Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7142700 | PMC |
http://dx.doi.org/10.1016/j.ekir.2020.04.002 | DOI Listing |
Hong Kong Med J
December 2024
Department of Pediatric Nephrology, Gazi University Faculty of Medicine, Gazi University, Ankara, Turkey.
Intern Med J
December 2024
Department of Medicine, University of Melbourne, Melbourne, Victoria, Australia.
BMC Nephrol
October 2024
Department of Pathology, Jawaharlal Institute of Postgraduate Medical Education and Research, Puducherry, 605006, India.
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.
View Article and Find Full Text PDFKidney Int Rep
September 2024
Division of Nephrology, Duke Molecular Physiology Institute, Duke University School of Medicine, Durham, North Carolina, USA.
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.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!