No therapies currently exist that can halt the progression of chronic kidney disease in children or restore the ability of kidney cells to filter blood.
Apr 9 2024 Children 's Hospital Los Angeles Recently, researchers at the GOFARR Laboratory for Organ Regenerative Research and Cell Therapeutics in Urology in The Saban Research Institute of Children 's Hospital Los Angeles found new clues to understanding how chronic kidney disease progresses.
We have a good idea of what happens in the process of various types of chronic kidney failure, but we still don't know precisely why and where it happens. Our goal was to scrutinize the molecular processes of any underlying mechanisms that could cause kidney podocytes to fail and lose their blood filtering capacity. Membranous nephropathy, which affects adults, can serve as a disease model for other chronic kidney disease processes that affect children and adults alike.
Previously, researchers believed that the membrane-attack-complex was the sole driver of podocyte injury, and that inhibiting it was key to halting disease progression. The GOFARR research team discovered instead that signaling in the C3a/C3aR pathway plays a critical role in the progression of membranous nephropathy.
Related Stories"By probing what is actually happening at the molecular level, we found that an entirely different pathway than we initially thought was the main driver for primary membranous neuropathy," says Dr. Da Sacco, Assistant Professor of Research Urology at the Keck School of Medicine of USC. "We had previous knowledge that this pathway could cause damage to podocytes, but no confirmation that it was important in membranous nephropathy.
This work was supported by grants from NIH/NIDDK and by the GOFARR Foundation from the Schenkman Family.Journal reference:Zhang, Q., et al. . C3aR-initiated signaling is a critical mechanism of podocyte injury in membranous nephropathy. JCI Insight. doi.org/10.1172/jci.insight.172976.
Chronic Chronic Kidney Disease Kidney Kidney Disease Nephropathy Antigen Autoantibodies Blood Cell CHIP Gene Genetic Glomerulus Hospital Laboratory Receptor Research Therapeutics Toxins Urology
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