Hemolytic-uremic syndrome risk factors: Difference between revisions
mNo edit summary |
|||
| Line 1: | Line 1: | ||
__NOTOC__ | __NOTOC__ | ||
{{HUS}} | {{HUS}} | ||
{{CMG}}; {{AE}} | |||
es: | |||
#HIV | |||
{{CMG}}; {{AE}} | |||
==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 | |||
==Risk Factors== | ==Risk Factors== | ||
| Line 24: | Line 15: | ||
'''etiology advance ''' | '''etiology advance ''' | ||
*Infection induced | *'''Infection induced''' | ||
#Shiga and verocytotoxin (shiga-like toxin)-producing bacteria;enterohemorrhagic Escherichia coli, Shigella dysenteriaen type 1,Citrobacter | #Shiga and verocytotoxin (shiga-like toxin)-producing bacteria;enterohemorrhagic Escherichia coli, Shigella dysenteriaen type 1,Citrobacter | ||
#Streptococcus pneumoniae, neuraminidase, and T-antigen exposure | #Streptococcus pneumoniae, neuraminidase, and T-antigen exposure | ||
*Disorders of complement | *'''Disorders of complement regulatio'''n | ||
**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 | *'''von Willebrand proteinase, ADAMTS13 deficiency''' | ||
# Genetic disorders of ADAMTS13 | # Genetic disorders of ADAMTS13 | ||
#Acquired von Willebrand proteinase deficiency; autoimmune, drug induced | #Acquired von Willebrand proteinase deficiency; autoimmune, drug induced | ||
*Defective cobalamine metabolism | *'''Defective cobalamine metabolism'''. | ||
'''Clinical associations with following diseases:''' | |||
#Malignancy, cancer chemotherapy and ionizing radiation | #Malignancy, cancer chemotherapy and ionizing radiation | ||
#Calcineurin inhibitors and transplantation | #Calcineurin inhibitors and transplantation | ||
| Line 54: | Line 45: | ||
{{WH}} | {{WH}} | ||
{{WS}} | {{WS}} | ||
[[Category:Nephrology]] | [[Category:Nephrology]] | ||
[[Category:Hematology]] | [[Category:Hematology]] | ||
Revision as of 16:49, 8 August 2018
|
Hemolytic-uremic syndrome Microchapters |
|
Differentiating Hemolytic-uremic syndrome from other Diseases |
|---|
|
Diagnosis |
|
Treatment |
|
Case Studies |
|
Hemolytic-uremic syndrome risk factors On the Web |
|
American Roentgen Ray Society Images of Hemolytic-uremic syndrome risk factors |
|
Risk calculators and risk factors for Hemolytic-uremic syndrome risk factors |
es:
- HIV
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
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