Document Detail


Excessive activation of the complement system in atypical hemolytic uremic syndrome: is it ready for prime time?
MedLine Citation:
PMID:  20118898     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Complement factor I (CFI) mutations are implicated in the pathogenesis of atypical hemolytic uremic syndrome (aHUS). Nevertheless, there is evidence that CFI deficiency is a weak effector of aHUS. Bienaime et al. report that homozygous deletion of CFHR-1 in the RCA gene cluster of chromosome 1q is a major risk factor for poor outcome for patients with CFI mutations. The basic and clinical implications of the findings are further elaborated here.
Authors:
Han-Mou Tsai
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Publication Detail:
Type:  Comment; Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Kidney international     Volume:  77     ISSN:  1523-1755     ISO Abbreviation:  Kidney Int.     Publication Date:  2010 Feb 
Date Detail:
Created Date:  2010-02-01     Completed Date:  2010-06-04     Revised Date:  2011-09-26    
Medline Journal Info:
Nlm Unique ID:  0323470     Medline TA:  Kidney Int     Country:  United States    
Other Details:
Languages:  eng     Pagination:  267-9     Citation Subset:  IM    
Affiliation:
Division of Hematology/Oncology, Pennsylvania State University, Milton S. Hershey Medical Center, Hershey, Pennsylvania 17033, USA. htsai@hmc.psu.edu
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MeSH Terms
Descriptor/Qualifier:
Complement Activation*
Hemolytic-Uremic Syndrome / immunology*
Humans
Grant Support
ID/Acronym/Agency:
R01 HL062136-10/HL/NHLBI NIH HHS; R01HL62136/HL/NHLBI NIH HHS
Comments/Corrections
Comment On:
Kidney Int. 2010 Feb;77(4):339-49   [PMID:  20016463 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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