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Kidney Week

Abstract: PO0809

COVID-19-Related Collapsing Focal Segmental Glomerulosclerosis and Apolipoprotein L1: A Report of Two Cases

Session Information

Category: Coronavirus (COVID-19)

  • 000 Coronavirus (COVID-19)

Authors

  • Magoon, Sandeep, Eastern Virginia Medical School, Norfolk, Virginia, United States
  • Malhotra, Varun, Eastern Virginia Medical School, Norfolk, Virginia, United States
  • Bichu, Prasad B., Nephrology Associates of Tidewater, Norfolk, Virginia, United States
Introduction


Acute kidney injury has been seen in approximately 15% of the patient with COVID-19 infection. Acute tubular injury was presumed to be the most common cause of AKI, but it did not explain significant proteinuria and hematuria. We present the case report of 2 patients with collapsing focal segmental glomerulopathy with COVID-19.

Case Description

Case 1, a 28 years old African American female and Case 2, a 58 years old African American male with baseline CKD III, admiited with COVID-19 infection and had acute kidney injury with significant proteinuria with hypoalbuminemia. Patients had kidney biopsies.
Please see table for all the details.

Discussion

Possible etiologies of acute kidney injury in COVID 19 are tubular injury due to cytokine storm, direct cytopathic effect and immune mediated glomerulonephritis.

Both the patients had collapsing FSGS in addition to tubular injury suggesting injury to the podocytes. Viral particles were not seen on both the biopsies, and hence direct cytopathic effect was not considered to be the mechanism of renal injury, although viral level below the detection threshold could not be excluded.

Collapsing FSGS has been seen with other viral infections including Parvo-virus infection, Cytomegalovirus infection and HIV. Variant of apolipoprotein L1 (APOL1) gene in African Americans have been shown to be associated with FSGS. These two patients had genetic susceptibility due to APOL1 and COVID infection caused interferon surge leading to a second hit.

Teaching Points:
Renal biopsy should be consedered in patients with COVID-19 and Nephrotic range proteinuria.
APOL1 testing should be done in patients with African American descent.

Demographic, clinical, laboratory, biopsy findings and follow up.
Patient No.Age/Sex/RaceOnset of AKIRisk FactorsUrinary findingsChemistryserologyRenal biopsyAPOL150 day follow up
128 Years
Female
AAa
7 days after the onset of feverAsthma, ObesityProteinuria 2 grams on spot UPCRb
No hematuria
No eosinophils
No casts
Crc 0.9 to 8.05 mg/dl
Albumin 3.3 to 1.3 g/dl
Mild transaminitis
Mild Rhabdomyolysis
CRPd 15.7 mg/dl
Complements normal.
Hepatitis B/C serologies negative.
HIVe PCR negative.
LMf: Tubular injury ++. Collapsing FSGS.
Mild IFTA

IFg: No IF pattern

EMh: No immune deposits.
Global podocyte foot process effacement.
Homozygous for G1 allelePatient is off dialysis, but renal functions are not at baseline
256 years
Male
AA
7-10 days after the onset of feverCKD 3
HTN,
Obesity
Proteinuria 20 grams on UPCR,
No hematuria
No eosinophils
No casts
Cr. 3.37 to 7.72 mg/dl
Albumin 2 to 0.8 g/dl
Mild transaminitis
Mild Rhabdomyolysis
CRP 9.0 mg/dl
Complements normal.
Hepatitis B/C serologies negative.
HIV PCR negative.
LM: Tubular injury ++.
Collapsing FSGS.
Mild IFTA

IF: No IF pattern

EM: No immune deposits. Global podocyte foot process effacement.
Heterozygous for G1 and G2 allelesPatient is off dialysis, but renal functions are not at baseline

a. AA: African American; b. UPCR: urine protein to creatinine ratio; c. Cr: Creatinine; d. CRP: C-reactive protein; e. HIV: Human immunodeficiency virus; f. LM: Light microscopy; g. IF: Immunofluorescence; h. EM: Electron microscopy.