IgA nephropathy is the most common primary glomerulonephritis and contributes to kidney failure. Growing evidence exists that the overactivation of the lectin pathway contributes to the pathogenesis of IgA nephropathy.
Although antifibrotic agents can contribute to suppressing renal function decline when administered in combination with existing treatments for chronic kidney disease, drugs targeting kidney fibrosis have yet to reach the clinic.
Scientists from INSERM and affiliated organizations presented findings from their work that aimed to investigate the involvement of heat shock protein 27 (HSP27) in the activation and pathological accumulation of parietal epithelial cells (PEC) during crescentic glomerulonephritis (CrGN).
The knockout of Col4a3 in mice is used as a model of Alport syndrome. Knockout mice develop glomerular disease associated with neutral lipid accumulation in the kidney and progressive renal failure, which can be treated with lipid-lowering agents.
Researchers at the Stony Brook University Renaissance School of Medicine performed a screening in search of Kruppel-like factor 15 (KLF15) agonists for treating proteinuric injuries in the kidney.
Patients receiving a kidney transplant and who are positive for BK virus (BKV) are at risk of losing their transplant due to BKV reactivation. At this time, there are no antiviral options available for the prevention of BKV-associated nephropathy. Researchers from Aicuris Anti-infective Cures GmbH presented preclinical data on AIC-468, an antisense RNA therapy that inhibits the splicing process of a viral mRNA encoding a protein critical for BKV replication.
Researchers from Southern Medical University and affiliated organizations presented the discovery and preclinical characterization of novel human urate transporter 1 (hURAT1) inhibitors being developed for the treatment of hyperuricemia.
Purespring Therapeutics Ltd. has raised £80 million (US$104.6 million) in a series B, putting it on course to be the first to take a gene therapy for a kidney disease into the clinic. The money enables the company to move the lead program, PS-002, for the treatment of IgA nephropathy to clinical proof of concept and advance programs in other complement-mediated kidney diseases, and in an undisclosed glomerular kidney disease.