Hemolytic-uremic syndrome risk factors: Difference between revisions
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==Overview== | ==Overview== | ||
The most potent risk factor in the development of Hemolytic Uremic Syndrome in childhood is infection with Verocytotoxin (shiga-like toxin)-producing bacteria, usually Enterohemorrhagic Escherichia coli (VTEC/STEC),and in some tropical regions Shigella dysenteriae type I . Other risk factors include genetic mutations in Complement factors, Pnemumococcal infections, Autoimmune diseases like SLE and Antiphospholipid Syndrome, Pregnancy, Antineoplastic and immunosupressive drugs, HIV infection and Organ transplantation. | The most potent risk factor in the development of Hemolytic Uremic Syndrome in childhood is infection with Verocytotoxin (shiga-like toxin)-producing bacteria, usually Enterohemorrhagic Escherichia coli (VTEC/STEC),and in some tropical regions Shigella dysenteriae type I . Other risk factors include genetic mutations in Complement factors, Pnemumococcal infections, Autoimmune diseases like SLE and Antiphospholipid Syndrome, Pregnancy, Antineoplastic and immunosupressive drugs, HIV infection and Organ transplantation. | ||
Revision as of 17:31, 13 August 2018
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Differentiating Hemolytic-uremic syndrome from other Diseases |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Anila Hussain, MD [2]
Overview
The most potent risk factor in the development of Hemolytic Uremic Syndrome in childhood is infection with Verocytotoxin (shiga-like toxin)-producing bacteria, usually Enterohemorrhagic Escherichia coli (VTEC/STEC),and in some tropical regions Shigella dysenteriae type I . Other risk factors include genetic mutations in Complement factors, Pnemumococcal infections, Autoimmune diseases like SLE and Antiphospholipid Syndrome, Pregnancy, Antineoplastic and immunosupressive drugs, HIV infection and Organ transplantation.
Risk Factors
The most potent risk factor in the development of HUS is etiology advanced and Clinical associations . Other risk factors include [etiology unknown].
etiology advance
- Infection induced
- Shiga and verocytotoxin (shiga-like toxin)-producing bacteria;enterohemorrhagic Escherichia coli, Shigella dysenteriaen type 1,Citrobacter
- Streptococcus pneumoniae, neuraminidase, and T-antigen exposure
- Disorders of complement regulation
- Complement factor H (CFH) mutation/ Factor H Defeciency (Autosomal Dominant)
- Complement Factor I(CFI) Defeciency (Acquired antibody mediated)
- Membrane co-factor protein Defeciency (MCP; CD46)
- Factor B Overactivity (Complement Factor B mutation)
- Diacylglycerol Kinase Epsilon gene mutations
- von Willebrand proteinase, ADAMTS13 deficiency
- Genetic disorders of ADAMTS13
- Acquired von Willebrand proteinase deficiency; autoimmune, drug induced
- Defective cobalamine metabolism.
Clinical associations with following diseases:
- Malignancy, cancer chemotherapy and ionizing radiation
- Calcineurin inhibitors and transplantation
- Pregnancy, HELLP syndrome and oral contraceptive pill
- Systemic lupus erythematosis and antiphospholipid antibody syndrome
- Glomerulopathy
- Familial, not included in part 1
- Unclassified