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Abstract: TH-PO532

Hepatitis B and C Dual Infection and Collapsing Glomerulopathy: Report of a Rare Association

Session Information

  • Trainee Case Reports - I
    October 25, 2018 | Location: Exhibit Hall, San Diego Convention Center
    Abstract Time: 10:00 AM - 12:00 PM

Category: Trainee Case Reports

  • 1201 Glomerular Diseases: Fibrosis and Extracellular Matrix


  • Espinoza, Flor, University of Texas Medical Branch, Galveston, Texas, United States
  • Afrouzian, Marjan, University of Texas Medical Branch, Galveston, Texas, United States
  • Omitogun, Tunde Olawale, University of Texas Medical Branch, Galveston, Texas, United States
  • Kassem, Hania, University of Texas Medical Branch, Galveston, Texas, United States

Collapsing Glomerulopathy (CG) is marked by severe hypertension and proteinuria, poor response to corticosteroids, and a rapid progression to end-stage renal disease. Many viral illnesses, including HIV, have been implicated in the pathogenesis of this disease. However, the association between CG and Hepatitis C virus (HCV) or Hepatitis B virus (HBV) remains less clear.

Case Description

A 55 y/o man with a history of HTN, Hepatitis B and C, and liver cirrhosis presented with altered mental status. He was hemodynamically stable, however, had significant laboratory derangements including a Cr of 19 mg/dl (recent baseline was 0.9), K of 7.3, CO2 11, and pH of 7.14. His lactic acid, coagulation panel and bilirubin levels were within normal limits. Urine microscopy showed muddy brown casts and no hematuria. He was also found to have nephrotic range proteinuria. HIV and Parvovirus B19 IgM antibodies were negative. Dialysis had to be initiated for uremia, hyperkalemia and acidemia. By light microscopy, the renal biopsy showed segmental glomerulosclerosis in 10/17 viable glomeruli with 3 glomeruli showing a collapsing pattern and podocyte hyperplasia. Severe interstitial fibrosis and tubular atrophy (IFTA) was noted. Immunofluorescence and electron microscopy showed tubulo-reticular inclusions (TRIs) within the endothelial cytoplasm.

Patient’s mental status, electrolytes and acidemia improved with dialysis. However, he remained dialysis dependent and given the severity of his kidney disease on presentation and the degree of IFTA, renal injury was deemed unlikely to recover.


The uncommon association of CG and HCV infection in HIV-negative patients has been reported, mainly in patients treated with interferon. There has been only one reported case of CG associated with HBV infection. As our patient was HIV-negative and was not treated with interferon, the occurrence of CG was attributed to his dual infection with HBV and HCV, especially since TRIs were found on electron microscopy. It is possible that a synergistic action during this dual infection led to the development of CG, a glomerular lesion that rarely occurs with either viral infection alone. This case highlights the need for further research to elucidate the pathogenetic role HBV and HCV may play in the development of CG.