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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7142700PMC
http://dx.doi.org/10.1016/j.ekir.2020.04.002DOI Listing

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Article Synopsis
  • * Among 94 patients, most were male and half had a history of hypertension; commonly observed kidney issues included collapsing glomerulopathy (CG), focal segmental glomerulosclerosis (FSGS), and thrombotic microangiopathy (TMA).
  • * Results indicated that FSGS and minimal change disease (MCD) were linked to better kidney survival compared to TMA, underscoring differences in kidney complications resulting from COVID-19 within this patient group.
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What is the spectrum of kidney pathology associated with COVID-19?

Intern Med J

December 2024

Department of Medicine, University of Melbourne, Melbourne, Victoria, Australia.

Article Synopsis
  • * A review of 14 studies, covering 159 patients, showed that direct viral infection isn't the primary cause of kidney damage; instead, factors like specific genotypes among patients of African descent contribute to conditions like collapsing glomerulopathy.
  • * Understanding COVID-19-related kidney problems is crucial for developing better treatment strategies and preventing chronic kidney disease, but more research is needed to grasp the long-term effects.
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Background: Podocytopathies, including minimal change disease (MCD), focal segmental glomerulosclerosis (FSGS), and collapsing glomerulopathy (CG), are kidney diseases that damage glomerular podocytes, leading to heavy proteinuria and nephrotic syndrome (NS). Inflammation plays a critical role in the progression of chronic kidney disease (CKD), with recent studies linking inflammatory biomarkers to declining kidney function. Tumor necrosis factor-alpha (TNF-α), an essential inflammatory cytokine, interacts with its circulating receptors, TNFR1 and TNFR2.

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Introduction: SARS-CoV-2 infection increases systemic inflammatory cytokines which act as a second-hit driver of Apolipoprotein L1 (APOL1)-mediated collapsing glomerulopathy. SARS-CoV-2 vaccination also increases cytokines. Recent reports of new glomerular disease in individuals with high-risk genotype (HRG) following SARS-CoV-2 vaccination raised the concern SARS-CoV-2 vaccination may also act as a second-hit driver of APOL1-mediated glomerulopathy.

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