Cases Of Hemolytic Uremic Syndrome Research Articles

Haemolytic uraemic syndrome is an immune‐mediated disease: role of anti‐CD36 antibodies

Haemolytic uraemic syndrome (HUS) is a disorder in which platelet microthrombi are formed that have a particular propensity to deposit in the kidney microvasculature, resulting in impaired renal function and thrombocytopenia. The mechanism of formation of these microthrombi is not known. In this study, we showed that plasma from five adult and six paediatric cases of HUS caused aggregation and release of adenosine triphosphate from normal platelets. The plasma reacted against platelet lysate in a protein blot and all samples showed reactivity against a band at 88 kDa, corresponding to the membrane antigen CD36. This was confirmed by probing with Mo91, a monoclonal antibody to CD36. CD36 was also identified in the immune complex formed by incubation of patient plasmas with normal platelet lysate. In other studies, bands of 32 and 7.7 kDa were obtained when purified verotoxin was protein blotted and probed with either patient plasma or with anti-CD36 antibody Mo91 suggesting structural homologies between CD36 and verotoxin. While a direct cause-effect relationship is not yet established, the data support the concept of an immunological pathogenesis for HUS and suggest that molecular mimicry involving one or both of the homologous domains in membrane-bound CD36 and verotoxin lead to the development of antibodies capable of inducing the pathophysiological events characteristic of HUS.

Non‐O157 Shiga Toxin–ProducingEscherichia coliInfections in the United States, 1983–2002

Shiga toxin-producing Escherichia coli (STEC) O157:H7 is a well-recognized cause of bloody diarrhea and hemolytic-uremic syndrome (HUS). Non-O157 STEC contribute to this burden of illness but have been underrecognized as a result of diagnostic limitations and inadequate surveillance. Between 1983 and 2002, 43 state public health laboratories submitted 940 human non-O157 STEC isolates from persons with sporadic illnesses to the Centers for Diseases Control and Prevention reference laboratory for confirmation and serotyping. The most common serogroups were O26 (22%), O111 (16%), O103 (12%), O121 (8%), O45 (7%), and O145 (5%). Non-O157 STEC infections were most frequent during the summer and among young persons (median age, 12 years; interquartile range, 3-37 years). Virulence gene profiles were as follows: 61% stx(1) but not stx(2); 22% stx(2) but not stx(1); 17% both stx(1) and stx(2); 84% intimin (eae); and 86% enterohemolysin (E-hly). stx(2) was strongly associated with an increased risk of HUS, and eae was strongly associated with an increased risk of bloody diarrhea. STEC O111 accounted for most cases of HUS and was also the cause of 3 of 7 non-O157 STEC outbreaks reported in the United States. Non-O157 STEC can cause severe illness that is comparable to the illness caused by STEC O157. Strains that produce Shiga toxin 2 are much more likely to cause HUS than are those that produce Shiga toxin 1 alone. Improving surveillance will more fully elucidate the incidence and pathological spectrum of these emerging agents. These efforts require increased clinical suspicion, improved clinical laboratory isolation, and continued serotyping of isolates in public health laboratories.

Public health implications of a case of haemolytic–uraemic syndrome associated with a concomitant outbreak of mild gastroenteritis in a small rural community

The concomitant occurrence of a case of haemolytic-uraemic syndrome (HUS) and 62 cases of mild gastroenteritis in schools of a small rural community in southern Italy induced the health authorities to suspect a foodborne outbreak of shiga-toxin-producing Escherichia coli (STEC) infection. The schools were closed and the catering service involved was investigated. However, STEC were not isolated from the HUS case or from the 56 cases of gastroenteritis examined, and the HUS case and the outbreak of gastroenteritis were probably just coincidental. A retrospective cohort study failed to show any correlation with consumption of school meals and suggested that the outbreak probably started outside the school setting and then spread within the schools by person-to-person transmission. All the cases examined were negative for common enteric pathogens and the responsible agent for the cases of gastroenteritis was not identified. The concern raised in the small community by the occurrence of a severe case of HUS and the lack of a rapid epidemiological assessment excluding the occurrence of a STEC outbreak, turned an epidemic episode of mild gastroenteritis into a public health emergency with relevant socioeconomic consequences. Prompt intervention in outbreaks following timely and effective risk communication are crucial for taking the most appropriate control measures and avoiding the spread of fear and panic in the community.

Epidemiology ofEscherichia coliO157:H7 Outbreaks, United States, 1982–2002

Escherichia coli O157:H7 causes 73,000 illnesses in the United States annually. We reviewed E. coli O157 outbreaks reported to Centers for Disease Control and Prevention (CDC) to better understand the epidemiology of E. coli O157. E. coli O157 outbreaks (>or=2 cases of E. coli O157 infection with a common epidemiologic exposure) reported to CDC from 1982 to 2002 were reviewed. In that period, 49 states reported 350 outbreaks, representing 8,598 cases, 1,493 (17%) hospitalizations, 354 (4%) hemolytic uremic syndrome cases, and 40 (0.5%) deaths. Transmission route for 183 (52%) was foodborne, 74 (21%) unknown, 50 (14%) person-to-person, 31 (9%) waterborne, 11 (3%) animal contact, and 1 (0.3%) laboratory-related. The food vehicle for 75 (41%) foodborne outbreaks was ground beef, and for 38 (21%) outbreaks, produce.

Escherichia Coli O157:H7 Outbreak Associated with Consumption of Ground Beef, June–July 2002

A case-control and environmental study tested the hypothesis that purchasing and eating ground beef from a specific source was the cause of a cluster of cases of hemolytic uremic syndrome (HUS) and Escherichia coli (E. coli) O157:H7 gastroenteritis. A case-control study comparing risk factors was conducted over the telephone on nine case-patients with 23 selected controls. An environmental investigation was conducted that consisted of reviewing beef handling practices at a specific local supermarket and obtaining ground beef samples from the store and two households with case-patients. The analysis of the case-control study showed that eight case-patients (89%) purchased ground beef at Grocery Chain A compared with four controls who did not develop illness (17%) (matched odds ratio=undefined; 95% confidence interval 2.8, infinity; p=0.006). The environmental investigation showed that Grocery Chain A received meat from Meatpacker A. Laboratory analysis of meat samples from Meatpacker A and Grocery Chain A and stool samples from some patients recovered an identical strain of E. coli O157:H7 according to pulse-field gel electrophoresis. Both the case-control and environmental studies showed that purchasing ground beef at Grocery Chain A, which received ground beef from Meatpacker A, was the major risk factor for illness in eight case-patients; the ninth case-patient was found to be unrelated to the outbreak. Furthermore, meat from Meatpacker A was associated with a nationwide outbreak of E. coli O157:H7 illness that resulted in the second largest recall of beef in U.S. history at the time.

Hemolytic Uremic Syndrome

Hemolytic uremic syndrome (HUS) is a thrombotic microangiopathy defined by thrombocytopenia, nonimmune microangiopathic hemolytic anemia, and acute renal failure. The most frequent form is associated with infections by Shiga-like toxin-producing bacteria (STEC-HUS). Rarer cases are triggered by neuraminidase-producing Streptococcus pneumoniae (pneumococcal-HUS). The designation of aHUS is used to refer to those cases in which an infection by Shiga-like toxin-producing bacteria or S. pneumoniae can be excluded. Studies performed in the last two decades have documented that hyperactivation of the complement system is the pathogenetic effector mechanism leading to the endothelial damage and the microvascular thrombosis in aHUS. Recent data suggested the involvement of the complement system in the pathogenesis of STEC-HUS and pneumococcal-HUS as well. Clinical signs and symptoms may overlap among the different forms of HUS; however, pneumococcal-HUS and aHUS have a worse prognosis compared with STEC-HUS. Early diagnosis and identification of underlying pathogenetic mechanism allows instating specific support measures and therapies. In clinical trials in patients with aHUS, complement inhibition by eculizumab administration leads to a rapid and sustained normalization of hematological parameters with improvement in long-term renal function. This review summarizes current concepts about the epidemiological findings, the pathological and clinical aspects of STEC-HUS, pneumococcal-HUS, and aHUS, and their diagnosis and management.

Three cases of hemolytic uremic syndrome in ovarian cancer patients treated with combination gemcitabine and pegylated liposomal doxorubicin

Background Hemolytic uremic syndrome (HUS) is a rare coagulation disorder characterized by microangiopathic hemolytic anemia, thrombocytopenia and acute uremia. Reports have described this fatal syndrome in association with cytotoxic agents. To our knowledge, no case reports of HUS in ovarian cancer patients receiving treatment with combination gemcitabine and pegylated liposomal doxorubicin (PLD) have been reported. Case Reports Three patients with recurrent ovarian carcinoma each developed profound hypertension and peripheral edema while receiving combination gemcitabine and PLD. The first patient had rapid hemolysis, thrombocytopenia, renal failure and respiratory distress. The other patients experienced slowly progressive renal failure and mild hematologic abnormalities. Two of the three patients had favorable outcomes. Conclusion The reported incidence of gemcitabine-induced HUS is rare. Clinicians should suspect HUS if blood pressure elevation or peripheral edema develop.

Thrombotic Thrombocytopenic Purpura and Hemolytic Uremic Syndrome in Children and Adolescents

Thrombotic thrombocytopenic purpura (TTP) and hemolytic uremic syndrome (HUS) are both uncommon disorders that present with a microangiopathic hemolytic anemia and thrombocytopenia. Although for TTP, neurologic manifestations predominate, and in HUS renal dysfunction is virtually always present, there is significant overlap in their clinical presentation. In recent years, tremendous progress has been made in our understanding of the pathogenesis of these disorders. It is now apparent that there are subcategories of both TTP and HUS that can differ in their clinical manifestations, etiology, and management. For instance, although most cases of HUS are due to infection with organisms that produce Shiga-like toxin, other cases may be caused by defined genetic abnormalities. Similarly, TTP is usually caused by genetic or acquired deficiency of the ADAMTS13 enzyme; however, in other cases the relationship with this enzyme remains to be established. Management includes supportive care, plasma transfusions for genetic protein deficiencies, and plasma exchange transfusion for autoimmune TTP.

Hemolytic uremic syndrome following prolonged gemcitabine therapy: report of four cases from a single institution

Hemolytic uremic syndrome (HUS) has been described following the administration of multiple antineoplastic agents, most notably mitomycin C. More recently, several cases of gemcitabine-induced HUS have been observed with the overall incidence of gemcitabine-induced HUS estimated at 0.015-0.25%. We here report on four patients who developed HUS following gemcitabine therapy at our institution within the last year (incidence 1.4%). All these patients had advanced-stage disease, were heavily pretreated, and received prolonged gemcitabine application, suggesting that in this subgroup of patients HUS may be more frequently encountered than documented so far.

Non-enteropathic hemolytic uremic syndrome: causes and short-term course

Background: Nondiarrheal or Streptococcus pneumoniae-related hemolytic uremic syndrome (HUS) represents a heterogeneous group of disorders. This study was performed to: (1) describe the current incidence, causes, demographic features, hospital courses, and short-term outcomes of non-enteropathic HUS; (2) compare findings in patients with non-enteropathic HUS with those obtained from a contemporaneous cohort of children with enteropathic or diarrhea-associated HUS (D+ HUS) diagnosed and treated at the same clinical sites; and (3) identify clinical or laboratory features that differentiate these 2 groups and predict disease severity and the short-term outcome in patients with non-enteropathic HUS. Methods: Data were collected from patients screened between 1997 and 2001 for enrollment in a multicenter trial of SYNSORB Pk (SYNSORB Biotech Inc, Calgary, Alberta, Canada) in D+ HUS, but who were ineligible because of lack of a diarrhea prodrome. The following features were recorded: age; sex; ethnicity; prodromal symptoms; cause; nadir values for hemoglobin, hematocrit, and platelet count; use of dialysis; and length of hospitalization. Results: Twenty-seven of 247 children with HUS had non-enteropathic HUS (11%). Twenty-four patients (15 boys, 9 girls), whose medical records were complete and available for review, comprise the study cohort. Mean age at onset was 4.2 ± 0.9 (SE) years. Infection caused by S pneumoniae was diagnosed in 9 patients (38%). Dialysis was performed in 17 patients (71%) for 40 ± 27 days. Median length of hospitalization was 22 days (range, 2 to 71 days). Children with S pneumoniae-related HUS had a longer hospital stay than those with other causes of non-enteropathic HUS, but all patients with S pneumoniae-related HUS recovered kidney function. Dialysis therapy was required more often (17 of 24 versus 59 of 145 children; P = 0.025) and hospital stays were longer (median, 22 versus 9 days; P = 0.002) in children with non-enteropathic HUS compared with patients with D+ HUS who were enrolled in the SYNSORB Pk clinical trial. Conclusion: (1) The incidence of non-enteropathic HUS is approximately one tenth that of D+ HUS; (2) patients with non-enteropathic HUS require dialysis therapy more often and are hospitalized more than twice as long during the acute episode compared with those with D+ HUS; (3) infection caused by S pneumoniae accounts for nearly 40% of cases of non-enteropathic HUS; and (4) although S pneumoniae-related HUS is associated with a less favorable short-term course than other types of non-enteropathic HUS or D+ HUS, the long-term prognosis for recovery of renal function appears to be good in these patients.

Hemolytic uremic syndrome revisited: Shiga toxin, factor H, and fibrin generation.

The hemolytic uremic syndrome (HUS) is a disease characterized by microangiopathic hemolytic anemia, thrombocytopenia, and renal failure. These features reflect the underlying histopathologic lesion: fibrin-rich thrombi that predominate in the renal microvasculature. HUS most commonly affects children younger than 5 years and is associated with Shiga toxin-producing enteric bacteria, the most important of which is Escherichia coli O157:H7. In this setting, HUS is epidemic and also might affect adults, particularly elderly people. Sporadic cases of HUS more commonly occur in adults and are associated with a wide variety of inciting agents and conditions. Although the disease manifestations might be similar and endothelial activation or injury likely represents a common etiologic event, differing responses to therapy suggest different pathogenic mechanisms. As more is understood about the underlying pathogenesis of the diseases that we now lump together as HUS, more efficacious and rational treatment and prevention strategies are likely to follow.

Incidence of thrombotic thrombocytopenic purpura/hemolytic uremic syndrome.

Thrombotic thrombocytopenic purpura and hemolytic uremic syndrome are rare disorders characterized by platelet aggregation, microthrombi, and resulting tissue damage. We studied the incidence and possible risk factors for these diseases in 3 large populations in the United States, United Kingdom, and Canada. Data were derived from a large health insurer in the United States, general practices in the United Kingdom, and the Province of Saskatchewan. We identified potential cases of thrombotic thrombocytopenia purpura and hemolytic uremic syndrome in computerized data and verified them by medical record review. We estimated incidence rates for thrombotic thrombocytopenia purpura and hemolytic uremic syndrome together and separately, and we conducted a case-control study to evaluate potential risk factors. The age-sex standardized incidence of thrombotic thrombocytopenia purpura and hemolytic uremic syndrome was higher than previously reported (6.5, 2.2, and 3.2 per million per year in the United States, United Kingdom, and Saskatchewan, respectively), but there was no secular trend. The incidence of thrombotic thrombocytopenia purpura and hemolytic uremic syndrome was higher in women than men. Most cases of hemolytic uremic syndrome occurred before 20 years of age. We confirmed several known risk factors for thrombotic thrombocytopenia purpura and hemolytic uremic syndrome (cancer, bone marrow transplantation, pregnancy). The incidence of thrombotic thrombocytopenia purpura and hemolytic uremic syndrome is higher than previously reported but does not appear to be rising. Apparent international differences in incidence could be the result of imprecision in identifying thrombotic thrombocytopenia purpura and hemolytic uremic syndrome in large research databases.

Phenotypic and genotypic analyses of enterohemorrhagic Escherichia coli O145 strains from patients in Germany.

Enterohemorrhagic Escherichia coli (EHEC) strains of serogroup O145 are emerging as causes of diarrhea and the hemolytic-uremic syndrome. However, there have been few genetic analyses of this EHEC group. We investigated the serotypes, virulence genes, plasmid profiles, pulsed-field gel electrophoresis (PFGE) patterns, and genetic variability of the fliC and eae genes in 120 EHEC O145 strains isolated from cases of hemolytic-uremic syndrome (n = 24) or diarrhea (n = 96) in Germany between 1996 and 2002. Three isolates belonged to serotype O145:H28, one to serotype O145:H25, and 116 were nonmotile (O145:H(-)). One hundred fourteen of the nonmotile strains shared fliC restriction fragment length polymorphism (RFLP) patterns identical to that of the O145:H28 strains. The remaining two nonmotile strains displayed a fliC-RFLP pattern identical to that of the O145:H25 strain. Each of the 117 strains with the fliC-RFLP(H28) pattern harbored eae gamma, whereas the three strains with the fliC-RFLP(H25) pattern possessed eae beta. Five different stx genotypes, six combinations of plasmid-encoded putative virulence genes, 29 plasmid profiles, and 47 PFGE types were identified. Strains within some of the PFGE types could be further subtyped by means of distinct plasmid profiles. These data demonstrate that the EHEC O145 serogroup is comprised of two different serotypes that possess distinct eae types. The heterogeneity of EHEC O145 strains at the chromosomal and plasmid level, in particular the high diversity in PFGE patterns, provides a basis for molecular subtyping of these pathogens.

The serological response to Verocytotoxigenic Escherichia coli in patients with haemolytic uraemic syndrome

To screen sera from 80 patients with clinical haemolytic uraemic syndrome (HUS) and serum antibodies to the lipopolysaccharide (LPS) of Escherichia coli O157, for antibodies to Verocytotoxin-producing Escherichia coli (VTEC) belonging to serogroups O5, O26, O104, O111, O128, O145, O153 and O165. Sera were screened by an LPS-based ELISA and SDS-PAGE/immunoblotting. None of the 80 sera contained antibodies binding to long-chain LPS of any of the LPS types employed; however, nine sera contained antibodies binding to R3 LPS-core epitopes. The presence of patients' serum antibodies to the LPS of E. coli O157, in the absence of antibodies to the LPS of a range of other VTEC, demonstrated that cases of HUS may be caused by strains of O157 VTEC alone and that concurrent infection with multiple strains of VTEC is not a prerequisite for cases of HUS. Antibodies to long-chain LPS of VTEC other than O157 were not detected, and so there was no evidence of infection with VTEC belonging to more than one serogroup. The results of immunoassays such as ELISAs and micro-agglutinations must take into consideration antibodies binding to R3 epitopes located on LPS-core.

Escherichia coli 0157: H7 reservoir, transmission, diagnosis and the African situation: a review

To provide an overview of the current understanding of verotoxigenic Escherichia coli 0157:H7 (VTEC) and to describe clinical picture, reservoir, transmission and diagnosis and African situations of VTEC. A literature review was performed of major published series between 1980 and 2001 inclusive, using the PUB MED and MEDLINE search. Some earlier published series were also reviewed in instances where they directly led to the understanding of current review. Data from laboratory studies on cultural and isolation, serological and molecular techniques are summarised in this review. Verotoxigenic Escherichia coli 0157:H7 (VTEC) is an important cause of uncomplicated diarrhoea, bloody diarrhoea (BD) and haemolytic uremic syndrome (HUS) in developed countries. The incidence and importance of 0157: H7 (VTEC) infections in most developing countries are not known; however, 0157: H7 (VTEC) cases have been isolated from many sporadic cases of diarrhoea, BD and HUS, while several cases have also been associated with diarrhoeal disease outbreaks in Africa. The morbidity and mortality associated with several recent outbreaks of VTEC disease have highlighted the threat these organisms pose to public health. For this reason, there is an increasing demand for improved diagnostic procedures for detection of VTEC in clinical specimen and in particular, in foods such as meat and dairy products in developing countries.

Familial haemolytic uraemic syndrome and an MCP mutation

Mutations in factor H (HF1) have been reported in a consistent number of diarrhoea-negative, non-Shiga toxin-associated cases of haemolytic uraemic syndrome (D-HUS). However, most patients with D-HUS have no HF1 mutations, despite decreased serum concentrations of C3. Our aim, therefore, was to assess whether genetic abnormalities in other complement regulatory proteins are involved. We screened genes that encode the complement regulatory proteins-ie, factor H related 5, complement receptor 1, and membrane cofactor protein (MCP)-by PCR-single-strand conformation polymorphism (PCR-SSCP) and by direct sequencing, in 25 consecutive patients with D-HUS, an abnormal complement profile, and no HF1 mutation, from our International Registry of Recurrent and Familial HUS/TTP (HUS/thrombotic thrombocytopenic purpura). We identified a heterozygous mutation in MCP, a surface-bound complement regulator, in two patients with a familial history of HUS. The mutation causes a change in three aminoacids at position 233-35 and insertion of a premature stop-codon, which results in loss of the transmembrane domain of the protein and severely reduced cell-surface expression of MCP. Results of previous studies on HF1 indicate an association between HF1 deficiency and D-HUS. Our findings of an MCP mutation in two related patients suggest that impaired regulation of complement activation might be a factor in the pathogenesis of genetic forms of HUS. MCP could be a second putative candidate gene for D-HUS. The protein is highly expressed in the kidney and plays a major part in regulation of glomerular C3 activation. We propose, therefore, that reduced expression of MCP in response to complement-activating stimuli could prevent restriction of complement deposition on glomerular endothelial cells, leading to microvascular cell damage and tissue injury.

Risk factors for poor renal prognosis in children with hemolytic uremic syndrome

Many factors have been proposed as predictors of poor renal prognosis in children with hemolytic uremic syndrome (HUS), but their role is still controversial. Our aim was to detect the most reliable early predictors of poor renal prognosis to promptly identify children at major risk of bad outcome who could eventually benefit from early specific treatments, such as plasmapheresis. Prognostic factors identifiable at onset of HUS were evaluated by survival analysis and a proportional hazard model. These included age at onset, prodromal diarrhea (D), leukocyte count, central nervous system (CNS) involvement, and evidence of Shiga toxin-producing Escherichia coli (STEC) infection. Three hundred and eighty-seven HUS cases were reported; 276 were investigated for STEC infection and 189 (68%) proved positive. Age at onset, leukocyte count, and CNS involvement were not associated with the time to recovery. Absence of prodromal D and lack of evidence of STEC infection were independently associated with a poor renal prognosis; only 34% of patients D(-)STEC(- )recovered normal renal function compared with 65%-76% of D(+)STEC(+), D(+)STEC(-) and D(-)STEC(+ )patients. In conclusion, absence of both D and evidence of STEC infection are needed to identify patients with HUS and worst prognosis, while D(-) but STEC(+) patients have a significantly better prognosis.

Study 2: steroid withdrawal in African American kidney transplant recipients receiving sirolimus and tacrolimus: analysis of renal function beyond 1 year

S teroid withdrawal in African American kidney transplant recipients has traditionally resulted in high rates of acute rejection. Conversely, we have previously reported excellent short-term outcomes among 30 African Americans withdrawn from prednisone between 3 and 5 months after primary kidney transplantation and maintained on a regimen of concentration-controlled doses of sirolimus (SRL) (target trough concentrations, 10-15 ng/mL) and tacrolimus (TAC) (target trough concentrations, 5-8 ng/ mL). After a mean follow-up of 14 months, only 2 of 30 patients (6.7%) experienced biopsy-proven acute rejection and 90% of patients remained steroid-free. This cohort of patients has now been followed up for 12 to 35 months (mean, 24 7 months). Acute rejection, prompting renewal of steroid therapy, has occurred in 4 patients (13%), including episodes in 2 patients occurring at 15 and 16 months, respectively, after steroid withdrawal. Two of the 4 episodes of acute rejection occurred in the setting of prolonged delayed graft function and were discovered on “protocol” biopsies. The other 2 episodes were related to gross noncompliance. There has been a single graft loss and no deaths (97% graft survival, 100% patient survival). Prednisone was renewed for medical reasons unrelated to rejection in 2 other patients, including 1 with a late case of hemolytic uremic syndrome and another with intractable bone pain prompting discontinuation of TAC. At last follow-up, 24 of 30 patients (80%) remained steroid-free. For the cohort of 29 patients with functioning grafts, serum creatinine concentration increased from 1.4 0.44 mg/dL before steroid withdrawal to 2.2 1.8 mg/dL at last follow-up (P .028). For the 24 patients who remain off prednisone and free of clinically overt acute rejection, serum creatinine concentration has increased from 1.44 0.4 to 1.65 0.4 mg/dL (P .006). Multiple linear regression was performed to determine the influence of age, gender, body weight, delayed graft function (occurring in 24% of patients), acute rejection, pretransplant panel reactive antibody (ranging from 0% to 84%), and the number of human leukocyte antigen mismatches (A, B, and DR loci) on serum creatinine level at last follow-up. For the entire cohort, independent correlates of serum creatinine level at last follow-up were acute rejection (P .0001), pretransplant panel reactive antibody levels (P .05), and body weight (P .004). For the steroid-free group, the independent correlates of serum creatinine at last follow-up were delayed graft function (P .05), panel reactive antibody (P .05), and male gender (P .003). Conclusion: Results of this uncontrolled study suggest that use of SRL and TAC allows the withdrawal of steroid therapy in African American kidney transplant recipients with a low incidence of acute rejection up to 3 years after transplantation. However, steroid withdrawal may be associated with longterm deterioration of renal function, even in the absence of clinically overt acute rejection. In addition to acute rejection, delayed graft function and pretransplant sensitization contribute to declining renal function over time and might be considered relative contraindications to withdrawing steroid therapy from African American kidney transplant recipients in future studies. From the Departments of Medicine and Surgery, University Hospitals of Cleveland, Cleveland, OH. © 2003 Elsevier Inc. All rights reserved. 0955-470X/03/1704-0000$30.00/0 doi:10.1016/j.trre.2003.10.029

Deficiency of ADAMTS-13 in thrombotic and thrombocytopenic purpura

Deficiency of ADAMTS-13 in thrombotic and thrombocytopenic purpura

Bovine non-O157 Shiga toxin 2-containing Escherichia coli isolates commonly possess stx2-EDL933 and/or stx2vhb subtypes.

stx(2) genes from 138 Shiga toxin-producing Escherichia coli (STEC) isolates, of which 127 were of bovine origin (58 serotypes) and 11 of human origin (one serotype; O113:H21), were subtyped. The bovine STEC isolates from Australian cattle carried ehxA and/or eaeA and predominantly possessed stx(2-EDL933) (103 of 127; 81.1%) either in combination with stx(2vhb) (32 of 127; 25.2%) or on its own (52 of 127; 40.4%). Of 22 (90.9%) bovine isolates of serotype O113:H21, a serotype increasingly recovered from patients with hemolytic uremic syndrome (HUS) or hemorrhagic colitis, 20 contained both stx(2-EDL933) and stx(2vhb); 2 isolates contained stx(2vhb) only. Although 7 of 11 (63.6%) human O113:H21 isolates associated with diarrhea possessed stx(2-EDL933), the remaining 4 isolates possessed a combination of stx(2-EDL933) and stx(2vhb). Three of the four were from separate sporadic cases of HUS, and one was from an unknown source.