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Abstract: FR-PO050

The Mosaic of Autoimmunity

Session Information

Category: Coronavirus (COVID-19)

  • 000 Coronavirus (COVID-19)


  • Joshi, Aditi Ashok, Saint Peter's University Hospital, New Brunswick, New Jersey, United States
  • Vasquez Espinosa, William Andres, Saint Peter's University Hospital, New Brunswick, New Jersey, United States
  • Arabi, Nida, Saint Peter's University Hospital, New Brunswick, New Jersey, United States

Lupus nephritis (LN) is one of the most common manifestations affecting 45% of patients with systemic lupus erythematosus (SLE). Here we present a case of rapid progression of LN in the setting of recent COVID-19 infection, suggesting a possible synergistic cascade of cytokines contributing to rapid disease flare up.

Case Description

52-year-old hispanic lady with past medical history of hypertension and newly diagnosed SLE presented to the clinic with chief complaint of generalized anasarca, fatigue and low back ache. She was found to have a hemoglobin of 8.8 along with severe leukopenia. Urinalysis was positive for large amount of blood, protein with a protein: creatinine ratio of 9 gm. ANA titer was positive along with low levels of C3 complement and normal levels of C4 complement. Creatinine of 2.3 which was 4 times higher than her baseline. Labs from 2 months ago showed creatinine of 0.57 . Of note, the patient was diagnosed with COVID-19 a month ago. She had a renal biopsy and was diagnosed with stage IV LN and was started on dialysis.


LN usually has an indolent course with people developing ESRD within 5 years of diagnosis of lupus. This case strikes out as a rapid progression of LN with progression to ESRD within less than 3 months of diagnosis of SLE. COVID-19 a few months before she was diagnosed with Lupus is a possible source of a cytokine storm. Suggested mechanisms of induction of autoimmunity include both molecular mimicry as well as bystander activation whereby the infection may lead to activation of antigen presenting cells that may in turn activate pre-primed auto-reactive T-cells, thus leading to pro-inflammatory mediators, which in turn may lead to tissue damage. Strategies to prevent rapid progression to ESRD in these patients needs to be studied and better understood. Perhaps patients with autoimmune conditions like SLE need more robust management of diseases like COVID-19 which is known to alter and activate the immunological cascade. As per recent literature exaggerated extrafollicular B cell response characteristic of active SLE also characterizes the B cell response to COVID-19. Understanding and targeting the B cell pathway could potentially help dampen a severe response and disease progression. Overlap including racial preponderance of disease severity also needs to be studied further.