2021
DOI: 10.1097/mnh.0000000000000750
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Kidney in the net of acute and long-haul coronavirus disease 2019: a potential role for lipid mediators in causing renal injury and fibrosis

Abstract: Purpose of reviewSevere COVID-19 disease is often complicated by acute kidney injury (AKI), which may transition to chronic kidney disease (CKD). Better understanding of underlying mechanisms is important in advancing therapeutic approaches.Recent findings SARS-CoV-2-induced endothelial injury initiates platelet activation, platelet-neutrophil partnership and release of neutrophil extracellular traps. The resulting thromboinflammation causes ischemia-reperfusion (I/R) injury to end organs. Severe COVID-19 indu… Show more

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Cited by 14 publications
(11 citation statements)
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“…Second, it can be attributed to the direct infection of renal cells by SARS‐Cov‐2, which promotes tubulointerstitial fibrosis at the molecular level 25,26 . In addition, lipid mediators storm, which plays a potential role in causing renal injury and fibrosis, increases the possibility of acute kidney disease to CKD 27 . Last but not least, SARS‐CoV‐2 produces cellular damage by alterations of the ACE2 pathway, various inflammatory cytokines, mitochondrial dysfunction, pro‐coagulation, and other immune aberrations, 16,17 of which the imbalance of anti‐inflammatory/pro‐inflammatory cytokines play a very important role.…”
Section: Discussionmentioning
confidence: 99%
“…Second, it can be attributed to the direct infection of renal cells by SARS‐Cov‐2, which promotes tubulointerstitial fibrosis at the molecular level 25,26 . In addition, lipid mediators storm, which plays a potential role in causing renal injury and fibrosis, increases the possibility of acute kidney disease to CKD 27 . Last but not least, SARS‐CoV‐2 produces cellular damage by alterations of the ACE2 pathway, various inflammatory cytokines, mitochondrial dysfunction, pro‐coagulation, and other immune aberrations, 16,17 of which the imbalance of anti‐inflammatory/pro‐inflammatory cytokines play a very important role.…”
Section: Discussionmentioning
confidence: 99%
“…Even in patients with mild symptoms, there is an increased risk of long-term renal damage [ 29 ]. The direct infection of renal cells and lipid mediator storm caused by SARS-Cov-2 can promote tubulointerstitial fibrosis at the molecular level, which increases the possibility of acute kidney involvement and CKD [ 30 , 31 ]. Although the incidence of hematuria and albuminuria is not high in this study, the kidney involvement represented by hematuria and albuminuria is likely to be the starting point of adverse renal outcomes in long-term follow-up.…”
Section: Discussionmentioning
confidence: 99%
“…In line with these organ-specific findings, SARS-CoV-2 antigen has been recovered from multiple body sites including the gastrointestinal tract, hepatic tissues, the brain, lymphoid tissues, and in circulation up to 7-month post-infection 34,40,207,208 Some groups proposed that, much like other chronic infections, persistent antigen exposure leads to chronic immune activation and subsequent systemic and compartmentalized inflammation, contributing to the wide array of clinical manifestations seen in long COVID. 105,165,177,178,181,183,189193,209212…”
Section: Long Covidmentioning
confidence: 99%