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Abstract: PO0837

AKI and Collapsing Glomerulopathy Associated with COVID-19 and APOL1 High-Risk Genotype

Session Information

Category: Coronavirus (COVID-19)

  • 000 Coronavirus (COVID-19)

Authors

  • Velez, Juan Carlos Q., Department of Nephrology, Ochsner Health System, New Orleans, Louisiana, United States
  • Larsen, Christopher Patrick, Arkana Laboratories, Little Rock, Arkansas, United States
  • Wu, Huijuan, Department of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee, United States
  • Caza, Tiffany, Arkana Laboratories, Little Rock, Arkansas, United States
  • Hernandez-Arroyo, Cesar F., Department of Nephrology, Ochsner Health System, New Orleans, Louisiana, United States
  • Mohamed, Muner, Department of Nephrology, Ochsner Health System, New Orleans, Louisiana, United States
  • Chughtai, Asim, Northwest Indiana Nephrology, Munster, Indiana, United States
  • Sharshir, Moh'd, Division of Nephrology, Tulane University School of Medicine, New Orleans, Louisiana, United States
  • Xie, Liping, Ascension All Saints Hospital - Spring Street Campus, Racine, Wisconsin, United States
  • Acheampong, Ellen, Department of Pathology, Massachusetts General Hospital, Boston, Massachusetts, United States
  • Rosales, Ivy, Department of Pathology, Massachusetts General Hospital, Boston, Massachusetts, United States
  • Colvin, Robert B., Department of Pathology, Massachusetts General Hospital, Boston, Massachusetts, United States
  • Fogo, Agnes B., Department of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee, United States

Group or Team Name

  • Ochsner Nephrology - Arkana - Vanderbilt
Background

Acute kidney injury (AKI), with or without proteinuria, has been described in patients with Coronavirus disease 2019 (COVID-19). Kidney involvement in COVID-19 has been reported to be of greater severity in African Americans (AA). Herein, we report genetic, histopathological and molecular findings in 6 AA patients with COVID-19 presenting with AKI and de novo nephrotic-range proteinuria.

Methods

Percutaneous kidney biopsies were performed in 6 patients with COVID-19 with respiratory manifestations and proteinuric AKI. Peripheral blood was obtained for apolipoprotein L1 (APOL1) risk allele assessment. Kidney tissue was also examined by in situ hybridization (ISH) for viral detection and by NanoString for COVID-19 associated genes and genes related to tubular injury.

Results

Six AA patients with COVID-19 (4 men, 2 women), mean age 55 years (37-65) were included in the series. At biopsy day, the mean serum creatinine was 6.5 mg/dL (2.9 – 11.4) and the mean urine protein-to-creatinine ratio was 11.5 g (3.6 – 25.0). Kidney biopsy specimen showed collapsing glomerulopathy, extensive foot process effacement, microcystic tubular dilation and focal or diffuse acute tubular injury. Three patients had reticular endothelial aggregates. No viral particles were identified. ISH and NanoString showed absence of SARS-CoV-2 RNA. NanoString analysis showed changes in genes related to acute tubular injury and an increase in chemokine gene expression. All 6 patients tested positive for 2 APOL1 risk alleles. Two patients died, 1 remained dialysis dependent, 2 partially recovered after transient need for dialysis and 1 partially recovered without needing dialysis.

Conclusion

Collapsing glomerulopathy in AA patients with COVID-19 was associated with high risk variants of APOL1. Direct viral infection in the kidneys was not observed, suggesting a possible “two-hit” phenomenon of genetic predisposition and cytokine-mediated host response to infection. Given the resemblance with HIV-associated nephropathy, we propose the term COVID-19-associated nephropathy (COVAN) to this new entity.