Abstract: PO0809
COVID-19-Related Collapsing Focal Segmental Glomerulosclerosis and Apolipoprotein L1: A Report of Two Cases
Session Information
- COVID-19: Clinical Characteristics and Cases
October 22, 2020 | Location: On-Demand
Abstract Time: 10:00 AM - 12:00 PM
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/Race | Onset of AKI | Risk Factors | Urinary findings | Chemistry | serology | Renal biopsy | APOL1 | 50 day follow up |
| 1 | 28 Years Female AAa | 7 days after the onset of fever | Asthma, Obesity | Proteinuria 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 allele | Patient is off dialysis, but renal functions are not at baseline |
| 2 | 56 years Male AA | 7-10 days after the onset of fever | CKD 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 alleles | Patient 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.