Biomaterial Database

Shiga toxin associated hemolytic uremic syndrome. 2015

Lindsay Susan Keir

Department of Molecular and Cell Biology, The Scripps Research Institute, MB 216, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA; Academic Renal Unit, University of Bristol, Dorothy Hodgkin Building, Whitson Street, Bristol BS1 3NY, UK. Electronic address: lskeir@doctors.org.uk.

Shiga toxin associated hemolytic uremic syndrome (Stx HUS), a thrombotic microangiopathy, is the most common cause of pediatric acute kidney injury but has no direct treatment. A better understanding of disease pathogenesis may help identify new therapeutic targets. For this reason, the role of complement is being actively studied while eculizumab, the C5 monoclonal antibody, is being used to treat Stx HUS but with conflicting results. A randomized controlled trial would help properly evaluate its use in Stx HUS while more research is required to fully evaluate the role complement plays in the disease pathogenesis.

UI	MeSH Term	Description	Entries
D002648	Child	A person 6 to 12 years of age. An individual 2 to 5 years old is CHILD, PRESCHOOL.	Children
D003165	Complement System Proteins	Serum glycoproteins participating in the host defense mechanism of COMPLEMENT ACTIVATION that creates the COMPLEMENT MEMBRANE ATTACK COMPLEX. Included are glycoproteins in the various pathways of complement activation (CLASSICAL COMPLEMENT PATHWAY; ALTERNATIVE COMPLEMENT PATHWAY; and LECTIN COMPLEMENT PATHWAY).	Complement Proteins,Complement,Complement Protein,Hemolytic Complement,Complement, Hemolytic,Protein, Complement,Proteins, Complement,Proteins, Complement System
D003170	Complement Pathway, Alternative	Complement activation initiated by the interaction of microbial ANTIGENS with COMPLEMENT C3B. When COMPLEMENT FACTOR B binds to the membrane-bound C3b, COMPLEMENT FACTOR D cleaves it to form alternative C3 CONVERTASE (C3BBB) which, stabilized by COMPLEMENT FACTOR P, is able to cleave multiple COMPLEMENT C3 to form alternative C5 CONVERTASE (C3BBB3B) leading to cleavage of COMPLEMENT C5 and the assembly of COMPLEMENT MEMBRANE ATTACK COMPLEX.	Alternative Complement Pathway,Properdin Pathway,Alternative Complement Activation Pathway,Complement Activation Pathway, Alternative
D006463	Hemolytic-Uremic Syndrome	A syndrome that is associated with microvascular diseases of the KIDNEY, such as RENAL CORTICAL NECROSIS. It is characterized by hemolytic anemia (ANEMIA, HEMOLYTIC); THROMBOCYTOPENIA; and ACUTE RENAL FAILURE.	Gasser's Syndrome,Gasser Syndrome,Gassers Syndrome,Hemolytic Uremic Syndrome,Syndrome, Hemolytic-Uremic
D006801	Humans	Members of the species Homo sapiens.	Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D054323	Shiga-Toxigenic Escherichia coli	Strains of ESCHERICHIA COLI with the ability to produce at least one or more of at least two antigenically distinct, usually bacteriophage-mediated cytotoxins: SHIGA TOXIN 1 and SHIGA TOXIN 2. These bacteria can cause severe disease in humans including bloody DIARRHEA and HEMOLYTIC UREMIC SYNDROME.	E coli, Verotoxigenic,Escherichia coli, Verotoxigenic,STEC,Verotoxigenic Escherichia coli,Shiga Toxigenic E. coli,Shiga Toxigenic Escherichia coli,Shiga Toxin-Producing Escherichia coli,VTEC,Vero Cytotoxin-Producing Escherichia coli,Verotoxigenic E. coli,Verotoxin-Producing Escherichia coli
D057049	Thrombotic Microangiopathies	Diseases that result in THROMBOSIS in MICROVASCULATURE. The two most prominent diseases are PURPURA, THROMBOTIC THROMBOCYTOPENIC; and HEMOLYTIC-UREMIC SYNDROME. Multiple etiological factors include VASCULAR ENDOTHELIAL CELL damage due to SHIGA TOXIN; FACTOR H deficiency; and aberrant VON WILLEBRAND FACTOR formation.	Microangiopathies, Thrombotic,Microangiopathy, Thrombotic,Thrombotic Microangiopathy
D058186	Acute Kidney Injury	Abrupt reduction in kidney function. Acute kidney injury encompasses the entire spectrum of the syndrome including acute kidney failure; ACUTE KIDNEY TUBULAR NECROSIS; and other less severe conditions.	Acute Kidney Failure,Acute Kidney Insufficiency,Acute Renal Failure,Acute Renal Injury,Acute Renal Insufficiency,Kidney Failure, Acute,Kidney Insufficiency, Acute,Renal Failure, Acute,Renal Insufficiency, Acute,Acute Kidney Failures,Acute Kidney Injuries,Acute Kidney Insufficiencies,Acute Renal Failures,Acute Renal Injuries,Acute Renal Insufficiencies,Kidney Failures, Acute,Kidney Injuries, Acute,Kidney Injury, Acute,Kidney Insufficiencies, Acute,Renal Failures, Acute,Renal Injuries, Acute,Renal Injury, Acute,Renal Insufficiencies, Acute
D018448	Models, Immunological	Theoretical representations that simulate the behavior or activity of immune system, processes, or phenomena. They include the use of mathematical equations, computers, and other electrical equipment.	Immunological Models,Immunologic Model,Model, Immunologic,Immunologic Models,Immunological Model,Model, Immunological,Models, Immunologic
D022621	Shiga Toxin	A toxin produced by SHIGELLA DYSENTERIAE. It is the prototype of class of toxins that inhibit protein synthesis by blocking the interaction of ribosomal RNA; (RNA, RIBOSOMAL) with PEPTIDE ELONGATION FACTORS.	Shigatoxin,Stx Protein, Shigella dysenteria,Shigella Cytotoxin,Shigella Toxin,Stx Protein,Cytotoxin, Shigella,Toxin, Shiga,Toxin, Shigella