Treatment of Microvascular Angiopathies
Introduction Acute injuries to smaller blood vessels and subsequent dysfunction of the tissue in which the injured blood vessels are located (microvascular angiopathies) are common features of a variety of diseases of different organs, such as kidney, heart and lungs. A subgroup of such diseases is unified by the presence of thrombotic microangiopathies (TMA), most commonly caused by the hemolytic uremic syndrome (HUS) that is responsible for acute renal failure or often more severe diseases. The current treatment of HUS consists primarily of supportive therapy (dialysis, transfusions and attention to fluid and electrolyte balance) and can be accompanied by the addition of plasma infusion and/or plasma exchange therapy in more severe cases. Unfortunately, some patients do not recover their renal function fully, and between 20 to 40% of patients will develop renal impairment or hypertension within 10-15 years, with as many as half of these patients progressing to dialysis. There is thus a great need for new therapeutic agents for the treatment of microvascular angiopathies, and in particular, TMA. Technology description University of Washington researchers have developed compositions and methods for the prevention or reduction of endothelial cell injury, or the repair of endothelial cells already injured. The invention specifically concerns the prevention and repair of injury to blood vessels and nonvascular tissue associated with microvascular angiopathies, and the prevention and treatment of HUS, by administering an effective amount of a vascular endothelial growth factor (VEGF), wherein VEGF promotes vascular endothelial cell growth. Business Opportunity The primary risk factor for HUS, the principal cause for acute kidney failure in children, is infection with shiga-toxin-producing strains of Escherichia coli. The Center for Disease Control and Prevention report 73,000 of these cases every year. TMA may present in multiple scenarios including pregnancy complications (eclampsia); malignant hypertension following radiation to the kidney; after transplantation; cancer chemotherapies; with certain infections; and in association with systemic lupus or the antiphospholipid syndrome. While current treatments are aimed at removing unknown factors responsible for TMA, UW scientists have developed a new therapy targeted at preventing or reducing endothelial cell injury and may represent a solution to maintain normal function of organs and avoid often irreversible consequences.
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