ABSTRACT
SARS-CoV-2 infections can induce kidney injury and glomerulopathy, with the most common pathology findings being acute tubular injury and collapsing glomerulopathy.Here we describe a rare case of membranous nephropathy in a man in his late 70s presented with nephrotic syndrome and rapidly progressive kidney dysfunction 1 month after SARS-CoV-2 infection. Phospholipase A2 receptor antibodies were positive. He was treated with rituximab, with proteinuria control. We review the cases reported in the literature.
Subject(s)
COVID-19 , Glomerulonephritis, Membranous , Nephrotic Syndrome , Male , Humans , Glomerulonephritis, Membranous/diagnosis , Glomerulonephritis, Membranous/drug therapy , Glomerulonephritis, Membranous/etiology , COVID-19/complications , COVID-19/pathology , SARS-CoV-2 , Kidney/pathology , Nephrotic Syndrome/drug therapy , Nephrotic Syndrome/etiology , Nephrotic Syndrome/pathologyABSTRACT
We report a case of a kidney transplant recipient who presented with acute kidney injury and nephrotic-range proteinuria in a context of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Kidney biopsy revealed collapsing glomerulopathy. Droplet-based digital polymerase chain reaction did not detect the presence of SARS-CoV-2 RNA in the biopsy fragment, and the virus was barely detectable in plasma at the time of the biopsy. SARS-CoV-2 RNAemia peaked several days later, followed by a seroconversion despite the absence of circulating CD19-positive lymphocytes at admission due to rituximab-based treatment of antibody-mediated rejection 3 months earlier. Genotyping for the 2 risk alleles of the apolipoprotein L1 (APOL1) gene revealed that the donor carried the low-risk G0/G2 genotype. This case illustrates that coronavirus disease 2019 infection may promote a collapsing glomerulopathy in kidney allografts with a low-risk APOL1 genotype in the absence of detectable SARS-CoV-2 RNA in the kidney and that podocyte injury may precede SARS-CoV-2 RNAemia.