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Abstract: PO0118

De Novo Henoch Schönlein Purpura (HSP) Post Kidney-Pancreas Transplant Triggered by COVID-19 Infection

Session Information

Category: Coronavirus (COVID-19)

  • 000 Coronavirus (COVID-19)

Authors

  • He, Mingyue, Lewis Katz School of Medicine at Temple University, Philadelphia, Pennsylvania, United States
  • Lee, Iris J., Lewis Katz School of Medicine at Temple University, Philadelphia, Pennsylvania, United States
  • Rakhman, Ilay, Lewis Katz School of Medicine at Temple University, Philadelphia, Pennsylvania, United States
  • Constantinescu, Serban, Lewis Katz School of Medicine at Temple University, Philadelphia, Pennsylvania, United States
Introduction

Histologic recurrence of immunoglobulin A (IgA) nephropathy after transplant is common, however, de novo development of HSP is rare post-kidney transplant. We describe a case of HSP with cutaneous and renal allograft findings, triggered by COVID-19 (SARS-CoV-2) infection.

Case Description

A 53-year-old African American (AA) male with history of ESRD secondary to diabetic nephropathy, underwent simultaneous pancreas-kidney transplant. Three months later, he presented with rash on the upper and lower extremities, hand and wrist pain, acute kidney injury and new onset nephrotic syndrome with 6.6g proteinuria and microscopic isomorphic hematuria. He had detectable SARS-CoV-2 RNA in the nasopharyngeal specimen and mild multifocal pneumonia treated with steroids and Remdesivir. Serologic work-up for nephrotic syndrome was negative. A skin biopsy demonstrated leukocytoclastic vasculitis. Renal allograft biopsy showed membrane proliferative and sclerosing glomerulonephritis with dominant IgA staining by immunofluorescence, consistent with IgA nephropathy. He received pulse dose steroids with improvement in kidney graft function and reduction of his proteinuria to 0.6 g four months after steroid treatment.

Discussion

We postulated that our patient developed de novo HSP and nephrotic syndrome as a result of COVID- 19 infection. Podocytopathy and nephrotic syndrome linked to viral infection have been well described, particularly in AA patients with high-risk APOL1 genotype. Key cytokines known to be elevated in COVID19 infection can drive autoimmune responses, such as interferon and IL-6. Cytokine release, uncontrolled activation of both innate and adaptive immune cells, along with genetic variants likely pre-dispose patients to the development of glomerular disease mediated by various immune mechanisms. Published biopsy series consistently demonstrate acute tubular injury as the most common renal manifestation of COVID-19, however, new onset autoimmune diseases such as IgAN may also be triggered by COVID infection. HSP can be a rare complication of COVID-19, and also rarely occurs post-transplant. Glomerular disease and systemic autoimmunity should be recognized as a complication of COVID-19, regardless of the presence or absence of pulmonary findings.