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COVID-19 & The Kidney
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Nearly half of patients hospitalized with COVID-19 present with or develop AKI, which is associated with poorer prognosis.
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The most common cause of AKI in patients with COVID-19 is acute tubular necrosis related to a high inflammatory state (termed “cytokine storm”).
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Treatment of COVID-19–related AKI is largely supportive.
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Urinalysis may reveal hematuria, reflecting endothelial injury and fibrin thrombi that are commonly observed on biopsy.
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Another emerging entity described is COVID-19–associated collapsing glomerulopathy, which is a type of focal segmental glomerulosclerosis.
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The role of corticosteroids in COVID-19–associated collapsing glomerulopathy is under investigation.
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Prior trials suggested that corticosteroids reduced proteinuria when administered to patients with GFR > 50 mL/min/1.73 m2 and persistent proteinuria > 1 g. However, more recent data failed to demonstrate slowing of GFR loss with corticosteroid therapy compared with use of ACE inhibitor or ARB alone; enthusiasm for glucocorticoid therapy therefore has waned.
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Pauci-Immune Glomerulonephritis (ANCA-Associated)
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Trials using the complement inhibitor avacopan in place of glucocorticoids in cyclophosphamide- or rituximab-based regimens are ongoing and appear promising.