Hemolytic‐uremic Syndrome: An Analysis of the Natural History and Prognostic Features

Loirat, Chantal; Sonsino, E; Moreno, Alberto; Pillion, G; Mercier, J; Beaufils, F.; Mathieu, H

doi:10.1111/j.1651-2227.1984.tb09962.x

Cited by 86 publications

(40 citation statements)

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“…Klebsiella spp has not been previously reported as a cause of HUS following episodes of diarrhoea but Klebsiella urinary tract infection has preceded HUS, (Loirat et al, 1984). K. pneumoniae was the only isolate in both the blood and pleural exudate in our patient, unlike previous reports where Klebsiella peritonitis was a secondary infection in HUS caused by Streptococcal Pneumoniae in a 2 year old, (Obata, 1998).…”

Section: Discussioncontrasting

confidence: 53%

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Haemolytic uraemic syndrome associated with Klebsiella empyema-case report and literature review

Agbedeyi¹,

Eke²

2011

J. Clin. Med. Res.

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We report a 13 month old male with haemolytic uraemic syndrome (HUS) associated with Klebsiella empyema. He presented with fever, gastroenteritis and respiratory distress. Investigations showed left pleural effusion, and HUS. Blood and pleural exudate cultures grew Klebsiella pneumoniae. He died during chest tube insertion. Post mortem showed fibrinous empyema. Renal histology confirmed HUS. Klebsiella has not been previously described to cause HUS. This is the first case of HUS and empyema associated with invasive K. pneumoniae in the Niger Delta Region.

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Section: Discussioncontrasting

confidence: 53%

“…Haemolytic uraemic syndrome, (HUS) is characterized by acute renal failure, (ARF), haemolytic anaemia, and thrombocytopenia, Loirat et al (1984). It is the commonest cause of ARF in children aged from 1 to 2 years.…”

Section: Introductionmentioning

confidence: 99%

Haemolytic uraemic syndrome associated with Klebsiella empyema-case report and literature review

Agbedeyi¹,

Eke²

2011

J. Clin. Med. Res.

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“…This organism also produces a toxin which plays a role in disease (verotoxin or Shiga-like toxin [SLT]). Most patients with EHEC infection recover uneventfully within a few days, but in about 8% of cases (23) the diarrhea is followed by hemolyticuremic syndrome (HUS), a life-threatening complication with a substantial morbidity in survivors (19,25). HUS appears to be caused by the interaction of SLT with endothelial cells.…”

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confidence: 99%

Human Response to Escherichia coli O157:H7 Infection: Antibodies to Secreted Virulence Factors

et al. 2000

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Vaccination has been proposed for the prevention of disease due to enterohemorrhagic Escherichia coli (EHEC), but the immune response following human infection, including the choice of potential antigens, has not been well characterized. To study this, sera were obtained from five pediatric patients with acute diarrhea caused by E. coli O157:H7 0, 8, and 60 days after hospitalization. These sera were used to examine the immune response to four different EHEC virulence factors: Tir (translocated intimin receptor, which is inserted into the host cell membrane), intimin (bacterial outer membrane protein which binds to Tir), EspA (secreted protein which forms filamentous structures on EHEC surface), and EspB (inserted into the host membrane and cytoplasm). The response to O157:H7 lipopolysaccharide was also examined. Sera were assayed against purified recombinant proteins using immunoblot analysis and by enzyme-linked immunosorbent assay to determine the sera's titers to each of the antigens in all patients. We found that there was little reaction to EspA, EspB, and intimin in the acute-phase sera, although there was some reactivity to Tir. By day 8, titers of antibody to all four virulence factors were present in all patients, with a very strong response against Tir (up to a titer of 1:256,000), especially in hemolytic-uremic syndrome patients, and lesser strong responses to the other three antigens. The titer to the antigens 60 days after hospitalization was decreased but was still highest for Tir. These results suggest that there is a strong immune response to Tir, and to a lesser extent to the other three virulence factors, following EHEC disease, indicating that these bacterial molecules are potential vaccine candidates for preventing EHEC disease. They also suggest that bacterial virulence factors that are inserted into host cells during infection by type III secretion systems (Tir or EspB) are still recognized by the host immune response.Enterohemorrhagic Escherichia coli (EHEC) (also called verotoxigenic E. coli) is an important cause of diarrhea. This organism also produces a toxin which plays a role in disease (verotoxin or Shiga-like toxin [SLT]). Most patients with EHEC infection recover uneventfully within a few days, but in about 8% of cases (23) the diarrhea is followed by hemolyticuremic syndrome (HUS), a life-threatening complication with a substantial morbidity in survivors (19,25). HUS appears to be caused by the interaction of SLT with endothelial cells. Worldwide, many serotypes of EHEC have been described, but in North America one type predominates, E. coli O157:H7 (11, 12). Epidemiological evidence shows that EHEC O157:H7 strains are present in the feces of healthy cattle, providing indirect evidence that EHEC O157:H7 can colonize the bovine intestine without causing disease.Because of the potential seriousness of EHEC infection (4), vaccination has been proposed, either to prevent the disease in humans or to reduce colonization in cattle. However, the immunological response to EHEC infection ...

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“…Endothelial injury is also involved in the initiation and propagation of glomerulosclerosis and ESRD (5)(6)(7)(8)(9)(10)(11).…”

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confidence: 99%

Protection of Endothelial Cells by Dextran Sulfate in Rats with Thrombotic Microangiopathy

Eto

Kojima

Uesugi

et al. 2005

Journal of the American Society of Nephrology

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The characteristic features of thrombotic microangiopathy (TMA) include glomerular and peritubular capillary endothelial cell injury in association with loss of heparan sulfate proteoglycans on the cell surface and thrombus formation, followed by subsequent ischemic tubulointerstitial damage. It therefore was hypothesized that dextran sulfate (DXS) may protect the kidney against endothelial damage in a model of TMA. TMA was induced in rats by renal artery perfusion of an antiglomerular endothelial antibody, followed by the administration of DXS or vehicle. Renal damage was assessed by histologic analysis and measurements of blood urea nitrogen and creatinine. Whereas control rats developed severe renal failure with extensive glomerular and tubular injury, administration of DXS significantly protected renal function and preserved the glomerular endothelium and peritubular capillaries. The beneficial effect of DXS could be attributed to the ability of DXS to protect endothelial cells from coagulation and complement activation, as demonstrated by the histologic analysis. In addition, binding of the administered DXS to the surface of the glomerular endothelium was confirmed in TMA rats, suggesting that DXS acts as a "repair coat" of injured glomerular endothelium. In conclusion, DXS protects the kidney from experimental TMA. This protection may be mediated by DXS's binding directly to the surface of glomerular endothelium and amelioration of coagulation, complement activation, and cellular matrix loss.

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Hemolytic‐uremic Syndrome: An Analysis of the Natural History and Prognostic Features

Cited by 86 publications

References 12 publications

Haemolytic uraemic syndrome associated with Klebsiella empyema-case report and literature review

Haemolytic uraemic syndrome associated with Klebsiella empyema-case report and literature review

Human Response to Escherichia coli O157:H7 Infection: Antibodies to Secreted Virulence Factors

Protection of Endothelial Cells by Dextran Sulfate in Rats with Thrombotic Microangiopathy

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