New Biomarker and Therapeutic Target for Sepsis and AKI

SANTA ROSA, Calif., Nov. 16, 2021 /PRNewswire/ -- Better Health Publishing -- A new biomarker and therapeutic target for sepsis and acute kidney injury (AKI) has been identified in two studies, offering a novel intervention for the leading causes of intensive care unit (ICU)-related deaths. With cytokine storms and organ failure the primary comorbidity in aggressive viral infections, these findings are especially relevant.

The research demonstrates that the pro-inflammatory biomarker protein, galectin-3 (Gal-3), serves as the primary driver of sepsis and AKI. Use of Gal-3 inhibitor, Modified Citrus Pectin (P-MCP), prevented kidney damage and reduced mortality in sepsis.

Galectin-3, Sepsis and AKI

Gal-3 is a multifunctional binding protein that controls the inflammatory immune response. Thousands of studies demonstrate that Gal-3 drives inflammatory, fibrotic, and degenerative conditions including cardiovascular disease, kidney failure, cancer, and others.

The first study highlighting the role of Gal-3 in sepsis and AKI is a human and animal translational study published March 2021 in Critical Care. Results demonstrate Gal-3's primary actions in promoting sepsis and AKI. The study also showed how pre-treatment with Gal-3 inhibitor P-MCP significantly prevented and reduced kidney damage, and reduced mortality from 61% to 22% in a proven sepsis-AKI animal model.  

A follow-up study, published October 2021 in Critical Care, expands on these findings by showing Gal-3 to be an early biomarker of AKI in patients after cardiac surgery entering the ICU. The study also analyzed Gal-3 inhibition by P-MCP in another type of AKI animal model. Findings again showed that P-MCP significantly decreased Gal-3 expression, reduced interleukin-6 (IL-6), and significantly reduced renal dysfunction and renal tubular injury.

Clinical findings from this study showed that post-cardiac surgery patients who had elevated Gal-3 levels at the time of admission to the ICU, went on to develop AKI. In the animal model, researchers examined Gal-3 levels and renal function in animals pretreated with P-MCP for one week before induced AKI, compared to controls. Results showed once again P-MCP decreased Gal-3 levels and reduced kidney injury.

P-MCP for Cardiac Surgery and AKI

This research adds to the growing body of data highlighting Gal-3 in the pathogenesis of sepsis, cytokine storms, AKI, and organ failure. It also expands the role of researched P-MCP as a potential adjunct in support against the cytokine storm and downstream effects, as well as other inflammatory conditions.

SOURCE Better Health Publishing

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