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Acute Kidney Injury (AKI) can be life-threatening in various patient populations.
Full recovery of kidney function is uncommon and leaves AKI patients at risk of long-term morbidity and death.
AKI affects almost 900,000 people in the United States with an annual cost of up to $24.0 billion. The most expensive patients are those with AKI of sufficient severity to require dialysis, where cost increases relative to patients without AKI and can reach up to $42,000 per hospitalization event.
In-hospital, mortality for patients with AKI has recently been estimated between 20 and 25%, while critically ill patients with dialysis-requiring AKI experience mortality rates in excess of 50%. Despite efforts to develop new therapeutic modalities, current therapeutic options are very limited. Global, regional, and national sepsis incidence and mortality, 1990–2017: Analysis for the global burden of disease study.
"Sepsis associated with 1 in 5 deaths globally..."
"...In 2017, an estimated 48.9 million (95% uncertainty interval [UI] 38.9-62.9) incident cases of sepsis were recorded worldwide and 11.0 million (10.1-12.0) sepsis-related deaths were reported, representing 19.7% (18.2-21.4) of all global deaths.
Global, regional, and national sepsis incidence and mortality, 1990-2017: analysis for the Global Burden of Disease Study.
The Lancet, 2020; DOI: 10.1016/S0140-6736(19)32989-7
Medical Device for Removal of Galectin-3
Studies demonstrate that Gal-3 has a causal role in AKI. AKI mediates not only local injury but also induces remote cardiac dysfunction, injury, and fibrosis via a gal-3-dependent pathway. Gal-3’s causal role in AKI makes it a potential point of therapeutic intervention.
Galectin-3 (Gal-3) is an important mediator and a known key driver of organ inflammation and fibrosis in numerous acute and chronic progressive conditions.In critically ill patients, the development of Sepsis and AKI is associated with increased plasma Gal-3 levels and increased biomarkers of kidney fibrosis and damage.
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Gal-3 is also associated with the progression of diabetes, heart failure, cancer, as well as liver and lung fibrosis. We have developed a unique medical device to allow Gal-3 removal from the circulation.
By targeting Gal-3 and selectively removing it from the bloodstream, we stop the rapid kidney function deterioration and effectively prevent long-term debilitating illnesses.
The addition of an extracorporeal procedure to intervene at an early stage to potentially slow down an aggressive disease or enhance the effectiveness of other therapies.
A recent proof-of-concept study shows that the removal of Gal-3 through a prototype device concept is both feasible and effective, yielding dramatic results in an induced fibrosis model.
The results, supported by previous models with Gal-3 inhibitors and genetic knockout animals, indicate that the removal of Gal-3 from the circulation can revolutionize the care of CKD patients, as well as of other potential Gal-3 mediated diseases including heart failure and cancer.
The single-use X-Gal-3 apheresis column selectively removes Galectin-3 from the body. Containing proprietary, highly effective molecule capturing, X-Gal-3 is built in a format that hospitals already know how to use.
