What's Happening?
Research led by Gabriel Cara-Fuentes has identified CD93, a protein released by endothelial cells, as a potential therapeutic target in idiopathic nephrotic syndrome (INS). The study found that high urinary
levels of CD93 correlate with poor clinical outcomes, such as rapid kidney disease progression and increased risk of relapse. This discovery suggests that CD93 plays a significant role in endothelial damage and podocyte injury, which are key factors in INS. The findings also indicate that CD93 is highly expressed in the glomerulus and released into urine in other proteinuric kidney diseases, including IgA nephropathy and lupus nephritis.
Why It's Important?
The identification of CD93 as a therapeutic target could lead to new treatment strategies for INS and other related kidney diseases. By focusing on endothelial damage, researchers may develop interventions that slow disease progression and improve patient outcomes. This research highlights the importance of understanding the molecular mechanisms underlying kidney diseases, which could pave the way for more effective therapies. The potential to target CD93 could also reduce the burden of kidney disease on healthcare systems by providing more precise and effective treatment options.
