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10.1016/j.xkme.2021.02.012

http://scihub22266oqcxt.onion/10.1016/j.xkme.2021.02.012
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33942030!8080498!33942030
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suck abstract from ncbi


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pmid33942030      Kidney+Med 2021 ; 3 (4): 653-658
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  • Molecular Analysis of the Kidney From a Patient With COVID-19-Associated Collapsing Glomerulopathy #MMPMID33942030
  • Meliambro K; Li X; Salem F; Yi Z; Sun Z; Chan L; Chung M; Chancay J; Vy HMT; Nadkarni G; Wong JS; Fu J; Lee K; Zhang W; He JC; Campbell KN
  • Kidney Med 2021[Jul]; 3 (4): 653-658 PMID33942030show ga
  • Recent case reports suggest that coronavirus disease 2019 (COVID-19) is associated with collapsing glomerulopathy in African Americans with apolipoprotein L1 gene (APOL1) risk alleles; however, it is unclear whether disease pathogenesis is similar to HIV-associated nephropathy. RNA sequencing analysis of a kidney biopsy specimen from a patient with COVID-19-associated collapsing glomerulopathy and APOL1 risk alleles (G1/G1) revealed similar levels of APOL1 and angiotensin-converting enzyme 2 (ACE2) messenger RNA transcripts as compared with 12 control kidney samples downloaded from the GTEx (Genotype-Tissue Expression) Portal. Whole-genome sequencing of the COVID-19-associated collapsing glomerulopathy kidney sample identified 4 indel gene variants, 3 of which are of unknown significance with respect to chronic kidney disease and/or focal segmental glomerulosclerosis. Molecular profiling of the kidney demonstrated activation of COVID-19-associated cell injury pathways such as inflammation and coagulation. Evidence for direct severe acute respiratory syndrome coronavirus 2 infection of kidney cells was lacking, which is consistent with the findings of several recent studies. Interestingly, immunostaining of kidney biopsy sections revealed increased expression of phospho-STAT3 (signal transducer and activator of transcription 3) in both COVID-19-associated collapsing glomerulopathy and HIV-associated nephropathy as compared with control kidney tissue. Importantly, interleukin 6-induced activation of STAT3 may be a targetable mechanism driving COVID-19-associated acute kidney injury.
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