Abstract

We report a case of a 69-year-old Caucasian male with a history of hypertension, Type 2 diabetes, and Stage IIIa chronic kidney disease (CKD), who presented to the emergency department with positional dizziness, generalized weakness, weight loss, and suppressed appetite. Two months earlier, the patient was diagnosed with coronavirus disease 2019 (COVID-19). The patient had non-oliguric acute kidney injury alongside preexisting CKD. The urinalysis showed hematuria and significant non-nephrotic proteinuria. His serological markers were positive for antineutrophil cytoplasmic antibodies with high titers. A kidney biopsy showed focal crescentic glomerulonephritis of the pauci-immune type. Initially, treatment with immunosuppressive medication was deferred because the biopsy findings suggested a poor renal outcome, as the cortical sample showed tubular atrophy and interstitial fibrosis of more than 50%. The patient was discharged but was later readmitted with worsening renal function, deep venous thrombosis in the lower extremities, and patchy lung consolidation suggesting possible pneumonia, which was ruled out. He required dialysis and brief empiric antibiotics for pneumonia, and anticoagulation for deep venous thrombosis, and was treated with intravenous (IV) pulsed steroids, followed by gradually tapering oral steroids and rituximab induction therapy. He continued dialysis three times a week. Three months after discharge, his renal function improved to near-baseline level, and he no longer required hemodialysis. He continues to be on maintenance IV rituximab therapy and low-dose oral steroids and is followed closely by a rheumatologist. Our case reflects the evolving state of understanding how COVID-19 impacts the immune system, its varying manifestations, and its management.

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