ABSTRACT
Background: Acute kidney injury (AKI) is a serious complication of infection with SARS-CoV-2 and it associated with high mortality. Post-mortem examination of kidney & lung of these patients allows a logistical assessment of the glomerular & vascular events. This is one of the largest North American autopsy series with details on renal lesions correlated with lung microthrombi. Method(s): From April 2020 to July 2021, a total of 94 autopsy cases were examined: 82 COVID-19 cases examined prospectively, & 12 control cases with similar comorbidities, retrospectively from the pre-COVID-19 era. Demographics, clinical presentation, cause of death, laboratory results were collected & pathologic findings, focusing on the following pathological lesions were studied: 1- collapsing glomerulopathy (CG), 2- evidence of thrombotic microangiopathy (TMA), i.e., presence of any glomerular microthrombi +/- thrombi in arteries/arterioles & acute tubular injury & necrosis (ATI-ATN);3- topography of the lesions in cortex;4- presence of pulmonary microthrombi. Beside routine stains used in renal pathology, Martius-scarlet-blue (MSB) stain and immunohistochemistry for fibrin were performed on 54 cases to detect microthrombi. Result(s): In the COVID-19 group composed of 82 cases, CG was observed in 40 (49%) cases, of whom only 14 (35%) were of African descent;TMA in 32 (39%);combined CG + TMA in 16 (19%) & ATI-ATN in 29 (35%). In the control group composed of 12 cases, TMA was observed in 3 (25%), ATI-ATN in 6 (50%) and no CG was found. Lung microthrombi examined in 35 cases were found in 19 cases (54%), 14 (40%) cases having TMA in the kidney. Statistical analysis of Variance showed a p-value of 0.0847, reflecting trending correlation between presence of TMA and CG. Conclusion(s): TMA, CG, and ATI-ATN were the main renal pathologic findings in our study. Wedge-shaped areas of cortical scarring suggesting a vascular pattern were observed. Co-incidence of TMA & CG was observed in half of the cases, suggesting an association between TMA & CG. Only a percentage of cases with CG were of African descent suggesting a second pathogenesis (other than podocyte injury related to APOL-1) for CG: In patients of non-African descent, TMA may be the pathogenesis behind the development of CG.