induced Fanconi syndrome associated with osteomalacia

• Park S
• Kim WI
• Cho DH
• Kim YJ
• Kim HS
• Kim JH
• Cha SK
• Park KS
• Lee JH
• Lee SM
• Lee EY

• KMID: 2428762
• DOI: http://doi.org/10.3350/cmh.2017.0009

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.

Keyword

Adefovir; Fanconi syndrome; Mitochondria; Proximal tubules; Osteomalacia

MeSH Terms

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
Fibroblast Growth Factors