Postmortem Kidney Pathology Findings in Patients with COVID-19

Abstract

BackgroundAKI is common among hospitalized patients with coronavirus disease 2019 (COVID-19) and is an independent risk factor for mortality. Although there are numerous potential mechanisms underlying COVID-19–associated AKI, our current knowledge of kidney pathologic findings in COVID-19 is limited.MethodsWe examined the postmortem kidneys from 42 patients who died of COVID-19. We reviewed light microscopy findings in all autopsies and performed immunofluorescence, electron microscopy, and in situ hybridization studies for SARS-CoV-2 on a subset of samples.ResultsThe cohort had a median age of 71.5 years (range, 38–97 years); 69% were men, 57% were Hispanic, and 73% had a history of hypertension. Among patients with available data, AKI developed in 31 of 33 patients (94%), including 6 with AKI stage 1, 9 with stage 2, and 16 with stage 3. The predominant finding correlating with AKI was acute tubular injury. However, the degree of acute tubular injury was often less severe than predicted for the degree of AKI, suggesting a role for hemodynamic factors, such as aggressive fluid management. Background changes of hypertensive arterionephrosclerosis and diabetic glomerulosclerosis were frequent but typically mild. We identified focal kidney fibrin thrombi in 6 of 42 (14%) autopsies. A single Black patient had collapsing FSGS. Immunofluorescence and electron microscopy were largely unrevealing, and in situ hybridization for SARS-CoV-2 showed no definitive positivity.ConclusionsAmong a cohort of 42 patients dying with COVID-19, autopsy histologic evaluation revealed acute tubular injury, which was typically mild relative to the degree of creatinine elevation. These findings suggest potential for reversibility upon resolution of SARS-CoV-2 infection.

Outcomes Among Patients Hospitalized With COVID-19 and Acute Kidney Injury

“…While in some cases the injury was mild, in many cases patients developed acute tubular injury with or without concomitant pathology including collapsing glomerulopathy or rarely thrombotic microangiopathy. [30][31][32][33] Second, it is important to understand the degree to which post-hospital nephrology follow-up care may be required, and accordingly the potential burden that COVID-19 conveys on the nephrology community. Third, for patients with AKI-KRT, knowledge on recovery and the ability to be discharged off dialysis can influence in-hospital decision making.…”

Effect of COVID-19 on Kidney Disease Incidence and Management

“…Post-mortem findings in another 63 patients revealed detectable SARS-CoV-2 ribonucleic acid (RNA) in kidney tissue of 72% of those with AKI and 43% of those without AKI (56). These findings do bring up the possibility that the virus may be causing direct tubular damage (23,57). Another case series of 10 kidney biopsies reported that staining by immunohistochemistry for SARS-CoV-2 was negative in all cases with COVID-19 and tubular injury.…”

“…In an autopsy series of 42 patients, ATN was the most predominant histological finding (23). Evidence of glomerulosclerosis, myoglobin cast nephropathy, thrombotic microangiopathy, crescentic glomerulonephritis, cortical necrosis, and collapsing glomerulopathy were also reported.…”

The Social Brain and Emotional Contagion: COVID-19 Effects

“…Even if healthcare organizations and researchers published guidelines and recommendations about postmortem investigation, frequently minimally invasive autopsies were performed avoiding brain extraction [27]. Postmortem investigations of the central nervous system (CNS) were restricted to a few individual reports and comprised cerebral swelling and focal hemorrhagic injuries scattered throughout the white matter with swollen axons at the borders of the hemorrhagic foci, responsive gliosis, and oligondendrocytic apoptosis around the injuries [28]. Brain pathological characteristics also include microthrombi and acute stroke, a central parenchymal infiltrate of CD3-positive T lymphocytes [29].…”