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Hemolytic uremic syndrome (HUS) is a rare, but menacing condition registered mainly in children. The paper gives a detailed description and analysis of a clinical case of HUS with a favorable outcome in an adult woman who developed the syndrome in the presence of bloody diarrhea. It considers an update on the etiology, pathogenesis, and clinical features of HUS associated with diarrheal syndrome and discusses differential diagnostic features, diagnostic problems, and characteristics of management tactics for patients.

Unlabelled: Shiga toxin-producing Escherichia coli (STEC) food-borne infections are reported worldwide and represent a serious problem for public healthcare. In the Russian Federation there is little information on epidemiology and etiology of STEC-infections as well as on molecular-genetic peculiarities of STEC pathogens., Objective: Our aim was to describe a food-borne outbreak as hemorrhagic colitis (HC) along with hemolytic uremic syndrome (HUS), enterocolitis, and acute gastroenteritis in children in St. Petersburg in 2013., Methods: Epidemiological, microbiological, molecular-genetic and bioinformatic methods were applied., Results: Objects to study were clinical specimens, milk and food samples, as well as STEC strains isolated during the outbreak. The outbreak of food-borne infection was found to be caused by STEC-contaminated raw milk as confirmed by epidemiological analysis, detection of STEC DNA and isolation of relevant pathogens in milk and sick children fecal specimens. The whole-genome sequencing revealed two groups ofpathogens, E. coli O157:H7 and E. coli O101:H33 among collected strains. Group I strains were attributed to the previously known sequence type ST24, while group II strains belonged to the previously non-described sequence type ST145. In strain genomes of both groups there were identified nucleotide sequences of VT2-like prophage carrying stx2c gene, plasmid enterohemolysin gene, and gene of the STEC main adhesion factor intimin. Gene of intimin gamma was identified in E. coli O157:H7 strains and intimin iota 2 in E. coli O101:H33 strains. The latter previously was identified only in enteropathogenic E. coli (EPEC) strains., Conclusion: The additional knowledge of epidemiology and biology of STEC pathogens would assist clinicians and epidemiologists in diagnosing, treating and preventing hemorrhagic colitis.

The clinical sign "anemia" is found in a majority of patients after solid organ transplantation. A variety of etiological factors cause reduced red blood counts--in different situations hemolysis is the culprit. Thrombotic microangiopathy (hemolytic uremic syndrome, transplant rejection or induced by immunosuppressive therapy), infections (bacterial, viral, fungal), and autoalloimmune reactions (differences in blood-group or Rhesus-antigens, drug induced RBC lysis) are most important pathologies to be considered in differential diagnostic steps. Methods applied in diagnostics, underlying pathologies and therapeutic consequences are described based on the clinical history of three transplant patients from a single university department. Therefore, hemolysis as a possible and important situation following organ transplantation should be considered, immediately traced back to the underlying disorder and effectively treated.

An examination was made of seventeen children having various stages of the hemolytic uremic syndrome: Stage 1 is the period of an expanded clinical picture of the disease, the patients' condition is grave (anuria, azotemia, severe hemolytic anemia and thrombocytopenia); Stage 2 is the period of recovery. The plasma levels of malonic dialdehyde, dienic conjugates, alpha-tocopherol at the first stage of the disease were considerably higher than the control ones, on recovery there were their reductions though their levels remained higher than the normal levels. The levels of malonic dialdehyde in the red blood cell membranes in ill children were also much higher than those in healthy donors, but at the second stage they decreased, but remained high. The activity of superoxide dismutase in the red blood cells of ill children in the acute period of the disease did not significantly differ from that of donors. At the second stage of the disease there was a significant fall in the activity of red blood cell superoxide dismutase. The activity of catalase in the red blood cells of ill children was thrice higher than in the controls; however, this index decreased during treatment and at the second stage it did not differ from that in the controls. There were no significant differences in the activity of red blood cell superoxide dismutase in donors and ill children. Mechanisms responsible for abnormal plasma and red blood cell peroxidation are considered in the hemolytic uremic syndrome. It is concluded that free radical reactions play a substantial role in the pathogenesis of this abnormality.

Current literature on the pathogenesis of the hemolytic-uremic syndrome (HUS) is analyzed. A variety of etiologic factors and mechanisms of HUS development is considered. The emphasis is laid on the endotoxinemia, damage of the renal vessel and glomerular mesangium endothelium and other mechanisms.

Morphology of the kidneys in hemolytic-uremic syndrome is considered basing on autopsy findings obtained for 3 infants with 5-17-day history of acute renal failure. A newborn infant of 17 days developed the disease after feto-fetal hemotransfusion when macerated fetus-donor hemolysis products entered the circulation of the fetus-recipient through monochorionic placenta. The second case in an infant of 6 months was due to ADTP Vaccine. The last infant aged 16 months manifested the syndrome in the presence of Proteus-induced ulcerative colitis. Varying in etiology, renal morphology exhibited similar features: fibrin deposits in the lumens of glomerular capillary loops, afferent glomerular arterioles and intrarenal arteries; fibrinoid necrosis of the wall in the arterioles. The renal affection ranged from acute thrombotic glomerulonephritis to cortical necrosis, these variations being dependent on the degree of thrombogenesis, caliber of impaired intrarenal vessels and time from the onset of acute renal failure.