Abstract: FR-PO0684
Tenofovir-Induced Tubulopathy and Podocytopathy in a Patient with Chronic Hepatitis B: A Double-Hit Hypothesis
Session Information
- Glomerular Diseases: Membranous Nephropathy, FSGS, and Podocytopathies
October 23, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics
Authors
- Mercado, Dick Darrel Paril, Veterans Memorial Medical Center, Quezon City, NCR, Philippines
- Mora, Joselito Aquino, Veterans Memorial Medical Center, Quezon City, NCR, Philippines
Introduction
Tenofovir Disoproxil Fumarate (TDF), a nucleotide analogue used for Hepatitis B and HIV, is a known cause of Fanconi syndrome, however glomerulopathy is rarely reported. We present rare case of Tenofovir-induced Fanconi syndrome (TFS) and Focal Segmental Glomerulosclerosis (FSGS), highlighting a direct tubular damage and a secondary glomerular maladaptation.
Case Description
A 56-year-old, female (history of hypertension and breast cancer on remission) on TDF for Hepatitis B for 3 years with undetectable HBV DNA, presented with generalized weakness and bubbly urine. Laboratories revealed Serum Creatinine (SCr) 2.3 mg/dL (eGFR 24 mL/min/1.73m2), K+ 2.7 meqs/L, normoglycemic glucosuria (+4 dipstick), UPCR 3.5 g/day and hyperchloremic metabolic acidosis and Urine K/Urine Creatinine 〉2.0.
Biopsy was done which revealed: FSGS not-otherwise-specified with 40% IFTA and incidental IgA (Figure 1). TDF was shifted to Entecavir 0.5 mg/day. PET SCAN and Liver Elastography ruled out malignancy and cirrhosis. Decreasing trend of SCr and UPCR with resolution of metabolic acidosis after 5 months discontinuation of TDF was noted.
Discussion
TFS cases were reported after a mean of 11 months of tenofovir exposure [1] which is attributed primarily to mitochondrial toxicity due to direct Complex V inhibition leading to ATP depletion. [2] In relation to our case, we hypothesize a dual mechanism of pathophysiology:
1. Primary Proximal Tubule Mitochondrial toxicity – ATP depletion leads to Fanconi Syndrome.
2. Secondary Glomerular maladaptation – Moderate IFTA-induced nephron loss leads to intraglomerular hypertension causing chronic mechanical strain on remaining podocyte manifesting as Secondary FSGS NOS. [3]
Nephrotic-range proteinuria and Tubulopathy resolution after TDF discontinuation could point to TDF as the cause.
In summary, this case underscores the necessity of consistent renal surveillance for patients receiving TDF, as the drug can trigger concurrent tubulopathy and podocytopathy, resulting in insidious and progressive renal damage. [4].
Acknowledgment
Sources:
1. Kapadia J, et al. Indian J Pharmacol. 2013; 45(2):191-2.
2. Sluis-Cremer N, et al. American Physiological Society. 2023; 4(3).
3. Mehmet MA, et al. Annual Review Pathology. 2025; 20:329-353.
4. Holt, SG, et al. AIDS Research Therapy. 2014; 11, 35.
Note: Final high resolution images are currently pending logistical processing and are expected by July 7, 2026. All relevant digital pathological files will be submitted directly to kidneyweek@asn-online.org.