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TDF Bone Toxicity — SCE Infectious Diseases MCQ

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ModerateHIV MedicineTDF Bone ToxicitySCE Infectious Diseases

A 35-year-old man with chronic hepatitis B on Tenofovir AF develops osteoporosis confirmed by DEXA scan (T-score -2.8 at the lumbar spine). His vitamin D is normal. His previous ART included Tenofovir DF for 5 years before switching to TAF. What is the relationship between his prior TDF use and bone disease?

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Correct answer: CTDF causes proximal renal tubular phosphate wasting and direct osteoclast activation, leading to reduced BMD — TAF has significantly less bone toxicity but prior TDF damage may persist

Tenofovir DF is associated with reduced bone mineral density through two mechanisms: (1) proximal tubular phosphate wasting (reducing phosphate available for bone mineralisation — Fanconi-like effect), and (2) direct promotion of osteoclast differentiation. TAF has significantly less bone (and renal) toxicity due to 90% lower plasma Tenofovir levels. Switching from TDF to TAF leads to partial BMD recovery in most patients. However, significant prior bone loss may persist. Standard osteoporosis management (calcium, vitamin D, bisphosphonates if indicated) should be provided.

Reference: BHIVA 2025 – ART guidelines; EACS 2025 – Bone health in HIV