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. 2020 Sep;31(9):1959-1968.
doi: 10.1681/ASN.2020060802. Epub 2020 Jul 17.

Kidney Biopsy Findings in Patients with COVID-19

Affiliations

Kidney Biopsy Findings in Patients with COVID-19

Satoru Kudose et al. J Am Soc Nephrol. 2020 Sep.

Abstract

Background: Coronavirus disease 2019 (COVID-19) is thought to cause kidney injury by a variety of mechanisms. To date, pathologic analyses have been limited to patient reports and autopsy series.

Methods: We evaluated biopsy samples of native and allograft kidneys from patients with COVID-19 at a single center in New York City between March and June of 2020. We also used immunohistochemistry, in situ hybridization, and electron microscopy to examine this tissue for presence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2).

Results: The study group included 17 patients with COVID-19 (12 men, 12 black; median age of 54 years). Sixteen patients had comorbidities, including hypertension, obesity, diabetes, malignancy, or a kidney or heart allograft. Nine patients developed COVID-19 pneumonia. Fifteen patients (88%) presented with AKI; nine had nephrotic-range proteinuria. Among 14 patients with a native kidney biopsy, 5 were diagnosed with collapsing glomerulopathy, 1 was diagnosed with minimal change disease, 2 were diagnosed with membranous glomerulopathy, 1 was diagnosed with crescentic transformation of lupus nephritis, 1 was diagnosed with anti-GBM nephritis, and 4 were diagnosed with isolated acute tubular injury. The three allograft specimens showed grade 2A acute T cell-mediated rejection, cortical infarction, or acute tubular injury. Genotyping of three patients with collapsing glomerulopathy and the patient with minimal change disease revealed that all four patients had APOL1 high-risk gene variants. We found no definitive evidence of SARS-CoV-2 in kidney cells. Biopsy diagnosis informed treatment and prognosis in all patients.

Conclusions: Patients with COVID-19 develop a wide spectrum of glomerular and tubular diseases. Our findings provide evidence against direct viral infection of the kidneys as the major pathomechanism for COVID-19-related kidney injury and implicate cytokine-mediated effects and heightened adaptive immune responses.

Keywords: COVID-19; kidney biopsy; renal pathology.

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Figures

None
Graphical abstract
Figure 1.
Figure 1.
Kidney biopsy findings in patients with COVID-19. (A) Light microscopy demonstrates a lesion of collapsing glomerulopathy characterized by hyperplasia of glomerular epithelial cells and collapse of the underlying glomerular capillaries. Jones methanamine silver. Magnification, ×600. (B) Diffuse foot process effacement and endothelial TRIs (arrow and inset) in a patient with minimal change disease. Electron micrograph. Magnification, ×8000. (C) Subepithelial electron dense deposits in PLA2R-associated membranous glomerulopathy. Electron micrograph. Magnification, ×15,000. (D) Multiple glomeruli with circumferential cellular crescents (arrows) in a patient with class 4+5 lupus nephritis. Periodic acid–Schiff. Magnification, ×100. (E) A glomerulus compressed by a crescent with global linear GBM staining for IgG in a patient with anti-GBM nephritis. Immunofluorescence for IgG. Magnification, ×400. (F) Tubular simplification and focal shedding of degenerating epithelial cells into the tubular lumina in a patient with isolated ATI. Hematoxylin and eosin. Magnification, ×400. (G) Severe lymphocytic tubulitis in a patient with acute T cell–mediated rejection. Periodic acid–Schiff. Magnification, ×600. (H) ISH for the virus by automated method showing undetectable viral RNA in the kidney (inset shows positive lung control). Automated ISH with hematoxylin counterstain. Magnification, ×400.

References

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