Renal pathology of 34 consecutive COVID autopsies: A single-institution experience

ABSTRACT

Background: Patients infected with the novel coronavirus 2019 (COVID19) have a wide spectrum of symptoms ranging from asymptomatic carriers to multisystem organ failure and death. While 20-40% of critically ill patients develop acute kidney injury (AKI) during the course of the disease, only few are biopsied. The most severely affected patients, frequently with multiple co-morbidities, provide insight into renal disease at autopsy. Methods: 30 of 34 autopsies performed on COVID patients had kidneys available for routine evaluation. Clinicopathologic features are presented. Results: The 34 patients range in age from 30-100 years (mean 68.5), 24 males and 10 females, 13 Caucasian, 10 Hispanic, 5 African American, 3 Indian, 3 Asian. All cases were positive by RT PCR nasal swab for SARS-CoV-2 except 3 (presumed false negative). All had on average 3.4 comorbidities (range 0-7, hypertension (HTN), diabetes (DM), obesity, COPD, asthma, stroke, dementia, cancer), frequently HTN (20) and DM (20), 11 required intubation. 18 patients had AKI (53%), 2 previously ESRD, and 5 required renal replacement therapy. Presenting Cr ranged from 0.7-9.6 mg/dl (mean 1.7). Renal pathology included diabetic nephropathy (14, 47%), with tubulointerstitial scarring ranging from <25% (60%), 25-50% (23%), to >50% (17%), and moderate (40%) or severe (40%) chronic vascular sclerosis. Other findings: obesity related glomerulopathy (2), atheroemboli (1), bilateral infarction (1), papillary necrosis (2), and thrombotic microangiopathy (2). No collapsing glomerulopathy was seen. Tubular autolysis prevents complete assessment of ATN. Platelet thrombi were seen by CD61 staining in 43% of cases to involve >20% of glomeruli and peritubular capillaries. C5b-9 staining was strong, 2-3+ arteriolar in 67% and glomeruli in 20%, suggesting localized complement activation. By electron microscopy, viral particles were identified within cells of glomeruli and tubulo-interstitium. Conclusions: Pathology in autopsy kidneys from 30 patients with COVID display pre-existing chronic disease correlating with co-morbidities, presenting with AKI or ESRD (59%). Despite varied tissue autolysis and the absence of significant proteinuria, the majority of AKI is presumed to be acute tubular injury due to ischemia and other causes. The viral particles in the renal glomerular and tubular cells may play a role in renal cytopathic injury.