ABSTRACT
African Americans (AAs) with high-risk APOL1 alleles are at an increased risk of developing early onset focal segmental glomerulosclerosis (FSGS) and rapid progression of chronic kidney disease. In some cases, severe COVID-19 pneumonia is associated with kidney injury known as COVID-19-Associated Nephropathy, the exact mechanisms of which are unclear. A 25-year-old AA female presented with mild respiratory symptoms and positive for SARS-CoV-2 and was admitted to Emergency in March 2020. Her serum creatinine (sCr) was 1.4 mg/dL, albumin 2.92 g/dL;she recovered clinically and was discharged. She returned to hospital 25 days later with severe kidney failure, sCr of 28 mg/dL, potassium of 5.6 mmol/L and urine protein/creatinine (uPCR) of 10355 mg/g. She was initiated on hemodialysis. Kidney biopsy showed CG with acute tubular necrosis with direct invasion of the glomerular cells by particles resembling coronavirus. Hemodialysis was discontinued and she was discharged home on oral prednisone at 1mg/kg/day. After 5 months, she was tapered off of prednisone and her sCr improved to 2.6 mg/dL with uPCR of 3133 mg/g. Genetic testing with Renasight, a 382 renal gene panel was performed, yielding homozygosity for the APOL1 risk allele (c.[1024A>G;1152T>G] (p. [Ser342Gly;Ile384Met]) (G1 allele). High-risk APOL1 risk variants occur in 13% of AAs.These individuals have an estimated 4% lifetime risk for incurring FSGS. However, a ‘2nd hit' is necessary for kidney disease to develop. COVID-19 may lead to kidney injury due to tissue ischemia, cytokine storm, hypercoagulability or direct viral-mediated mechanisms. In COVID-19 related kidney biopsies, CG is often described. Although glucocorticoid sensitivity in such patients is not well-defined, our patient showed response to oral prednisone. This case adds to growing evidence that SARS-CoV-2 infection contributes to CG. The dual effect of high-risk APOL1 variants and SARS-CoV-2 in effecting CG remains to be elucidated. Testing with a broad renal genetic panel could help define genetic variants that promote complications from SARS-CoV-2 infection.