scholarly journals Infections in Pediatric Postdiarrheal Hemolytic Uremic Syndrome

2012 ◽  
Vol 166 (10) ◽  
pp. 902 ◽  
Author(s):  
Rajal K. Mody ◽  
Ruth E. Luna-Gierke ◽  
Timothy F. Jones ◽  
Nicole Comstock ◽  
Sharon Hurd ◽  
...  
Keyword(s):  
Hemolytic Uremic Syndrome ◽  
Uremic Syndrome ◽  
Postdiarrheal Hemolytic Uremic Syndrome

Involvement of the fractalkine pathway in the pathogenesis of childhood hemolytic uremic syndrome

Blood ◽  
2006 ◽  
Vol 109 (6) ◽  
pp. 2438-2445 ◽  
Author(s):  
María Victoria Ramos ◽  
Gabriela C. Fernández ◽  
Natasha Patey ◽  
Pablo Schierloh ◽  
Ramón Exeni ◽  
...  
Keyword(s):  
Renal Failure ◽  
Endothelial Cells ◽  
Hemolytic Uremic Syndrome ◽  
Cell Damage ◽  
Mononuclear Leukocytes ◽  
Selective Depletion ◽  
Inflammatory Processes ◽  
Uremic Syndrome ◽  
Globotriaosyl Ceramide ◽  
Postdiarrheal Hemolytic Uremic Syndrome

Abstract Thrombotic microangiopathy and acute renal failure are cardinal features of postdiarrheal hemolytic uremic syndrome (HUS). These conditions are related to endothelial and epithelial cell damage induced by Shiga toxin (Stx) through the interaction with its globotriaosyl ceramide receptor. However, inflammatory processes contribute to the pathogenesis of HUS by sensitizing cells to Stx fractalkine (FKN), a CX3C transmembrane chemokine expressed on epithelial and endothelial cells upon activation, is involved in the selective migration and adhesion of specific leukocyte subsets to tissues. Here, we demonstrated a selective depletion of circulating mononuclear leukocytes expressing the receptor for FKN (CX3CR1) in patients with HUS. We found a unique phenotype in children with HUS distinct from that seen in healthy, uremic, or infected controls, in which monocytes lost CX3CR1, down-modulated CD62L, and increased CD16. In addition, the CD56dim natural killer (NK) subpopulation was decreased, leading to an altered peripheral CD56dim/CD56bright ratio from 10.0 to 4.5. It is noteworthy that a negative correlation existed between the percentage of circulating CX3CR1+ leukocytes and the severity of renal failure. Finally, CX3CR1+ leukocytes were observed in renal biopsies from patients with HUS. We suggest that the interaction of CX3CR1+ cells with FKN present on activated endothelial cells may contribute to renal injury in HUS.

POSTDIARRHEAL HEMOLYTIC UREMIC SYNDROME IN PERSONS AGED 65 AND OLDER IN FOODNET SITES, 2000-2006

2011 ◽  
Vol 59 (2) ◽  
pp. 366-368 ◽  
Author(s):  
L. Hannah Gould ◽  
John G. Jordan ◽  
John Dunn ◽  
Mirasol Apostol ◽  
Patricia M. Griffin ◽  
...  
Keyword(s):  
Hemolytic Uremic Syndrome ◽  
Uremic Syndrome ◽  
Postdiarrheal Hemolytic Uremic Syndrome

Prognostic significance of microalbuminuria in postdiarrheal hemolytic uremic syndrome

2007 ◽  
Vol 22 (1) ◽  
pp. 117-120 ◽  
Author(s):  
Randall Lou-Meda ◽  
Robert S. Oakes ◽  
Jarom N. Gilstrap ◽  
Christopher G. Williams ◽  
Richard L. Siegler
Keyword(s):  
Hemolytic Uremic Syndrome ◽  
Prognostic Significance ◽  
Uremic Syndrome ◽  
Postdiarrheal Hemolytic Uremic Syndrome

A 20-Year Population-Based Study of Postdiarrheal Hemolytic Uremic Syndrome in Utah

PEDIATRICS ◽  
1994 ◽  
Vol 94 (1) ◽  
pp. 35-40
Author(s):  
Richard L. Siegler ◽  
Ryan D. Christofferson ◽  
Mark K. Milligan ◽  
Andrew T. Pavia
Keyword(s):  
Hemolytic Uremic Syndrome ◽  
Severe Disease ◽  
Public Health Problem ◽  
Population Based ◽  
Etiologic Agent ◽  
Population Based Study ◽  
Cell Counts ◽  
Uremic Syndrome ◽  
Postdiarrheal Hemolytic Uremic Syndrome ◽  
Epidemiologic Features

Objective. To determine epidemiologic features, trends in frequency, and predictors of clinical outcome of postdiarrheal hemolytic uremic syndrome (HUS) in Utah. Design. A 20-year population-based study of HUS with a review of the HUS registry, hospital records, transplant registry, and a survey of pediatricians and pediatric nephrologists to ensure completeness of ascertainment. Population. All Utah residents under 18 years of age with HUS occurring after a diarrheal prodrome between 1971 and 1990. Outcome measures. Incidence of HUS, severity, complications, and long-term sequelae. Results. There were 157 cases during 20 years; 140 (89%) occurred after a diarrheal prodrome. The mean annual incidence was 1.42/100 000 children (range 0.2 to 3.4/100 000 children/year). Periods of high incidence occurred; however, there was no overall sustained increase in incidence. Escherichia coli O157:H7 was isolated from the stool of 62% of children who had specimens submitted. There were no differences between the first and second decade in the proportion with diarrheal prodrome, bloody diarrhea, most abnormal laboratory values, hospital course, or outcome. However, admission laboratory abnormalities were more severe during the first decade suggesting a delay in diagnosis. Age <2 years, anuria before admission, and higher white blood cell counts on admission predicted severe disease. Bad outcome (death, end-stage renal disease, or stroke) occurred in 11%; 5% died. Chronic renal sequelae, usually mild, were found on follow-up (median 6.5 years) in 51% of survivors. Conclusions. HUS has been an important clinical and public health problem in Utah for 20 years. The consistency of the clinical and epidemiologic features over 2 decades suggests that a common etiologic agent has accounted for most cases of HUS in this region since 1971.

Hemorrhagic colitis in postdiarrheal hemolytic uremic syndrome: retrospective analysis of 54 children

2011 ◽  
Vol 27 (2) ◽  
pp. 229-233 ◽  
Author(s):  
Ricardo C. Rahman ◽  
Carlos J. Cobeñas ◽  
Ricardo Drut ◽  
Oscar R. Amoreo ◽  
Javier D. Ruscasso ◽  
...  
Keyword(s):  
Hemolytic Uremic Syndrome ◽  
Retrospective Analysis ◽  
Hemorrhagic Colitis ◽  
Uremic Syndrome ◽  
Postdiarrheal Hemolytic Uremic Syndrome

scholarly journals Response to Single and Divided Doses of Shiga Toxin-1 in a Primate Model of Hemolytic Uremic Syndrome

2001 ◽  
Vol 12 (7) ◽  
pp. 1458-1467 ◽  
Author(s):  
RICHARD L. SIEGLER ◽  
THEODORE J. PYSHER ◽  
VERNON L. TESH ◽  
FLETCHER B. TAYLOR
Keyword(s):  
Hemolytic Uremic Syndrome ◽  
Shiga Toxin ◽  
Capillary Endothelium ◽  
Primate Model ◽  
Disease Expression ◽  
Uremic Syndrome ◽  
Flocculent Material ◽  
Factor Α ◽  
Postdiarrheal Hemolytic Uremic Syndrome

Abstract. Postdiarrheal hemolytic uremic syndrome is caused by Shiga toxin (Stx)-producing Escherichia coli. It was shown previously that the baboon, like the human, has glycolipid receptors for Stx in the gut and the kidney and that a single 50- to 200-ng/kg intravenous dose of purified Stx-1 results in thrombocytopenia, hemolytic anemia, and renal thrombotic microangiopathy. For further characterization of factors that modulate disease expression, the baboon's response to the intravenous administration of 100 ng/kg Stx-1 given either rapidly as a single bolus or slowly as four 25-ng/kg doses at 12-h intervals was compared. Animals that received the Stx-1 as a single dose developed thrombocytopenia, schistocytosis, and acute renal failure. Urinary but not plasma tumor necrosis factor-α concentrations rose significantly by 6 h and then declined rapidly. Urinary and plasma interleukin-6 concentrations rose later. Glomeruli showed reduced patency of capillary loops, fragmented red blood cells, fibrin and platelet microthrombi, necrosis and detachment of endothelial cells, and accumulation of flocculent material in subendothelial spaces. Damage to tubular epithelium and peritubular capillary endothelium also was seen. Animals that received four divided doses of Stx-1 developed no clinical or histologic features of hemolytic uremic syndrome. It is concluded that in the primate model, disease expression is modulated by the rate of Stx administration, and it is speculated that in the human, the rate of Stx absorption from the gut is one determinant of disease severity.

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