Postmortem Kidney Pathology Findings in Patients with COVID-19

Abstract

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.

Keywords: COVID-19; SARS-CoV-2; acute kidney injury; acute renal failure; acute tubular injury; pathology.

Graphical abstract

Figure 1.

Autopsy kidneys deomstarted arteriosclerosis, variable degrees of autolysis and, rarely, fibrin thrombi. (A) A low-magnification view reveals complete autolysis in an autopsy with a prolonged PMI. Tubular nuclei are not visible, and tubular injury cannot be assessed. In contrast, chronic changes of glomerulosclerosis, arteriosclerosis, and TA/IF are still visualized. (Hematoxylin and eosin, ×100.) (B) A glomerulus exhibits mild changes of NDGS. (Hematoxylin and eosin, ×400.) (C) A glomerulus displays red blood cell congestion and an intracapillary fibrin thrombus. (Hematoxylin and eosin, ×400.) (D) A fibrin thrombus is seen in the lumen of an artery. (Hematoxylin and eosin, ×400.) (E) In this area of microscopic infarction, tubules exhibit coagulative-type necrosis, and there is prominent neutrophil infiltration with neutrophilic debris. (Hematoxylin and eosin, ×200.) (F) In this patient with hypertensive arterionephrosclerosis, an artery exhibits severe intimal sclerosis, compromising >50% of the lumen. (Hematoxylin and eosin, ×400.)

Figure 2.

ATI is the main finding in autopsy kidneys from patients with COVID-19 and AKI. (A) A low-magnification view reveals intact renal cortex, without evidence of ATI. (Hematoxylin and eosin, ×40.) (B) In this patient with AKI stage 1 with an increase in creatinine from 1.09 to 1.6 mg/dl, histologic evaluation revealed mild ATI characterized by mild luminal ectasia, irregular luminal contours, and vacuolization. Prominent cytoplasmic simplification and loss of brush border are not apparent. (Hematoxylin and eosin, ×100.) (C) In this patient with AKI stage 3 with an increase in creatinine from 0.94 to 6.83 mg/dl requiring CRRT, only mild ATI is noted, characterized by luminal ectasia and mild vacuolization. (Hematoxylin and eosin, ×200.) (D) In this patient with AKI stage 3 with an increase in creatinine from 0.67 to 3.48 mg/dl, the kidneys exhibit severe ATI, with more prominent luminal ectasia, cytoplasmic simplification, vacuolization, and loss of brush border. (Hematoxylin and eosin, ×200.) (E) In this patient with AKI stage 3 requiring CRRT, severe ATI is also apparent. (Hematoxylin and eosin, ×100.)