Biomarkers of Kidney Disease Progression in ADPKD.

Autosomal dominant polycystic kidney disease (ADPKD) is the most common monogenic kidney disorder and the fourth leading cause of kidney failure (KF) in adults. Characterized by a reduction in glomerular filtration rate (GFR) and increased kidney size, ADPKD exhibits significant variability in progression, highlighting the urgent need for reliable and predictive biomarkers to optimize management and treatment approaches. This review explores the roles of diverse biomarkers-including clinical, genetic, molecular, and imaging biomarkers-in evaluating disease progression and customizing treatments for ADPKD.

Spontaneous Coronary Artery Dissection in Patients with Autosomal Dominant Polycystic Kidney Disease: A Systematic Review of the Literature.

Spontaneous coronary artery dissection (SCAD) is a spontaneous intimal tear of the coronary artery wall. A factor rarely associated with SCAD is autosomal dominant polycystic kidney disease (ADPKD). Using the PRISMA guidelines, we identified 10 unique cases of SCAD in ADPKD patients reported between 1998 and 2021.

Epstein-Barr Virus DNA Exacerbates Arthritis in a Mouse Model via Toll-like Receptor 9.

Epstein-Barr virus (EBV) DNA is known to be shed upon reactivation of latent EBV. Based on our previous findings linking Toll-like receptor-9 (TLR9) to an EBV DNA-driven surge in IL-17A production, we aimed to examine the therapeutic potential of TLR9 inhibition in EBV DNA-exacerbated arthritis in a collagen-induced arthritis (CIA) mouse model. C57BL/6J mice were administered either collagen, EBV DNA + collagen, EBV DNA + collagen + TLR9 inhibitor, or only the TLR9 inhibitor.

The Effects of Endosomal Toll-like Receptor Inhibitors in an EBV DNA-Exacerbated Inflammatory Bowel Disease Mouse Model.

Epstein-Barr virus (EBV), a family member, is associated with an increased risk of autoimmune disease development in the host. We previously demonstrated that EBV DNA elevates levels of the pro-inflammatory cytokine IL-17A and that inhibiting Toll-like receptor (TLR) 3, 7, or 9 reduces its levels. Moreover, this DNA exacerbated colitis in a mouse model of inflammatory bowel disease (IBD).

The role of Epstein-Barr virus in autoimmune and autoinflammatory diseases.

Epstein-Barr Virus (EBV), a dsDNA herpesvirus, is believed to play a significant role in exacerbating and potentially triggering autoimmune and autoinflammatory maladies. Around 90% of the world is infected with the virus, which establishes latency within lymphocytes. EBV is also known to cause infectious mononucleosis, a self-limited flu-like illness, in adolescents.