Haemolytic uraemic syndrome

Author(s):  
Paul Warwicker ◽  
Timothy H J Goodship

The haemolytic uraemic syndrome (HUS) is characterized by the triad of: (1) microangiopathic haemolytic anaemia, (2) thrombocytopenia, and (3) acute renal failure. Endothelial cell activation leads to a change in phenotype from an anticoagulant to a procoagulant state. Diarrhoeal associated (D+) HUS—this accounts for over 90% of cases and is the commonest cause of acute renal failure in children. The usual pathogen is enterohaemorrhagic ...

1980 ◽  
Vol 25 (4) ◽  
pp. 323-326
Author(s):  
Catriona Williams ◽  
J. L. Anderton ◽  
P. A. Yates

A patient who developed chronic renal failure secondary to the haemolytic uraemic syndrome subsequently developed life threatening microangiopathic haemolytic anaemia following renal transplantation. Transplant nephrectomy was necessary to prevent the progression ofthrombocytopenia and associated pulmonary haemorrhage.


1999 ◽  
Vol 13 (6) ◽  
pp. 487-492 ◽  
Author(s):  
Corinne H. F. Nevard ◽  
Andrew D. Blann ◽  
Karen M. Jurd ◽  
George B. Haycock ◽  
B. J. Hunt

Author(s):  
Mohammad Ammad Ud Din ◽  
Hania Liaqat ◽  
Prabhsimrat Gill ◽  
Soon Khai Low

Severe haemolytic anaemia is a rare complication of haemodialysis that is often difficult to recognize, especially when there are other potential differential diagnoses. Here, we present the case of 19-year-old man on haemodialysis who developed severe haemolytic anaemia while recovering from acute renal failure secondary to rhabdomyolysis. Other causes of haemolytic anaemia such as thrombotic thrombocytopenic purpura and haemolytic uraemic syndrome were ruled out. As his blood counts were dropping on days following haemodialysis, haemolysis secondary to the mechanical sheering effect of the catheter was considered and his haemodialysis catheter was exchanged, which led to the resolution of anaemia.


2020 ◽  
Vol 14 (7) ◽  
pp. e0007656
Author(s):  
João Conrado Khouri Dos-Santos ◽  
João Luiz Silva-Filho ◽  
Carla C. Judice ◽  
Ana Carolina Andrade Vitor Kayano ◽  
Júlio Aliberti ◽  
...  

2021 ◽  
Author(s):  
Melanie Bergmann ◽  
Anna Heidbreder ◽  
Ambra Stefani ◽  
Cecilia Raccagni ◽  
Elisabeth Brandauer ◽  
...  

2015 ◽  
Vol 76 ◽  
pp. 15
Author(s):  
Eva Zilian ◽  
Hendry Saragih ◽  
Oliver Hiller ◽  
Abid Aljabri ◽  
Constanca Figueiredo ◽  
...  

2021 ◽  
Vol 9 (6) ◽  
pp. 1305
Author(s):  
Carlos Alonso Domínguez-Alemán ◽  
Luis Alberto Sánchez-Vargas ◽  
Karina Guadalupe Hernández-Flores ◽  
Andrea Isabel Torres-Zugaide ◽  
Arturo Reyes-Sandoval ◽  
...  

A common hallmark of dengue infections is the dysfunction of the vascular endothelium induced by different biological mechanisms. In this paper, we studied the role of recombinant NS1 proteins representing the four dengue serotypes, and their role in promoting the expression and release of endocan, which is a highly specific biomarker of endothelial cell activation. We evaluated mRNA expression and the levels of endocan protein in vitro following the stimulation of HUVEC and HMEC-1 cell lines with recombinant NS1 proteins. NS1 proteins increase endocan mRNA expression 48 h post-activation in both endothelial cell lines. Endocan mRNA expression levels were higher in HUVEC and HMEC-1 cells stimulated with NS1 proteins than in non-stimulated cells (p < 0.05). A two-fold to three-fold increase in endocan protein release was observed after the stimulation of HUVECs or HMEC-1 cells with NS1 proteins compared with that in non-stimulated cells (p < 0.05). The blockade of Toll-like receptor 4 (TLR-4) signaling on HMEC-1 cells with an antagonistic antibody prevented NS1-dependent endocan production. Dengue-infected patients showed elevated serum endocan levels (≥30 ng/mL) during early dengue infection. High endocan serum levels were associated with laboratory abnormalities, such as lymphopenia and thrombocytopenia, and are associated with the presence of NS1 in the serum.


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