Lessons for the clinical nephrologist: recurrence of nephrotic syndrome induced by SARS-CoV-2

J Nephrol. 2020 Dec;33(6):1369-1372. doi: 10.1007/s40620-020-00855-5. Epub 2020 Sep 5.

Abstract

SARS-CoV-2 is characterized by a multiorgan tropism including the kidneys. Recent autopsy series indicated that SARS-CoV-2 can infect both tubular and glomerular cells. Whereas tubular cell infiltration may contribute to acute kidney injury, data on a potential clinical correlative to glomerular affection is rare. We describe the first case of nephrotic syndrome in the context of COVID-19 in a renal transplant recipient. A 35 year old male patient received a kidney allograft for primary focal segmental glomerulosclerosis (FSGS). Three months posttransplant a recurrence of podocytopathy was successfully managed by plasma exchange, ivIG, and a conversion from tacrolimus to belatacept (initial proteinuria > 6 g/l decreased to 169 mg/l). Six weeks later he was tested positive for SARS-CoV-2 and developed a second increase of proteinuria (5.6 g/l). Renal allograft biopsy revealed diffuse podocyte effacement and was positive for SARS-CoV-2 in RNA in-situ hybridation indicating a SARS-CoV-2 associated recurrence of podocytopathy. Noteworthy, nephrotic proteinuria resolved spontaneously after recovering from COVID-19. The present case expands the spectrum of renal involvement in COVID-19 from acute tubular injury to podocytopathy in renal transplant recipients. Thus, it may be wise to test for SARS-CoV-2 prior to initiation of immunosuppression in new onset glomerulopathy during the pandemic.

Keywords: COVID-19; Podocytopathy; SARS-CoV-2.

Publication types

  • Case Reports

MeSH terms

  • Adult
  • Biopsy
  • COVID-19 / complications*
  • COVID-19 / epidemiology
  • Humans
  • Kidney Glomerulus / pathology*
  • Male
  • Nephrologists / standards*
  • Nephrotic Syndrome / diagnosis
  • Nephrotic Syndrome / etiology*
  • Pandemics
  • Recurrence