ABSTRACT
Introduction: The most common COVID-19 associated glomerular diseases are COVID associated nephropathy (COVAN) and Thrombotic Microangiopathy (TMA). Other less common glomerular diseases associated with COVID reported are antineutrophil cytoplasmic antibody (ANCA) vasculitis, anti-glomerular basement membrane (Anti GBM) antibody disease, podocytopathies, and IgA nephropathy. We report a case of TMA due to COVID-19 infection. Case Description: A 67-year-old woman with asthma was admitted for COVID related respiratory failure and was noted to have acute kidney injury with anemia and thrombocytopenia. She was hypertensive and urine analysis was notable for hematuria and proteinuria. ANA, ANCA, Anti GBM, Coombs, ADAMTS13, disseminated intravascular coagulation panel, serum immune fixation and free light chains, cryoglobulins, and infectious work up were unrevealing. Complement C3 and C4 were low, lactate dehydrogenase and bilirubin were high, haptoglobin was undetectable, and schistocytes were seen on peripheral smear which raised concern for thrombotic microangiopathy. Renal function deteriorated rapidly with ensuing anuria prompting initiation of dialysis. Kidney biopsy confirmed acute thrombotic microangiopathy. She was started on plasma exchange (PLEX) for COVID related thrombotic microangiopathy and she started producing urine with rapid improvement in creatinine (Cr) after two treatments. Cr was down to 3.11mg/dL from a peak of 7.45 mg/dL after PLEX and normalized at discharge. The patient is currently being monitored with renal panel and complete blood picture every three months, as an outpatient. Discussion: COVID is known to cause TMA that is presumed to be secondary to endothelial dysfunction and complement activation. There are no standard guidelines for treatment. Terminal complement blockade was not used in our patient. Our case demonstrates the efficacy of PLEX in the treatment of COVID related TMA. Early recognition and treatment is crucial and may reduce morbidity and mortality.
ABSTRACT
Introduction: Acute kidney injury (AKI) occurs in > 20% of hospitalized patients with SARS-CoV2 infection. Etiology of renal injury includes acute tubular injury, collapsing focal segmental glomerulosclerosis, and thrombotic microangiopathy. Rarely COVID-19 has been associated with antineutrophil cytoplasmic antibody associated vasculitis, anti-glomerular basement membrane antibody disease, and IgA nephropathy. We report a case of crescentic IgA nephropathy in a patient with recent COVID-19 infection. Case Description: A 55-year-old man with prolonged hospitalization for COVID-19 complicated by pulmonary embolism presented with hemorrhage secondary to a spontaneous retroperitoneal bleed. On admission, he was hemodynamically stable but received large-volume blood product transfusion. Significant admission labs included serum creatinine 3.54 mg/dl (baseline 1.34mg/dl), urinalysis with large blood and protein, spot urine protein to creatinine ratio 6,697 mg/g. Renal function and hemoglobin continued to decline despite stabilization of his bleed. Hemolysis workup revealed haptoglobin <10, lactate dehydrogenase 714, occasional schistocytes on the peripheral blood smear, concerning for TMA secondary to COVID-19 infection. Renal biopsy revealed crescentic IgA nephropathy with moderate acute tubular injury. He was started on prednisone 80mg daily for crescentic IgA nephropathy. Unfortunately his kidney function continued to worsen, and renal replacement therapy was initiated. He continued to require dialysis while inpatient with no meaningful renal recovery. Discussion: AKI is a common complication in COVID-19, however, this is not typically due to glomerular disease. Although viral infections such as COVID-19 can trigger IgA nephropathy, to the best of our knowledge, there is only one other case report of IgA nephropathy in a patient with a COVID-19 infection. COVID-19 associated glomerular disease, including IgA nephropathy, should be considered in patients with nephrotic range proteinuria, and hematuria in the setting of recent COVID-19 infection.