In:
Journal of the American Society of Nephrology, Ovid Technologies (Wolters Kluwer Health), Vol. 31, No. 9 ( 2020-9), p. 2158-2167
Abstract:
More than one third of hospitalized patients with coronavirus disease 2019 (COVID-19) develop AKI. The pathogenesis of AKI in this setting is poorly understood, and pathologic descriptions are limited. The authors examined kidney histopathology of 42 patients who died of COVID-19. The most significant findings included mild acute tubular injury as well as the absence of classic viral nephropathy, diffuse thrombotic microangiopathy, or acute GN. In situ hybridization could not identify definitive positivity for SARS-CoV-2. The finding of only mild acute tubular injury in the setting of severe creatinine elevation suggests a pathogenesis involving tubular injury and hemodynamic factors (such as aggressive fluid management) and potential for recovery of renal function upon resolution of infection. Background AKI 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. Methods We 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. Results The 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. Conclusions Among 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.
Type of Medium:
Online Resource
ISSN:
1046-6673
,
1533-3450
DOI:
10.1681/ASN.2020050744
Language:
English
Publisher:
Ovid Technologies (Wolters Kluwer Health)
Publication Date:
2020
detail.hit.zdb_id:
2029124-3
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