Abstract: SA-PO383
Looking Beyond Tenofovir Renal Toxicity as the Cause of Bone Disease in HIV
Session Information
- Genetic and Diagnostic Trainee Case Reports
November 09, 2019 | Location: Exhibit Hall, Walter E. Washington Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Trainee Case Report
- 402 Bone and Mineral Metabolism: Clinical
Authors
- Maibam, Amita, University of Kentucky, Lexington, Kentucky, United States
- Castellanos, Ana L., University of Kentucky, Lexington, Kentucky, United States
- Thornton, Alice, University of Kentucky, Lexington, Kentucky, United States
- Rao, Madhumathi, University of Kentucky, Lexington, Kentucky, United States
Introduction
Chronic kidney disease (CKD) with tubular dysfunction from tenofovir therapy in HIV disease is frequently associated with bone disease. Here we present a patient referred for evaluation of osteoporosis.
Case Description
A 48-year-old African American phenotypic female with CKD stage 3a-A3 and sub-nephrotic proteinuria, was referred for osteopenia on bone densitometry in the setting of prior history of right hand fracture with minor trauma. Her past medical history was notable for HIV/AIDS diagnosed 24 years ago, for which she was on antiretroviral therapy (ART) including Tenofovir Disoproxil Fumarate (TDF) and protease inhibitors (PI). Upon evaluation, laboratory data showed serum creatinine of 1.5 mg/dL (eGFR 50 mL/min), low normal serum phosphorus with fractional excretion of phosphorus in the urine ~15% and glycosuria. There was mild elevation of serum alkaline phosphatase although bone alkaline phosphatase was normal. Other bone turnover markers (osteocalcin, C-Telopeptide and N-Telopeptide) were in the normal range. Patient underwent bone biopsy with double tetracycline labeling to evaluate turnover and mineralization; histological results showed high turnover osteoporosis with normal mineralization. Patient was started on anti-resorptive therapy with Alendronate.
Patient was transitioned to combination ART (dolutegravir, abacavir, lamivudine) 2 years earlier, with improvements in renal parameters. Further review of medications revealed she was being treated with estradiol for gender dysphoria (male to female transition) and had levels below target; estradiol therapy was increased to better support hormone status and thereby mitigate bone loss.
Discussion
Although the impacts of HIV, ART with TDF and PI’s, CKD, and tubular dysfunction contribute cumulatively to long-term consequences for bone health, in this patient, hypogonadism related to transgender status was likely a major contributing factor at the time of evaluation. This report highlights that bone disease in CKD patients with HIV is multifactorial and a potentially dynamic process over time in the context of evolving risk factors. Accurate diagnosis remains critical for optimal management.