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Hemolytic uremic syndrome; pathogenesis, treatment,and outcomeRichard Siegler and Robert Oakes The hemolytic uremic syndrome (HUS) is the most common As with any syndrome, the hemolytic uremic syndrome cause of acute renal failure in infants and young children, (HUS) is a constellation of features, namely the triad of and is a substantial cause of acute mortality and chronic microangiopathic hemolytic anemia, thrombocytopenia, morbidity. It is therefore relevant and appropriate that and acute nephropathy. Like any syndrome, HUS has pediatricians remain familiar with the various subsets of the many causes, but in the pediatric age group 90% will be disease including its classification, management, and of the post diarrheal variety (D+ HUS), due to Shiga tox- in (Stx) producing E. coli (e.g., 0157:H7). It is best to refer to the renal involvement in D+ HUS as acute nephrology, This review will focus on recent information relative to since not all patients with this syndrome develop acute epidemiology, pathogenesis, treatment, and outcome. It will renal failure with azotemia; a few express only hematuria include some of the newer associations between HUS and and proteinuria. Moreover, with D+ HUS some patients a variety of infections, including, but not limited to E. coli experience an incomplete form of the syndrome with one 0157:H7 (Shiga toxin-mediated) HUS, as well as the or more of the features missing. It is important for the pe- ever-increasing number of associations between HUS and diatrician to remain cognizant of the ever-increasing num- a variety of drugs. It will review some of the newer therapies ber of cases caused by other (i.e., non E. coli) infectious for the more common subsets, but will acknowledge that agents, and drugs. Moreover, we are just beginning to choosing evidence-based therapies is often limited by our identify and dissect the pathogenic cascades of the nu- incomplete understanding of the various pathogenic merous subsets that comprise the 10% of cases labeled cascades, and that with the possible exception of Shiga toxin-mediated HUS(D+HUS), long-term outcomeinformation is often limited by small numbers and limited To provide the context for the recent articles (October 2003–October 2004) included in this review, we have in- cluded a substantial amount of older material that is This review should provide a framework for making the not cited in the reference section, but is available upon proper diagnosis, implementing appropriate treatment, and advising the family about anticipated outcome.
Of the hundreds of manuscripts dealing with some aspect of HUS during this time interval, we have chosen about ACE inhibitors, complement system, factor H, hemolytic 50 that we felt most relevant and useful to the pediatri- cian. Our selection of those of special or outstanding in-terest was of course subjective, and we apologize to the Curr Opin Pediatr 17:200–204. ª 2005 Lippincott Williams & Wilkins.
numerous authors who wrote excellent articles that werenot included due to either their very specialized nature Department of Pediatrics, Division of Nephrology, University of Utah School of and/or the length constraints of this review.
Correspondence to Richard Siegler, Department of Pediatrics, Division of Nephrology, University of Utah School of Medicine (801 581-7609 Hemolytic), Although 90% of childhood hemolytic uremic syndrome 30 North 1900 East Salt Lake City, UT, 84132 USATel: 801 587 9243; fax: 801 581 8043; e-mail: (HUS) follows a colitis prodrome caused by Shiga toxin(Stx) producing E. coli (e.g., E. coli 0157), there is increas- Current Opinion in Pediatrics 2005, 17:200–204 ing awareness that other organisms, drugs, and conditions(e.g., bone marrow transplant, SLE, glomerulonephritis, ª 2005 Lippincott Williams & Wilkins.
1040-8703 malignant hypertension, systemic sclerosis, cancer, etc.),can also initiate the triad of microangiopathic hemolyticanemia, thrombocytopenia, and acute nephropathy thatdefines HUS. A definite causal relation has not been prov-en in many of the reports. Even so, the list of drugs, in-fectious agents, and conditions associated with atypical(non-diarrheal) HUS continues to grow.
Hemolytic uremic syndrome Siegler and Oakes 201 The antiplatelet drug ticlopididine for example, a rare but and secondary TMA (HUS). Quantitative deficiencies known cause of HUS, has largely been replaced by clopi- can be suspected by a low serum C3, and documented dogrel, initially thought to be free of this side effect. It too by a measurement of factor H. Determining qualitative has been reported to cause HUS [1]. Though rare in chil- (functional) abnormalities are more difficult and are avail- dren and adolescents, advanced pancreatic cancer is usu- able in only a few research laboratories. This defect in fac- ally managed with gemcitabine, also recently reported to tor H can be inherited as either a heterozygous or homo- cause HUS [2,3]. Of greater relevance to pediatricians is zygous disorder, and is the result of a number of mutations a recent report of a child who developed HUS during in- including nucleotide substitutions, insertions, or dele- duction therapy with L-asparaginase and vincristine for tions, and is thus polymorphous relative to molecular ab- ALL [4]. A comprehensive yet concise review of drug-in- normalities. This helps to explain the variability in clinical duced HUS/TTP is available [5••].
The occurrence of HUS as a complication of bone marrow Recently, reduced expression of the membrane co-factor transplant is well known, but recent evidence suggests (MCF; CD46), also a widely expressed transmembrane that the relation may be augmented by concurrent complement regulator, has been recognized as a cause H. pylori infection [6]. A report of HUS occurring in a of familial HUS [20,21]. It inhibits complement activa- 12-month-old infant with infectious mononucleosis [7] tion by its regulation of C3b deposition on target cells is the third such reported association, though the patho- genesis remains obscure. There are two recent reports ofQ fever (C. burnetti, infection) [8,9], one in Greece and Customary maintenance therapy for these disorders has the other in Canada, associated with HUS. The syndrome been plasma manipulation (plasma infusion or exchange), has also been reported to follow Staphylococcus-induced and potential definitive therapy for factor H deficiency perianal abscess [10], as well as group A beta hemolytic has been a liver transplant (the site of factor H produc- streptococcal infections [11]. CMV infection following tion) [22] or a combined kidney-liver transplant [22], liver transplant [12], relapsing viral hepatitis A [13], though the outcomes to date have largely been poor.
Hanta virus [14], and envenomization due to scorpion Helpful reviews of factor H in both health and disease bites [15] are additional novel associations and probable [23••], and the role of CD46 [24••] are both recom- More common and better-understood causes of non- Although largely a disease of adults, thrombotic thrombo- E. coli (Shiga toxin) mediated HUS are those caused by cytopenic purpura (TTP), a disorder with many overlap- S. pneumonia. In these cases the neuroaminidase producing ping clinical features with classic D+ HUS, is known to S. pneumonia exposes the cryptic T-antigen present on occur due to either a congenital absence (Upshaw- erythrocytes, platelets, and glomeruli. This exposed cryp- Schulman-Syndrome) of von Willebrand factor (vWF) tic antigen then reacts with anti-T antibodies that are nor- cleaving protease enzyme (ADAMTS 13) activity, or to mally present in the plasma, that in turn damage red blood an acquired IGg antibody directed against this enzyme.
cells, platelets, glomerular endothelial cells and results in Recently, an additional cause has been discovered, namely glomerular thrombotic microangiopathy (TMA). When an novel mutations that either reduce vWF synthesis or re- individual presents with pneumococcal pneumonia or sult in abnormal mRNA that reduces vWF activity during meningitis, the T-antigen should be tested for and if pres- severe episodes to less than 3% of normal.
ent only washed red blood cells/or platelets should be ad-ministered and plasma products avoided [16].
We are rapidly learning more of the epidemiology andpathogenesis of classic post-diarrheal HUS (D+HUS).
Factor H deficiency is another fairly common atypical sub- We know that the syndrome is caused by Sigha toxin set that is characterized by complement dysregulation. It (Stx) producing enterohemorrhagic E. coli (EHEC). These is arguably the most difficult D-subset to manage and organisms produce subunit cytotoxins composed of a single most cases progress to end stage kidney disease despite A subunit surrounded by five B subunits. They are highly aggressive therapy [17]. Although serum complement is lethal and belong to a new family of AB [5] toxins [25].
vital to innate immunity, newly generated complement ac- The pathogenic cascade starts with the ingestion of tivation products are extremely toxic and are consequently EHEC. Although cattle and other domestic (e.g., sheep) highly restricted in terms of time and space [18]. This and wild (e.g., deer, seagulls) fauna as well as humans and protection is partly mediated by factor H, the regulator food, beverage, and water contaminated with E. coli of the alternative complement pathway. Defects in this vi- 0157:H7 are the major vectors, and serotypes, respective- tal regulatory factor activate the complement system, ly, there are dozens of non-0157: H7 Shiga toxin (Stx) pro- resulting in complement deposition on glomerular endo- ducing strains that can cause HUS as illustrated in an thelial cells with subsequent endothelial cells damage outbreak among attendees of a cheerleading camp [26] where the most likely vectors were salad and ice, and the molecular fingerprinting as the same strain of E. coli col- lected from the patients stools [36]. Surveys have foundactive disease producing E. coli in environments up to A general overview of the cascade of events starts with the 10 months following initial contamination [36].
ingestion of EHEC that causes a colitis that is usuallybloody. The inflamed colon facilitates transmural absorp- tion of Shiga toxins and lipopolysaccharide (LPS) into the Since there have been no major treatment ‘‘break- circulation. The Stxs are then engaged by glycoprotein throughs’’ during the past 30 years when dialysis for in- (Gb3) receptors on target cells in the gut, kidney, and oc- fants and pediatric intensive care units became available casionally other vital organs. It has been shown, however, in the developed countries, the emphasis continues to be that Stx binding to glomerular cells is heterogeneous due on prevention. This includes safer slaughterhouse, meat to variation in Gb3 expression within glomeruli [27]. Sub- processing, food handling and cooking standards and irra- sequent cellular internalization leads to inhibition of pro- diation of raw meat products. However, these hardy patho- tein production, resulting in damage and/or death of the gens are now ubiquitous, and cases of Stx-mediated HUS cells and detachment from their basement membranes.
This is followed by secondary activation of platelets andthe coagulation cascade that in concert results in the The most promising preventive measure for those who have E. coli 0157:H7 colitis but have not yet shown signsof HUS is the administration of humanized monoclonal E. coli 0157:H7 may be the most prevalent EHEC to cause antibodies (i.e., passive immunity) against the Shiga toxins D+ HUS because it possesses certain virulence factors during the 3 to 5 day window from colitis to onset of HUS.
[28••]. Some of the virulence factors that account for the To make this test practical in the outpatient setting (e.g., pathogenicity of E. coli 0157:H7 are certain virulence genes emergency room) it must be coupled to a rapid detection (e.g., stx2, eae intimin, Z1640) [29–32]. Of the intimin test for Shiga toxins in the stool [37,38,39•]. Another pos- genes, eae has been studied and characterized the most, sible technique would be to administer Stx receptor (Gb3) but at least 10 others have been identified [33]. The analogues to bind the Stxs in the circulation and effectively intimin gene eae is located within the so-called pathoge- inactivate them before they could attach to Gb3 [40].
nicity island of the enterocyte effacement lesion, and isresponsible for the tight adherence of the bacteria to There still may be time to interrupt the pathogenic cas- the enterocyte. This tight attachment is thought to facil- cade and ameliorate full expression of the syndrome by itate the transluminal passage of the toxins into the gen- inhibiting the p38 MAP kinase pathway, and thus block the genes required for production of prothrombotic andpro-inflammatory cytokines (e.g., TNF-a) [41•]. For now It is interesting that activated platelets bind to Shiga tox- however, therapy includes attention to fluid and electro- in, further amplifying the pro-thrombotic state [34].
lyte balance, providing full nutritional support coupled There is reason to believe that lipopolysaccharides with the judicious use of blood transfusions, treatment (LPS) and apoptosis also play a role. Recently it has been of hypertension, and dialysis or blood pump assisted con- shown in cell culture of human glomerular endothelial tinuous venous-venous hemofiltration-dialysis (CVVHD).
cells that there is a reduction of thrombomodulin (TM) The latter, also known as continuous renal replacement expression (a protein that ordinarily inhibits coagulation), therapy (CRRT), requires an intensive care environment, following co-incubation with Shiga toxin2. There is also and is best used with a citrate (heparin free), anticoagu- good evidence that the proinflammatory cytokines (e.g., lation system. CRRT is very useful for hemodynamically TNF-alpha) as well as LPS participate in the genesis of the TMA. TNF-alpha and certain other cytokines areknown to activate the p38 MAP kinase cascade, known There is no reason to use plasma manipulation (e.g., plasma to mediate gene expression and production of inflamma- infusions, plasma exchange) in those with classical D+ tory cytokines. Moreover administration of a p38 MAP ki- HUS (unless one can document that they also have Factor nase inhibitor suppresses gene expression and prevents H or vWF cleaving protease deficiency).
the development of glomerular TMA in a mouse modelof HUS [35].
Although about one half of patients with D+ HUS requirea period of dialysis, mortality rate is now down to 3 to 5%.
Another virulence factor for the 0157:H7 serotype may be Even so, some patients develop life-threatening extra- the hardiness of this organism. This was recently demon- renal complications including intestinal necrosis and brain strated when an outbreak at a county fair was traced to a infarction with or without cerebral edema. Cerebral edema contaminated multipurpose building. Organisms collected without stroke can occur and lead to fatal brain stem herni- in sawdust 42 weeks after the outbreak were identified by ation syndrome. Mild pancreatic involvement is common, Hemolytic uremic syndrome Siegler and Oakes 203 but on occasion can be severe with necrosis and/or pseu- Manor SM, Guillory GS, Jain SP. Clopidogrel-induced thrombotic thrombo-cytopenic purpura-hemolytic uremic syndrome after coronary artery stenting.
docysts [42], that can leave the patient with insulin de- pendent diabetes, and on rare occasion, exocrine dysfunc- Humphreys BD, Sharman JP, Henderson JM, et al. Gemcitabine-associated tion. Less frequent involvement of vital organs includes thrombotic microangiopathy. Cancer 2004; 100:2664–2670.
the heart. Troponin subtype cTnI is useful in detecting Tuinmann G, Hegewisch-Becker S, Zschaber R, et al. Gemcitabine and mi- tomycin C in advanced pancreatic cancer: a single-institution experience. An- myocardial injury, as exemplified in a child with congestive heart failure due to D+HUS [43•]. This life-threatening Chandra D, Lawson S, Ramani P. Atypical haemolytic uraemic syndrome as complication has been successfully treated with extracor- a complication of induction chemotherapy for acute lymphoblastic leukemia. JClin Pathol 2004; 57:667–669.
poreal membrane oxygenation (ECMO), which should be Dlott JS, Danielson CF, Blue-Hnidy DE, McCarthy LJ. Drug-induced throm- reserved for the most severe cases [44].
botic thrombocytopenic purpura/hemolytic uremic syndrome: a concise re-view. Ther Apher Dial 2004; 8:102–111.
This very comprehensive, yet concise review of drug-induced HUS/TTP is of in- When dialysis is required, it is usually for about 5 to 7 days, terest to the physician because it not only lists and classifies numerous groups though long-term dialysis support is needed for some who of drugs, but includes pathogenesis when known, and includes tables that provideclinically useful information.
eventually recover kidney function, though are usually left Takatsuka H, Wakae T, Toda A, et al. Association of Helicobacter pylori with with residual kidney damage. Amazingly, recovery has thrombotic thrombocytopenic purpura and hemolytic uremic syndrome after been reported in two children following anuria and dialysis bone marrow transplantation. Clin Transplant 2004; 18:547–551.
that persisted for 8 and 16 months, respectively [45].
Simonetti GD, Dumont-Dos Santos K, Pachlopnik JM, et al. Hemolytic uremicsyndrome linked to infectious mononucleosis. Pediatr Nephrol 2003;18:1193–1194.
Long-term follow-up is appropriate since about 30 to 50% Marrie TJ. Q fever pneumonia. Curr Opin Infect Dis 2004; 17:137–142.
of those surviving the acute phase of D+HUS are later Maltezou HC, Constantopoulou I, Kallergi C, et al. Q fever in children in found to have signs of kidney damage and/or hypertension Greece. Am J Trop Med Hyg 2004; 70:540–544.
[46]. Some who experienced pancreatic damage (hyper- 10 Campos B, Gracia O, Sanjuan A, et al. [Self-limited thrombotic microangiop- athy associated with perianal abscess.] Nefrologia 2004; 24 (suppl 3): glycemia) during the acute phase of their disease and regain normal glucose levels, years later develop insulin 11 Yildiz B, Kural N, Yarar C. Atypical hemolytic uremic syndrome associated dependent diabetes. Those with proteinuria with or with- with group A beta hemolytic streptococcus. Pediatr Nephrol 2004; 19:943–944 author reply 945.
out an impaired glomerular filtration rate (GFR) are prob- 12 Ramasubbu K, Mullick T, Koo A, et al. Thrombotic microangiopathy an cyto- ably suffering from hyperfiltration injury that can progress megalovirus in liver transplant recipients: a case-based review. Transpl Infect to eventual end-stage renal disease (ESRD) requiring re- nal replacement therapy (dialysis or transplant) for surviv- 13 Tagle M, Barriga JA, Gutierrez S, et al. [Relapsing viral hepatitis type A com- plicated with renal failure.] Rev Gastroenterol Peru 2004; 24:92–96.
al. There is evidence that the HUS population, like others 14 Keyaerts E, Ghijsels E, Lemey P, et al. Plasma exchange-associated immuno- with renal damage, benefit from the use of angiotensin- globulin m-negative hantavirus disease after a camping holiday in southern converting enzyme (ACE) inhibitors as they slow the pro- France. Clin Infect Dis 2004; 38:1350–1356.
gression of hyperfiltration injury [47•,48•]. In the 5 to 10% 15 Bahloul M, Ben Hmida M, Belhoul W, et al. [Hemolytic-uremic syndrome sec- ondary to scorpion envenomation (apropos of 2 cases).] Nephrologie 2004; of HUS survivors who eventually develop ESRD, renal transplant should be the goal for those who had D+ 16 Cochran JB, Panzarino VM, Maes LY, Tecklenburg FW. Pneumococcal-in- HUS. The recurrence rate is for D+ HUS is low [49•].
duced T-antigen activation in hemolytic uremic syndrome and anemia. PediatrNephrol 2004; 19:317–321.
Those with atypical (e.g., Factor H deficiency) HUS expe- 17 Filler G, Radhakrishnan S, Strain L, et al. Challenges in the management of rience a much higher recurrence risk [49•] and should be infantile factor H associated hemolytic uremic syndrome. Pediatr Nephrol 18 Jozsi M, Manuelian T, Heinen S, et al. Attachment of the soluble complement regulator factor H to cell and tissue surfaces: relevance for pathology. HistolHistopathol 2004; 19:251–258.
Hemolytic uremic syndrome is a trilogy that is usually 19 Dragon-Durey MA, Fremeaux-Bacchi V, Loirat C, et al. Heterozygous and ho- caused by Shiga toxin producing E. coli, but can be precip- mozygous factor H deficiencies associated with hemolytic uremic syndrome itated by a variety of infections, drugs, and conditions.
or membranoproliferative glomerulonephritis: report and genetic analysis of16 cases. J Am Soc Nephrol 2004; 15:787–795.
Treatment and natural history varies with the type of 20 Richards A, Kemp EJ, Liszewski MK, et al. Mutations in human complement HUS, but is generally favorable with D+HUS of child- regulator, membrane cofactor protein (CD46), predispose to development of hood; less than 5% of cases are fatal, and most survivors familial hemolytic uremic syndrome. Proc Natl Acad Sci USA 2003; 100:12966–12971.
escape severe sequelae. The management and outcome 21 Noris M, Brioschi S, Caprioli J, et al. Familial haemolytic uraemic syndrome of the D-subsets is less favorable and is hampered by and an MCP mutation. Lancet 2003; 362:1542–1547.
our limited understanding of the multiple pathogenic cas- 22 Cheong HI, Lee BS, Kang HG, et al. Attempted treatment of factor H deficiency cades that characterizes this challenging group of patients.
by liver transplantation. Pediatr Nephrol 2004; 19:454–458.
23 Rodriguez de Cordoba S, Esparza-Gordillo J, Goicoechea de Jorge E, et al.
•• The human complement factor H: functional roles, genetic variations and dis- ease associations. Mol Immunol 2004; 41:355–367.
Papers of particular interest, published within the annual period of review, have This is an excellent review that provides the practitioner with an understanding of the importance of factor H in both health and disease. It walks the reader through the complex structure, function, molecular biology, and relationship of factor H to renal disease, with an emphasis on HUS.
24 Riley-Vargas RC, Gill DB, Kemper C, et al. CD46: expanding beyond com- 39 Tazzari PL, Ricci F, Carnicelli D, et al. Flow cytometry detection of Shiga tox- plement regulation. Trends Immunol 2004; 25:496–503.
ins in the blood from children with hemolytic uremic syndrome. Cytometry The article describes the expression pattern, function, and signaling that this com- plement regulating protein participates in, and the diseases, especially HUS, This article provides the practitioner with a review of specific new strategies for the which occur in the context of its deficiency.
rapid detection of E. coli Stx 1 and 2, and their potential utilization in clinical 25 Paton AW, Srimanote P, Talbot UM, et al. A new family of potent AB(5) cy- totoxins produced by Shiga toxigenic Escherichia coli. J Exp Med 2004; 40 Karmali MA. Prospects for preventing serious systemic toxemic complications of Shiga toxin-producing Escherichia coli infections using Shiga toxin recep-tor analogues. J Infect Dis 2004; 189:355–359.
26 Brooks JT, Bergmire-Sweat D, Kennedy M, et al. Outbreak of Shiga toxin-pro- ducing Escherichia coli O111:H8 infections among attendees of a high 41 Fu XJ, Iijima K, Nozu K, et al. Role of p38 MAP kinase pathway in a toxin- school cheerleading camp. Clin Infect Dis 2004; 38:190–198.
induced model of hemolytic uremic syndrome. Pediatr Nephrol 2004; 19:844–852.
27 Chark D, Nutikka A, Trusevych N, et al. Differential carbohydrate epitope rec- This gives the physician an overview of p38 MAP activity, and how blocking it pre- ognition of globotriaosyl ceramide by verotoxins and a monoclonal antibody.
vented TMA in a rat model of HUS. This may provide a strategy to prevent the pro- duction of prothrombotic and pro-inflammatory cytokines that are thought to 28 Khan A, Datta S, Das SC, et al. Shiga toxin producing Escherichia coli infection: augment the host response to Shiga toxins.
current progress & future challenges. Indian J Med Res 2003; 118:1–24.
42 Rebouissoux L, Llanas B, Jouvencel P, et al. Pancreatic pseudocyst compli- This review provides physicians with an overview of the current progress in treat- cating hemolytic-uremic syndrome. J Pediatr Gastroenterol Nutr 2004; ing Shiga toxin producing E. coli infections. Virulence factors are described in de- tail. It also provides genomic insight of potential therapeutic strategies.
43 Askiti V, Hendrickson K, Fish AJ, et al. Troponin I levels in a hemolytic uremic 29 Werber D, Fruth A, Buchholz U, et al. Strong association between shiga toxin- syndrome patient with severe cardiac failure. Pediatr Nephrol 2004; 19:345– producing Escherichia coli O157 and virulence genes stx2 and eae as pos- sible explanation for predominance of serogroup O157 in patients with hae- This case report describes the treatment of a patient with congestive heart failure molytic uraemic syndrome. Eur J Clin Microbiol Infect Dis 2003; 22:726–730.
due to D+ HUS and provides the physician information regarding the utility of us- 30 Ritchie JM, Thorpe CM, Rogers AB, Waldor MK. Critical roles for stx2, eae, ing of Trooping subtype catnip in diagnosing heart involvement in HUS.
and tir in enterohemorrhagic Escherichia coli-induced diarrhea and intestinal 44 Thomas NJ, Messina JJ, DeBruin WJ, Carcillo JA. Cardiac failure in hemolytic inflammation in infant rabbits. Infect Immun 2003; 71:7129–7139.
uremic syndrome and rescue with extracorporeal life support. Pediatr Cardiol 31 Ethelberg S, Olsen KE, Scheutz F, et al. Virulence factors for hemolytic uremic syndrome, Denmark. Emerg Infect Dis 2004; 10:842–847.
45 Brunner K, Bianchetti MG, Neuhaus TJ. Recovery of renal function after long- 32 Shen S, Mascarenhas M, Rahn K, et al. Evidence for a hybrid genomic island term dialysis in hemolytic uremic syndrome. Pediatr Nephrol 2004; 19:229– in verocytotoxin-producing Escherichia coli CL3 (serotype O113:H21) con- taining segments of EDL933 (serotype O157:H7) O islands 122 and 48. In- 46 De Petris L, Gianviti A, Giordano U, et al. Blood pressure in the long-term follow-up of children with hemolytic uremic syndrome. Pediatr Nephrol 2004.
33 Ramachandran V, Brett K, Hornitzky MA, et al. Distribution of intimin subtypes 47 Van Dyck M, Proesmans W. Renoprotection by ACE inhibitors after severe among Escherichia coli isolates from ruminant and human sources. J Clin Mi- hemolytic uremic syndrome. Pediatr Nephrol 2004; 19:688–690.
Evidence that angiotensin-converting enzyme (ACE) inhibitors can be used to re- 34 Ghosh SA, Polanowska-Grabowska RK, Fujii J, et al. Shiga toxin binds to ac- duce hyperfiltration injury in D+ HUS patients left with renal damage is docu- tivated platelets. J Thromb Haemost 2004; 2:499–506.
mented in this study. It is important reading for all who care for the 30 to 50%of patients left with renal damage following D+ HUS.
35 Fernandez GC, Te Loo MW, van der Velden TJ, et al. Decrease of thrombo- modulin contributes to the procoagulant state of endothelium in hemolytic 48 Caletti MG, Lejarraga H, Kelmansky D, Missoni M. Two different therapeutic uremic syndrome. Pediatr Nephrol 2003; 18:1066–1068.
regimes in patients with sequelae of hemolytic-uremic syndrome. PediatrNephrol 2004; 19:1148–1152.
36 Varma JK, Greene KD, Reller ME, et al. An outbreak of Escherichia coli O157 These observations provide further evidence that angiotensin-converting enzyme infection following exposure to a contaminated building. JAMA 2003; (ACE) inhibitors may be used to preserve renal function in D+ HUS patients by substantially slowing the progression of hyperfiltration injury.
37 Lin FY, Sherman PM, Li D. Development of a novel hand-held immunoassay 49 Loirat C, Niaudet P. The risk of recurrence of hemolytic uremic syndrome for the detection of enterohemorrhagic Escherichia coli O157:H7. Biomed after renal transplantation in children. Pediatr Nephrol 2003; 18:1095– 38 Bukhari Z, Weihe J, LeChevallier M. Development of procedures for rapid de- This article compares the recurrence rates among different types of HUS following tection of E. coli O157:H7 from source and finished water samples. Water renal transplantation, and thus provides the physician with critically important


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