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Abstract: SA-OR02

Renal Pathology of Fatal Cases of COVID-19: A Study of 94 Autopsies

Session Information

Category: Coronavirus (COVID-19)

  • 000 Coronavirus (COVID-19)

Authors

  • Pourmehdi Lahiji, Arian, The University of Texas Medical Branch at Galveston, Galveston, Texas, United States
  • Gietzen, Rachelle Ariele, The University of Texas Medical Branch at Galveston, Galveston, Texas, United States
  • Walker, David D., The University of Texas Medical Branch at Galveston, Galveston, Texas, United States
  • Aronson, Judith, The University of Texas Medical Branch at Galveston, Galveston, Texas, United States
  • Afrouzian, Marjan, The University of Texas Medical Branch at Galveston, Galveston, Texas, United States
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.

Methods

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.

Results

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

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.