Laboratory and Clinical Variables to Predict Outcome in Hemolytic-Uremic Syndrome

Havens, Peter L.; O’Rourke, P. Pearl; Hahn, Jin S.; Higgins, Joseph; Walker, Alexander M.

doi:10.1001/archpedi.1988.02150090059022

Cited by 11 publications

(12 citation statements)

References 5 publications

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“…1 Previously identified predictors of D + HUS-related in-hospital death include marked leukocytosis 1-3 and greater hematocrit or hemoglobin values. [1][2][3][4] Studies that explore how these and other factors interact are lacking and clinical profiles predictive of death have not been well defined.…”

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

Postdiarrheal Hemolytic Uremic Syndrome in United States Children: Clinical Spectrum and Predictors of In-Hospital Death

Mody¹,

Gu²,

Griffin³

et al. 2015

The Journal of Pediatrics

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Section: Resultsmentioning

confidence: 99%

“…Like others, we identified central nervous system complications as the most common contributing factors to in-hospital death. 1 Past observational studies have identified leukocytosis 1-3,8-13 and greater hematocrit or hemoglobin, 1,2,4,8,12,14 as predictors of death and other poor outcomes in children with D + HUS.…”

Section: Discussionmentioning

confidence: 99%

Postdiarrheal Hemolytic Uremic Syndrome in United States Children: Clinical Spectrum and Predictors of In-Hospital Death

Mody¹,

Gu²,

Griffin³

et al. 2015

The Journal of Pediatrics

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“…Recently, some investigators have questioned the risk of transfusing plasma in patients demonstrating T-activation [24,26,43]. Others have suggested that these events are the result of infection with a verocytotoxin-producing strain of S. pneumoniae, and not the result of neuraminidase activity [44,45,46,47]. Regardless, detection of T-activation has been proposed as an early indicator of a more serious condition [48,49].…”

Section: Discussionmentioning

confidence: 99%

Pneumococcus-induced T-antigen activation in hemolytic uremic syndrome and anemia

Cochran

Panzarino

Maes

et al. 2004

Pediatric Nephrology

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The hemolytic uremic syndrome (HUS) is most commonly associated with Escherichia coli, but has been associated with other infections such as Streptococcus pneumoniae. Pneumococcus-induced HUS carries an increased risk of mortality and renal morbidity compared with E. coli-induced HUS. The pneumococcal organism produces an enzyme, which can expose an antigen (T-antigen) present on erythrocytes, platelets, and glomeruli. Antibodies to the T-antigen, normally found in human serum, bind the exposed T-antigen, and the resultant antigen-antibody reaction (T-activation) can lead to HUS and anemia. Clinicians need to be aware to request specific testing when pneumococcus-induced HUS/anemia is suspected, as current blood banking techniques do not routinely test for the presence of the T-antigen. Once this association is documented, washing all blood products and avoiding plasma products, if possible, is recommended. Plasmapheresis can be considered for the more critically ill patient. The incidence of pneumococcus-induced HUS may be increasing. We report six cases of pneumococcus-induced HUS/anemia presenting at our hospital.

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“…However, two case reports detail Shiga toxinmediated HUS associated with polyuria and persistent production of isosmotic urine (29,57). Thus, direct tubular insult by Stx2 may participate in HUS-associated renal failure, and we hypothesize that collecting duct damage may facilitate dehydration that contributes to worse outcomes in some patients (24,44). Although not without technical difficulty (66), testing prodromal HUS patients for urine-concentrating defects may identify those with severe disease and at greater risk for dehydration with a worse outcome.…”

Section: Vol 77 2009mentioning

confidence: 99%

Shiga Toxin 2 Targets the Murine Renal Collecting Duct Epithelium

et al. 2009

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Hemolytic-uremic syndrome (HUS) caused by Shiga toxin-producingEscherichia coli infection is a leading cause of pediatric acute renal failure. Bacterial toxins produced in the gut enter the circulation and cause a systemic toxemia and targeted cell damage. It had been previously shown that injection of Shiga toxin 2 (Stx2) and lipopolysaccharide (LPS) caused signs and symptoms of HUS in mice, but the mechanism leading to renal failure remained uncharacterized. The current study elucidated that murine cells of the glomerular filtration barrier were unresponsive to Stx2 because they lacked the receptor glycosphingolipid globotriaosylceramide (Gb 3 ) in vitro and in vivo. In contrast to the analogous human cells, Stx2 did not alter inflammatory kinase activity, cytokine release, or cell viability of the murine glomerular cells. However, murine renal cortical and medullary tubular cells expressed Gb 3 and responded to Stx2 by undergoing apoptosis. Stx2-induced loss of functioning collecting ducts in vivo caused production of increased dilute urine, resulted in dehydration, and contributed to renal failure. Stx2-mediated renal dysfunction was ameliorated by administration of the nonselective caspase inhibitor Q-VD-OPH in vivo. Stx2 therefore targets the murine collecting duct, and this Stx2-induced injury can be blocked by inhibitors of apoptosis in vivo.

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Laboratory and Clinical Variables to Predict Outcome in Hemolytic-Uremic Syndrome

Cited by 11 publications

References 5 publications

Postdiarrheal Hemolytic Uremic Syndrome in United States Children: Clinical Spectrum and Predictors of In-Hospital Death

Postdiarrheal Hemolytic Uremic Syndrome in United States Children: Clinical Spectrum and Predictors of In-Hospital Death

Pneumococcus-induced T-antigen activation in hemolytic uremic syndrome and anemia

Shiga Toxin 2 Targets the Murine Renal Collecting Duct Epithelium

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