Renal histopathological analysis of 26 postmortem findings of patients with COVID-19 in China

Although the respiratory and immune systems are the major targets of Coronavirus Disease 2019 (COVID-19), acute kidney injury and proteinuria have also been observed. Currently, detailed pathologic examination of kidney damage in critically ill patients with COVID-19 has been lacking. To help define this we analyzed kidney abnormalities in 26 autopsies of patients with COVID-19 by light microscopy, ultrastructural observation and immunostaining. Patients were on average 69 years (19 male and 7 female) with respiratory failure associated with multiple organ dysfunction syndrome as the cause of death. Nine of the 26 showed clinical signs of kidney injury that included increased serum creatinine and/or new-onset proteinuria. By light microscopy, diffuse proximal tubule injury with the loss of brush border, non-isometric vacuolar degeneration, and even frank necrosis was observed. Occasional hemosiderin granules and pigmented casts were identified. There were prominent erythrocyte aggregates obstructing the lumen of capillaries without platelet or fibrinoid material. Evidence of vasculitis, interstitial inflammation or hemorrhage was absent. Electron microscopic examination showed clusters of coronavirus-like particles with distinctive spikes in the tubular epithelium and podocytes. Furthermore, the receptor of SARS-CoV-2, ACE2 was found to be upregulated in patients with COVID-19, and immunostaining with SARS-CoV nucleoprotein antibody was positive in tubules. In addition to the direct virulence of SARS-CoV-2, factors contributing to acute kidney injury included systemic hypoxia, abnormal coagulation, and possible drug or hyperventilation-relevant rhabdomyolysis. Thus, our studies provide direct evidence of the invasion of SARSCoV-2 into kidney tissue. These findings will greatly add to the current understanding of SARS-CoV-2 infection. Although the respiratory and immune systems are the major targets of Coronavirus Disease 2019 (COVID-19), acute kidney injury and proteinuria have also been observed. Currently, detailed pathologic examination of kidney damage in critically ill patients with COVID-19 has been lacking. To help define this we analyzed kidney abnormalities in 26 autopsies of patients with COVID-19 by light microscopy, ultrastructural observation and immunostaining. Patients were on average 69 years (19 male and 7 female) with respiratory failure associated with multiple organ dysfunction syndrome as the cause of death. Nine of the 26 showed clinical signs of kidney injury that included increased serum creatinine and/or new-onset proteinuria. By light microscopy, diffuse proximal tubule injury with the loss of brush border, non-isometric vacuolar degeneration, and even frank necrosis was observed. Occasional hemosiderin granules and pigmented casts were identified. There were prominent erythrocyte aggregates obstructing the lumen of capillaries without platelet or fibrinoid material. Evidence of vasculitis, interstitial inflammation or hemorrhage was absent. Electron microscopic examination showed clusters of coronavirus-like particles with distinctive spikes in the tubular epithelium and podocytes. Furthermore, the receptor of SARS-CoV-2, ACE2 was found to be upregulated in patients with COVID-19, and immunostaining with SARS-CoV nucleoprotein antibody was positive in tubules. In addition to the direct virulence of SARS-CoV-2, factors contributing to acute kidney injury included systemic hypoxia, abnormal coagulation, and possible drug or hyperventilation-relevant rhabdomyolysis. Thus, our studies provide direct evidence of the invasion of SARSCoV-2 into kidney tissue. These findings will greatly add to the current understanding of SARS-CoV-2 infection. Editor’s NoteThe Editors recommend that the readers also view the letter to the editor by Kissling et al. (see page 228) reporting a case of COVID-19–associated collapsing glomerulopathy featuring cytoplasmic vacuoles containing numerous spherical particles. The nature of those intracellular organelles as viral particles is questioned in 2 letters to the editor, Nadasdy et al. (see page 233) and Miller and Brealey (see page 231), that provide important information when examining viral-like electron microscopy structures in the kidney. The Editors recommend that the readers also view the letter to the editor by Kissling et al. (see page 228) reporting a case of COVID-19–associated collapsing glomerulopathy featuring cytoplasmic vacuoles containing numerous spherical particles. The nature of those intracellular organelles as viral particles is questioned in 2 letters to the editor, Nadasdy et al. (see page 233) and Miller and Brealey (see page 231), that provide important information when examining viral-like electron microscopy structures in the kidney. In December 2019, a cluster of patients with pneumonia of unknown etiology was reported in Wuhan, Hubei Province, China. On January 9, 2020, the Chinese Center for Disease Control and Prevention identified the causative agent as a novel coronavirus, which now is officially termed severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2).1Lu R. Zhao X. Li J. et al.Genomic characterisation and epidemiology of 2019 novel coronavirus: implications for virus origins and receptor binding.Lancet. 2020; 395: 565-574Abstract Full Text Full Text PDF PubMed Scopus (7711) Google Scholar The illness caused by SARS-CoV-2, coronavirus disease 2019 (COVID-19), mainly manifests with fever, dry cough, dyspnea, myalgia, and diarrhea. However, COVID-19 presentations can range from asymptomatic infection, self-limited influenza-type symptoms, and acute pneumonia to severe respiratory failure with high mortality. Currently, the epidemic in China is being gradually controlled with major domestic efforts and international support. However, the global epidemic has now become a pandemic. Without knowing the detailed mechanisms of COVID-19, specific management is lacking. The reported mortality in different countries varies according to extent of testing performed, ranging from 0.3% to 10%. The respiratory, immune, and coagulation systems are the major targets of this pandemic disease.2Guan W.J. Ni Z.Y. Hu Y. et al.Clinical characteristics of coronavirus disease 2019 in China.N Engl J Med. 2020; 382: 1708-1720Crossref PubMed Scopus (19246) Google Scholar Kidney injury has appeared relatively less with COVID-19 than with Middle East respiratory syndrome or hantavirus infections, perhaps due to the different underlying mechanisms and ensuing pathologic manifestations. Clinically, the incidence of acute kidney injury (AKI) in COVID-19 varied from 0.9% to 29% in different centers. New onset proteinuria was also reported by several institutions.3Alsaad K.O. Hajeer A.H. Al Balwi M. et al.Histopathology of Middle East respiratory syndrome coronavirus (MERS-CoV) infection—clinicopathological and ultrastructural study.Histopathology. 2018; 72: 516-524Crossref PubMed Scopus (215) Google Scholar Currently, the pathologic investigation has primarily focused on respiratory, hematopoietic, and immune systems, whereas morphologic data of kidney injury are lacking. In this study, we report on our experience of kidney findings at autopsy in patients with severe COVID-19. The 26 patients with COVID-19 included 19 males and 7 females, with an average age of 69 years (range, 39–87 years). All 26 cases had positive results for SARS-CoV-2 by nucleic acid testing and characteristic radiologic alterations in lungs. Eleven patients had history of hypertension or diabetes or both. Data on angiotensin-converting enzyme (ACE) inhibitors or angiotensin-receptor blockers for hypertension or diabetes or both before the terminal hospitalization were not available. Patients were treated with calcium-channel blockers if needed for hypertension during the terminal hospitalization, without ACE inhibitors or angiotensin-receptor blockers or both, due to uncertainty regarding possible effects. Six patients had history of tumor. The clinical information is summarized in Tables 1 and 2.Table 1Clinical information of 26 patients with COVID-19IDSexAge (y)History of HT, DM, CKD or tumorHypotension/vasopressorBUN (mmol/l)Cr (μmol/l)UrineHb (g/l)WBC (g/l)LY (g/l)LY%PLT (T/l)D-dimer (μg/ml)ALT (U/l)AST (U/l)TBIL (μmol/l)CK (U/l)PROBLDWBC1M77NY22.52239.8N/AN/AN/AN/A25.10.371.5033>8.006071N/AN/A2F60NNN/AN/A−2+1+11217.870.824.601032.35N/AN/AN/AN/A3M51Pancreas CaY18.9671.3Trace−−9631.870.752.40385.61102126110.23284M87DM, HT, CKDY42.45229.8N/AN/AN/A7013.630.261.902191.0813169.5995M39Gastric CaN7.1831N/AN/AN/A9811.40.443.902736.1151823.9876M66Liver CaY41.84161.4N/AN/AN/A8912.520.241.90570.918415049.110017M77Skin CaY24.14460.2N/AN/AN/A9323.590.813.401055.32214813.63128F87DM, HT, CKDYN/AN/A3+3+1+1018.980.485.40110>8.00N/AN/AN/AN/A9M70Lung CaN12.86207.3N/AN/AN/A1125.760.8114.102152.8536784014.9245910F84HTN14.28114.7N/AN/AN/A607.690.536.80752.86293016.15411F83HTY21.54108N/AN/AN/A692.280.177.30302.087179546.549512M63HTY7.345.9−±−10241.480.531.301791.02107448.515813M52NY7.5158.72+−±7311.190.665.903422.69975218.919414M61HTY13.9994.21+1+±8015.670.644.10802.3887741.325915F70HT, Lung CaY5.7944.1N/AN/AN/A10218.891.216.40106>8.00543526.13716M64HTY20.42137.3N/AN/AN/A933.350.5616.80237.69213818.96417M66HTY3.2457.92+3+1+810.260.0829.90154.953491573.2N/A18F62NY11.8661.8N/AN/AN/A889.140.697.60763.42191814.22319M55DM, HTY9.2443.72+1+3+781.280.086.20182.05599119957.73420M83N/AN/AN/AN/AN/AN/AN/AN/AN/AN/AN/AN/AN/AN/AN/AN/AN/A21F86N/AN/AN/AN/AN/AN/AN/AN/AN/AN/AN/AN/AN/AN/AN/AN/AN/A22M78N/AN/AN/AN/AN/AN/AN/AN/AN/AN/AN/AN/AN/AN/AN/AN/AN/A23M62N/AN/AN/AN/AN/AN/AN/AN/AN/AN/AN/AN/AN/AN/AN/AN/AN/A24M51N/AN/AN/AN/AN/AN/AN/AN/AN/AN/AN/AN/AN/AN/AN/AN/AN/A25M72N/AN/AN/AN/AN/AN/AN/AN/AN/AN/AN/AN/AN/AN/AN/AN/AN/A26M86HTY4.3663.61+−−9745.440.380.801553.77153524.5213ALT, alanine aminotransferase; AST, aspartate aminotransferase; BLD, blood; BUN, blood urea nitrogen; Ca, cancer; CK, creatine kinase; CKD, chronic kidney disease; Cr, creatinine; DM, diabetes; F, female; Hb, hemoglobin; HT, hypertension; ID, identification number; LY, lymphocytes; M, male; N, no; N/A, not available; PLT, platelet; PRO, proteinuria; TBIL, total bilirubin; WBC, white blood cell; Y, yes.The cause of death in all patients was respiratory failure. In addition, patients 1, 5, 14, 15, 16, 25, and 26 had multiorgan failure. Open table in a new tab Table 2Treatment historyIDExposure to nephrotoxic drugRenal replacement therapyAntiviralsSteroid1NNArbidolY2YCRRTArbidolY3NNRibavirinN4NNRibavirin, arbidolN5NNArbidolY6NNArbidolY7NCRRTArbidolY8NNArbidolN9NNNN10NCRRTArbidolY11NNArbidolY12NNArbidolY13YNLopinavir/ritonavirY14YNNY15NNLopinavir/ritonavirY16NNLopinavir/ritonavirY17YNNY18NCRRTNY19NCRRTLopinavir/ritonavirY20N/AN/AN/AN/A21N/AN/AN/AN/A22N/AN/AN/AN/A23N/AN/AN/AN/A24N/AN/AN/AN/A25N/AN/AN/AN/A26NNLopinavir/ritonavirYCRRT, continuous renal replacement therapy; ID, identification number; N, no; N/A, not available; Y, yes. Open table in a new tab ALT, alanine aminotransferase; AST, aspartate aminotransferase; BLD, blood; BUN, blood urea nitrogen; Ca, cancer; CK, creatine kinase; CKD, chronic kidney disease; Cr, creatinine; DM, diabetes; F, female; Hb, hemoglobin; HT, hypertension; ID, identification number; LY, lymphocytes; M, male; N, no; N/A, not available; PLT, platelet; PRO, proteinuria; TBIL, total bilirubin; WBC, white blood cell; Y, yes. The cause of death in all patients was respiratory failure. In addition, patients 1, 5, 14, 15, 16, 25, and 26 had multiorgan failure. CRRT, continuous renal replacement therapy; ID, identification number; N, no; N/A, not available; Y, yes. All tissue samples were well preserved without autolysis. There was prominent proximal acute tubule injury (ATI) manifested as the loss of brush border, vacuolar degeneration, dilatation of the tubular lumen with cellular debris, and occasionally even frank necrosis and detachment of epithelium with bare tubular basement membrane noted (the latter observed in 4 cases). The majority of the vacuoles in cytoplasm were variable in size; however, focal isometric fine vacuolization was uncommonly present and is associated with, for example, mannitol or i.v. Ig therapy (Figure 1a and b). In 2 patients, consistent with corresponding pathologic findings in their lungs, acute pyelonephritis was observed with multiple foci of bacteria and diffuse polymorphonuclear casts in the lumen of tubules. In 1 of these 2 patients, an arcuate artery was infiltrated with numerous inflammatory cells (Figure 1c and d), likely representing reaction to bacterial infection. Diffuse erythrocyte aggregation and obstruction were present in peritubular and glomerular capillary loops without distinct fragmentation of erythrocytes or platelets or fibrin thrombi. Occasional hemosiderin granules in tubular epithelium were identified in 4 patients with hematuria by dipstick (Figure 1e). In 3 cases, pigmented casts were found with high levels of creatine phosphokinase, possibly representing rhabdomyolysis (Figure 1f). Distal tubules and collecting ducts showed only occasional cellular swelling and edematous expansion of the interstitial space without significant inflammation. Lymphocytic infiltrates were present in areas of nonspecific fibrosis including subcapsular areas. Glomeruli showed varied degrees of underlying morphologic changes, such as nodular mesangial expanding and hyalinosis of arterioles, which constituted evidence of diabetic nephropathy in 2 of the patients with diabetes, and arteriosclerosis of medium-size arteries with ischemic glomeruli in 11 of the patients with hypertension. Focal obsolescent glomeruli were detected proportional to the age in this population. Endothelial cell swelling with variable foamy degeneration was present in 5 of the patients with COVID-19, and they were usually older and had hypertensive or diabetic histories. In 3 cases, a few areas of segmental fibrin thrombus in glomerular capillary loops were identified associated with severe injury of the endothelium (Figure 1g). Occasional podocyte vacuolation and even detachment from the glomerular basement membrane was noted. Focal segmental glomerulosclerosis was observed in 2 patients with overt proteinuria as well as history of diabetes. Ischemic changes with shrinkage of capillary loops with accumulation of plasma in Bowman’s space was present in 7 cases, occasionally with pseudocrescent appearance (Figure 1h). Crescents and hypercellular or inflammatory lesions of glomeruli were not present. The pathologic findings are summarized in Table 3.Table 3The pathologic abnormalities of kidney in 26 cases of deceased patients with COVID-19IDLMEMIFTubule interstitiumGlomeruliATIMultiple foci of bacteriaPigmented castsArteriosclerosisSegmental fibrin thrombusFSGSCoronavirus-like particlesDense depositsSubendothelial lucent expansionIgGIgASARS-CoV NP1SevereNNMild to moderateNNN/AN/AN/AN/AN/AN/A2ModerateNNMildNNYNNN/AN/AN/A3Mild to moderateNYMildNNYNYN/AN/AN/A4SevereNNSevereNYYNYN/AN/AN/A5MildNNMildNNN/AN/AN/AN/AN/AN/A6Mild to moderateNYMildNNN/AN/AN/AN/AN/AN/A7SevereNNMild to moderateNNN/AN/AN/AN/AN/AN/A8ModerateNNSevereFocalYN/AN/AN/AN/AN/AN/A9ModerateNYModerateNNN/AN/AN/AN/AN/AN/A10ModerateNNModerate to severeNNN/AN/AN/AN/AN/AN/A11Moderate to severeNNModerate to severeFocalNN/AN/AN/AN/AN/AN/A12Moderate to severeNNModerateNNYNYN/AN/AN/A13Mild to moderateNNMildNNN/AN/AN/AN/AN/AN/A14SevereMultiple focalNModerateDiffuseNN/AN/AN/AN/AN/AN/A15Mild to moderateNNModerate to severeNNN/AN/AN/AN/AN/AN/A16SevereMultiple focalNModerate to severeNNN/AN/AN/AN/AN/AN/A17ModerateNNModerateNNN/AN/AN/AN/AN/AN/A18ModerateNNMildNNN/AN/AN/AN/AN/AN/A19MildNNModerate to to to to to severeNNModerate to to acute tubular COVID-19, coronavirus disease electron focal segmental ID, identification number; light N, not N/A, not available; severe acute syndrome Y, Open table in a new tab acute tubular COVID-19, coronavirus disease electron focal segmental ID, identification number; light N, not N/A, not available; severe acute syndrome Y, particles were identified in the cytoplasm of renal proximal tubular epithelium as well as in the and less in tubules. The of particles varied from to with distinctive to in a of this coronavirus included membrane with to the viral and the of the particles (Figure In 1 and with segmental mesangial and increased were present (Figure and were noted in were These 2 patients not have evidence of bacterial at autopsy in or In 2 of 3 patients with diabetes, characteristic changes of diabetic nephropathy were present by electron microscopy including increased of the glomerular basement membrane without mesangial expansion and segmental and erythrocytes were observed obstructing peritubular capillary with of endothelium (Figure or fibrin were not detected in with this of erythrocytes in segmental glomerular capillary loops was without inflammation or In glomerular capillary a varied extent of injury was including lucent and without The ultrastructural findings are summarized in Table for inflammatory cells not specific accumulation of these with of and cells in areas of nonspecific with and present in the obstruction was of for showed in the significant platelet and for cells showed of peritubular capillary (Figure In an of a was and without COVID-19, for ACE of proximal tubules without glomerular was which is consistent with was observed in the kidney (Figure ACE2 was also in 5 of the patients ACE2 in 3 of these ACE2 was prominent in proximal tubular in areas with severe In addition, focal cells was as well as occasional podocyte (Figure or was from in cases, and nonspecific and were present. showed segmental capillary however, without the capillary with by case showed in mesangial as well as capillary associated with corresponding mesangial and by By an the of SARS-CoV nucleoprotein was analyzed in the cases, and 3 showed positive in a or cytoplasm in tubular epithelium (Figure and positive showed The immunostaining findings are summarized in Table In the present study, we report the kidney and immunostaining findings from autopsies of 26 patients from respiratory failure due to COVID-19. is the report of kidney pathologic presentations in patients with SARS-CoV-2 infection. autopsy the range of abnormalities present and the specific kidney cells likely with the and provide important information for studies in less ill patients with COVID-19 and kidney observed significant the of mainly by erythrocytes with ensuing as well as glomerular and changes of underlying diabetic or hypertensive of these findings are in with mechanisms for in kidney. also findings that distinct mechanisms of this novel coronavirus infection, direct kidney and likely Thus, these pathologic provide a for understanding of COVID-19. observed diffuse acute proximal tubular injury with loss of brush and which be caused by the direct virulence of SARS-CoV-2, by our ultrastructural and immunostaining The tubular cytoplasmic vacuoles were variable in However, in a few patients, focal isometric fine vacuolization was present and is likely to with or such as i.v. 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