RGD Reference Report - Genetic Susceptibility to Postdiarrheal Hemolytic-Uremic Syndrome After Shiga Toxin-Producing Escherichia coli Infection: A Centers for Disease Control and Prevention FoodNet Study. - Rat Genome Database

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Genetic Susceptibility to Postdiarrheal Hemolytic-Uremic Syndrome After Shiga Toxin-Producing Escherichia coli Infection: A Centers for Disease Control and Prevention FoodNet Study.

Authors: Kallianpur, Asha R  Bradford, Yuki  Mody, Rajal K  Garman, Katie N  Comstock, Nicole  Lathrop, Sarah L  Lyons, Carol  Saupe, Amy  Wymore, Katie  Canter, Jeffrey A  Olson, Lana M  Palmer, Amanda  Jones, Timothy F 
Citation: Kallianpur AR, etal., J Infect Dis. 2018 Mar 5;217(6):1000-1010. doi: 10.1093/infdis/jix633.
RGD ID: 42722620
Pubmed: PMID:29216383   (View Abstract at PubMed)
DOI: DOI:10.1093/infdis/jix633   (Journal Full-text)


Background: Postdiarrheal hemolytic-uremic syndrome (D+HUS) following Shiga toxin-producing Escherichia coli (STEC) infection is a serious condition lacking specific treatment. Host immune dysregulation and genetic susceptibility to complement hyperactivation are implicated in non-STEC-related HUS. However, genetic susceptibility to D+HUS remains largely uncharacterized.
Methods: Patients with culture-confirmed STEC diarrhea, identified through the Centers for Disease Control and Prevention FoodNet surveillance system (2007-2012), were serotyped and classified by laboratory and/or clinical criteria as having suspected, probable, or confirmed D+HUS or as controls and underwent genotyping at 200 loci linked to nondiarrheal HUS or similar pathologies. Genetic associations with D+HUS were explored by multivariable regression, with adjustment for known risk factors.
Results: Of 641 enrollees with STEC O157:H7, 80 had suspected D+HUS (41 with probable and 32 with confirmed D+HUS). Twelve genes related to cytokine signaling, complement pathways, platelet function, pathogen recognition, iron transport, and endothelial function were associated with D+HUS in multivariable-adjusted analyses (P <= .05). Of 12 significant single-nucleotide polymorphisms (SNPs), 5 were associated with all levels of D+HUS (intergenic SNP rs10874639, TFRC rs3804141, EDN1 rs5370, GP1BA rs121908064, and B2M rs16966334), and 7 SNPs (6 non-complement related) were associated with confirmed D+HUS (all P < .05).
Conclusions: Polymorphisms in many non-complement-related genes may contribute to D+HUS susceptibility. These results require replication, but they suggest novel therapeutic targets in patients with D+HUS.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Diarrhea prodrome + Hemolytic-Uremic Syndrome  IAGP 42722620associated with Escherichia Coli Infections and DNA:SNP:exon: (rs121908064) (human)RGD 
Diarrhea prodrome + Hemolytic-Uremic Syndrome  ISOGP1BA (Homo sapiens)42722620; 42722620associated with Escherichia Coli Infections and DNA:SNP:exon: (rs121908064) (human)RGD 

Objects Annotated

Genes (Rattus norvegicus)
Gp1ba  (glycoprotein Ib platelet subunit alpha)

Genes (Mus musculus)
Gp1ba  (glycoprotein 1b, alpha polypeptide)

Genes (Homo sapiens)
GP1BA  (glycoprotein Ib platelet subunit alpha)


Additional Information