Adefovir-induced Fanconi syndrome associated with osteomalacia

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...

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Main Authors: Samel Park, 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
Format: Article
Language:English
Published: Korean Association for the Study of the Liver 2018-09-01
Series:Clinical and Molecular Hepatology
Subjects:
Online Access:http://e-cmh.org/upload/pdf/cmh-2017-0009.pdf
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author Samel Park
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_facet Samel Park
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_sort Samel Park
collection DOAJ
description 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.
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spelling doaj.art-d68f87b0062d4e90855c26cfd8df88962022-12-22T02:02:33ZengKorean Association for the Study of the LiverClinical and Molecular Hepatology2287-27282287-285X2018-09-0124333934410.3350/cmh.2017.00091372Adefovir-induced Fanconi syndrome associated with osteomalaciaSamel Park0Woo-Il Kim1Dai-Hyun Cho2Yeo-Joo Kim3Hong-Soo Kim4Ji-Hee Kim5Seung-Kuy Cha6Kyu-Sang Park7Ji-Hye Lee8Sang Mi Lee9Eun Young Lee10 Department of Internal Medicine, Soonchunhyang University Cheonan Hospital, Cheonan, Korea Department of Internal Medicine, Soonchunhyang University Cheonan Hospital, Cheonan, Korea Department of Internal Medicine, Soonchunhyang University Cheonan Hospital, Cheonan, Korea Department of Internal Medicine, Soonchunhyang University Cheonan Hospital, Cheonan, Korea Department of Internal Medicine, Soonchunhyang University Cheonan Hospital, Cheonan, Korea Department of Physiology, Yonsei University Wonju College of Medicine, Wonju, Korea Department of Physiology, Yonsei University Wonju College of Medicine, Wonju, Korea Department of Physiology, Yonsei University Wonju College of Medicine, Wonju, Korea Department of Pathology, Soonchunhyang University Cheonan Hospital, Cheonan, Korea Department of Nuclear Medicine, Soonchunhyang University Cheonan Hospital, Cheonan, Korea Department of Internal Medicine, Soonchunhyang University Cheonan Hospital, Cheonan, KoreaFanconi 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.http://e-cmh.org/upload/pdf/cmh-2017-0009.pdfAdefovirFanconi syndromeMitochondriaProximal tubulesOsteomalacia
spellingShingle Samel Park
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
Adefovir-induced Fanconi syndrome associated with osteomalacia
Clinical and Molecular Hepatology
Adefovir
Fanconi syndrome
Mitochondria
Proximal tubules
Osteomalacia
title Adefovir-induced Fanconi syndrome associated with osteomalacia
title_full Adefovir-induced Fanconi syndrome associated with osteomalacia
title_fullStr Adefovir-induced Fanconi syndrome associated with osteomalacia
title_full_unstemmed Adefovir-induced Fanconi syndrome associated with osteomalacia
title_short Adefovir-induced Fanconi syndrome associated with osteomalacia
title_sort adefovir induced fanconi syndrome associated with osteomalacia
topic Adefovir
Fanconi syndrome
Mitochondria
Proximal tubules
Osteomalacia
url http://e-cmh.org/upload/pdf/cmh-2017-0009.pdf
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