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Abstract Atypical hemolytic uremic syndrome (aHUS) is a thrombotic microangiopathy (TMA) that affects multiple organs and the kidneys in particular. aHUS can be sporadic or familial and is most commonly caused by dysregulation of the alternative complement pathway. The initial attack of aHUS can occur at any age, and is associated with a high rate of progression to end stage renal disease. Many aHUS patients relapse in the native or transplanted kidneys, and require close monitoring and long-term management. Availability of anticomplement therapy has revolutionized the management of aHUS, and can change the natural course of aHUS by inducing hematologic remission, improving or stabilizing kidney functions, and preventing graft failure. As a result, it is important to succeed in the challenging task of differentiating aHUS from other TMAs and initiate adequate treatment early during the course of disease. Considering the high cost of currently available anticomplement therapy, it is important also from a financial point of view to accurately diagnose aHUS early during the course of disease and determine the necessary length of therapy. This highlights the need for development of precise complement functional and genetic studies with rapid turnaround time.
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Goldwater, Paul N. "Treatment and prevention of enterohemorrhagicEscherichia coliinfection and hemolytic uremic syndrome." Expert Review of Anti-infective Therapy 5, no. 4 (August 2007): 653–63. http://dx.doi.org/10.1586/14787210.5.4.653.
Haslam, David B. "Molecular Decoys: Novel Approaches to the Prevention of Hemolytic Uremic Syndrome." Pediatric Research 48, no. 3 (September 2000): 267–68. http://dx.doi.org/10.1203/00006450-200009000-00001.
The severity of human infection by one of the many Shiga toxin-producing Escherichia coli (STEC) is determined by a number of factors: the bacterial genome, the capacity of human societies to prevent foodborne epidemics, the medical condition of infected patients (in particular their hydration status, often compromised by severe diarrhea), and by our capacity to devise new therapeutic approaches, most specifically to combat the bacterial virulence factors, as opposed to our current strategies that essentially aim to palliate organ deficiencies. The last major outbreak in 2011 in Germany, which killed more than 50 people in Europe, was evidence that an effective treatment was still lacking. Herein, we review the current knowledge of STEC virulence, how societies organize the prevention of human disease, and how physicians treat (and, hopefully, will treat) its potentially fatal complications. In particular, we focus on STEC-induced hemolytic and uremic syndrome (HUS), where the intrusion of toxins inside endothelial cells results in massive cell death, activation of the coagulation within capillaries, and eventually organ failure.
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TARR, PHILLIP I. "Escherichia coli O157: H7: Overview of Clinical and Epidemiological Issues." Journal of Food Protection 57, no. 7 (July 1, 1994): 632–37. http://dx.doi.org/10.4315/0362-028x-57.7.632.
Escherichia coli O157:H7 is an important and common human pathogen which causes diarrhea, bloody diarrhea (hemorrhagic colitis) and the life threatening post-diarrheal disorder, hemolytic uremic syndrome (HUS). Escherichia coli O157:H7 produces one or two potent cytotoxins, designated Shiga-like toxins (or verocytotoxins) I and II. While additional serotypes of cytotoxin-producing E. coli may cause human disease, E. coli O157:H7 is the most important such enteric pathogen in the United States. Epidemiologic data suggest that the incidence of hemolytic uremic syndrome is probably increasing. Until data emerge from controlled studies, conservative management of infected patients remains the mainstay of therapy, rather than specific antibacterial or antitoxin therapy. The serious nature of illness caused by E. coli O157:H7 should make prevention of human infection with this pathogen a high priority for the food industry.
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Davin, Jean-Claude, Charles Majoie, Jaap Groothoff, Valentina Gracchi, Antonia Bouts, Timothy H. J. Goodship, and Chantal Loirat. "Prevention of large-vessel stenoses in atypical hemolytic uremic syndrome associated with complement dysregulation." Pediatric Nephrology 26, no. 1 (July 24, 2010): 155–57. http://dx.doi.org/10.1007/s00467-010-1608-9.
Nuernberger, Jens, Oliver Witzke, Russell P. Rother, Thomas Philipp, Udo Vester, Hideo Baba, Lothar Bernd Zimmerhackl, and Andreas Kribben. "Successful Treatment of Atypical Hemolytic Uremic Syndrome with the Complement Inhibitor Eculizumab." Blood 112, no. 11 (November 16, 2008): 2294. http://dx.doi.org/10.1182/blood.v112.11.2294.2294.
Abstract Background: Atypical hemolytic uremic syndrome (aHUS) is a rare microangiopathic hemolytic anemia characterized by the uncontrolled progression of the alternative complement pathway due to genetic or acquired dysregulation of steady state alternative pathway activity leading to a proinflammatory and prothrombotic condition. Atypical HUS is characterized by intravascular hemolysis, consumptive thrombocytopenia, and microvascular glomerular thrombosis with the formation of thrombi in glomerular capillaries. As the thrombotic microangiopathy is particularly severe in the renal microvasculature, the disease inevitably leads to acute kidney injury with most cases progressing to end-stage-renal-disease. Eculizumab is a complement inhibitor that has been shown to completely and consistently block the activation of the terminal complement cascade thereby preventing the generation of the proinflammatory and prothrombotic molecules C5a and C5b-9. In recent phase 3 clinical studies in patients with the rare hemolytic disease paroxysmal nocturnal hemoglobinuria, chronic eculizumab treatment was shown to be safe, and demonstrated an effective reduction in intravascular hemolysis and a 85% reduction in thrombotic events. Aim: The safety and efficacy of eculizumab in the management of aHUS. We sought to investigate the potential benefit of the complement inhibitor eculizumab in aHUS, a disease characterized by uncontrolled progression of the alternative complement pathway. Methods: Two aHUS patients that were unresponsive to plasmapheresis were dosed with 600 mg of eculizumab to inhibit the terminal complement cascade. The patients were monitored closely for adverse events and platelet counts, creatinine and haptoglobin were assessed. PK/PD analyses were performed on one of the two patients. Results: We report aHUS in two patients successfully treated with the complement inhibitor eculizumab. The first was a 37-year old female with recurrence of aHUS after renal transplantation. At the age of 25 years, the patient developed aHUS with end-stage-renal- disease and stayed on dialysis until she received a first cadaveric kidney transplant 5 years later. This first transplant was lost 5 weeks after transplantation due to chronic aHUS. A second attempt of kidney transplantation was undertaken using a calcineurin-inhibitor free immunosuppressive protocol and despite immediate plasmapheresis (4 times), aHUS worsened (platelet count dropping, haptoglobin decreasing, creatinine increasing) indicating a high probability of repeated renal transplant loss. The patient was characterized as having a missense mutation in the gene encoding the complement regulatory protein factor H. The current literature indicates that patients with such mutations have a high incidence of graft rejection (7 of 8 grafts rejected). Eculizumab was therefore administered and resulted in immediate and complete inhibition of terminal complement activation for at least 5 days. During the week following treatment, platelet count increased, hemolysis normalized (as assessed by haptoglobin levels), and transplant function recovered (as assessed by creatinine levels) indicating successful reversal of aHUS (see Figure A). The second patient was an 18-year old female with first the initial manifestation of aHUS. After a total of 18 plasmaphereses, the young patient was referred to our hospital with aHUS. When symptoms persisted despite another three plasmaphereses in our University hospital, we decided to administer eculizumab. Over the following week, platelet count normalized, hemolysis was reversed, and renal function partially recovered (see Figure B). Summary: This is the first report evaluating the use of a complement inhibitor as a potential therapy for the treatment of aHUS. These data suggest that eculizumab therapy results in a reduction in thrombotic microangiopathy and hemolysis as evidenced by a reversal of thrombocytopenia, the normalization of hemolytic parameters, and the recovery of kidney transplant function. These data suggest the eculizumab modifies the course of aHUS and warrant further clinical investigation to confirm whether complement inhibition with eculizumab is an effective treatment of this devastating and life-threatening disease. Figure Figure
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Noris, Marina, and Giuseppe Remuzzi. "Managing and preventing atypical hemolytic uremic syndrome recurrence after kidney transplantation." Current Opinion in Nephrology and Hypertension 22, no. 6 (November 2013): 704–12. http://dx.doi.org/10.1097/mnh.0b013e328365b3fe.
Avila Bernabeu, Ana Isabel, Teresa Cavero Escribano, and Mercedes Cao Vilarino. "Atypical Hemolytic Uremic Syndrome: New Challenges in the Complement Blockage Era." Nephron 144, no. 11 (2020): 537–49. http://dx.doi.org/10.1159/000508920.
Atypical hemolytic uremic syndrome (aHUS) is a rare cause of thrombotic microangiopathy (TMA), characterized by microangiopathic hemolytic anemia, consumptive thrombocytopenia, and multisystem end organ involvement, most commonly affecting the kidney. Diagnosis is clinical, after exclusion of other TMA causes. Primary aHUS arises from genetic abnormalities, resulting in uncontrolled complement activity, while a variety of clinical scenarios cause secondary aHUS, including infection, pregnancy, malignancy, autoimmune disease, and medications. They can also induce a temporary complement deregulation with an overlap between both scenarios, which can make differential diagnosis difficult. Primary aHUS can be sporadic or familial and is associated with a high rate of progression to ESRD. Many aHUS patients relapse in the native or transplanted kidneys, leading to kidney failure. The introduction of eculizumab has changed the prognosis of aHUS, by inducing hematologic remission, improving or stabilizing kidney functions, and preventing graft failure. The early institution of appropriate therapy can prevent multiorgan damage, so is essential to recognize and differentiate the TMA syndromes. Eculizumab is considered now the first-line treatment, and it is recommended lifelong therapy. However, the high cost of therapy has led to make efforts to develop precise complement functional and genetic studies that help physicians to determine the appropriate duration of eculizumab therapy. Nowadays, more studies are needed to select candidates to adjustment of therapy.
Dissertations / Theses on the topic "Hemolytic uremic syndrome Prevention":
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Srimanote, Potjanee. "Analysis of putative virulence factors of a locus of enterocyte effacement-negative shiga-toxigenic Escherichia coli O113:H21 strain." Title page, contents and abstract only, 2003. http://web4.library.adelaide.edu.au/theses/09PH/09php863.pdf.
"February 2003." Addendum and corrigenda inserted at back Includes bibliographical references (leaves 249-272) Aims to identify and characterise potential virulence-associated factors from the locus of enterocyte effacement-negative shiga-toxigenic Escherichia coli O113:H21 strain 98NK2 which was responsible for an outbreak of haemolytic uremic syndrome. Particular attention was focused on putative virulence genes encoded on the megaplasmid of this strain.
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Noris, Marina. "Genetics of hemolytic uremic syndrome." Maastricht : Maastricht : Universiteit Maastricht ; University Library, Maastricht University [Host], 2006. http://arno.unimaas.nl/show.cgi?fid=7591.
Maga, Tara Kristen. "Unraveling the complex genetics of atypical hemolytic uremic syndrome." Diss., University of Iowa, 2012. https://ir.uiowa.edu/etd/2935.
Atypical hemolytic uremic syndrome (aHUS) is characterized by acute renal failure, thrombocytopenia, and microangiopathic hemolytic anemia. aHUS is far less common and more severe than typical HUS, which is caused by E. coli infection and manifests as diarrheal illness. The pathogenesis of the disease is linked to dysregulation of the alternative pathway of the complement cascade. Mutations in the complement regulators factor H (CFH), membrane cofactor protein (MCP), factor B (CFB), and factor I (CFI) have been implicated in aHUS. These loss or gain of function mutations lead to uncontrolled complement activity and immune-mediated host cell damage. Establishing a genetic etiology is important as it helps to direct treatment during the acute phase of disease and when transplantation is considered. It has been shown in previous studies that the age of onset as well the severity of the disease is correlated with the type of mutation a patient is found to carry. In forty percent of aHUS patients a mutation in CFH, MCP, CFB, CFI, C3 or THBD is not detected. These data strongly suggest that other genetic factors are involved in the pathogenesis of aHUS and that comprehensive mutation detection in aHUS patients is essential to provide diagnostic and prognostic information, and improve their clinical care.
My thesis work has aimed to identify the other genetic contributors to this disease. To achieve this goal we began by screening the largest American cohort of aHUS patients for mutations in CFH, MCP, CFB, CFI, C3, THBD as well as CFHR5. This study identified over thirty novel mutations and suggests a more comprehensive genetic screening method that would better serve patients. To complement these studies multiplex ligation-dependent probe amplification was used to detect genetic rearrangements within the factor H related genes. A number of unique fusion proteins were seen in aHUS patients, all of which are predicted to affect the function of CFH. To discover mutations in novel genes that are causally related to aHUS, we have optimized a platform called CASCADE (Capture and Sequencing of Complement-Associated Disease Exons), which is based on targeted-genome capture and next-generation sequencing. This study revealed an unexpected role for ADAMTS13 and other genes in the coagulation pathway as modifiers of aHUS. Using functional assays we show two of the ADAMTS13 variants alter the behavior of this protein. This work has changed how we view this disease by identifying several novel candidate genes, for which we hope future analysis will lead to a better understanding of their role in aHUS. Using this knowledge we can provide better and more personalized treatments for patients.
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Edwards, Kelly Katherine. "Bacterial factors contributing to the pathogenesis of the hemolytic uremic syndrome." MU has:, 2002. http://wwwlib.umi.com/cr/mo/fullcit?p3060096.
Bu, Fengxiao. "Exploring the genetics of a complex disease - atypical hemolytic uremic syndrome." Diss., University of Iowa, 2016. https://ir.uiowa.edu/etd/3055.
Atypical hemolytic uremic syndrome (aHUS) is a rare renal disorder characterized by thrombotic microangiopathy, thrombocytopenia, and acute kidney injury. Its pathogenesis has been attributed to a ‘triggering' event that leads to dysregulation of the complement cascade at the level of the endothelial cell surface. Consistent with this understanding of the disease, mutations in complement genes have been definitively implicated in aHUS. However, the existence of other genetic contributors is supported by two observations. First, in ~50% of cases, disease-causing variants are not identified in complement genes, and second, disease penetrance is typically incomplete and highly variable.
To test this hypothesis, we identified pathways established to have crosstalk with the complement cascade, focusing initially on the coagulation pathway. Using targeted genomic enrichment and massively parallel sequencing we screened 36 European-American patients with sporadic aHUS patients for genetic variants in 85 complement and coagulation genes, identifying deleterious rare variants in several coagulation genes. The most frequently mutated coagulation gene in our study cohort was PLG, which encodes a zymogen of plasmin and plays key role in fibrinolysis. These results implicate the coagulation pathway in the pathogenesis of aHUS.
Based on this outcome, we developed a clinical genetic testing panel to screen disease-related genes in a group of ultra-rare complement-mediated diseases that includes, in addition to aHUS, thrombotic thrombocytopenic purpura (TTP), C3 glomerulonephritis (C3GN) and dense deposit disease (DDD) patients. Data from 193 patients validate the usage of this panel in clinical practice and also provide confirmatory insight into the pathogeneses of these diseases. Specifically, we found that in aHUS and TTP patients, variants were frequently identified in complement regulator genes, while in C3GN and DDD patients, variants were additionally found in C3 convertase genes.
To understand variability in disease penetrance, we completed targeted genetic screening in two aHUS families grossly discordant for disease penetrance, identifying in one family a co-segregating Factor X-deficiency variant (F10 p.Glu142Lys) that abrogated the effect of the complement mutation. Functional studies of the F10 p.Glu142Lys variant show that it decreases Factor X activity predicting to a hypo-coagulable state and further illustrating the importance of complement-coagulation crosstalk in exacerbating, but also mitigating the aHUS phenotype.
In our final studies, we have sought to complete a comprehensive analysis for other potentially related pathways by using bioinformatics to identify candidate pathways coupled with whole exome sequencing. Preliminary data from 43 aHUS patients and 300 controls suggest that pathways for dermatan and heparan sulfate synthesis, which are relevant to the formation of the extra-cellular matrix and cell surface adhesion, may be implicated in the aHUS.
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Karpman, Diana O. "Studies of the pathogenesis of hemolytic uremic syndrome and thrombotic thrombocytopenic purpura." Lund : Lund University, 1997. http://catalog.hathitrust.org/api/volumes/oclc/68945090.html.
Valoti, Elisabetta. "Genetic factors associated with anti-factor H autoantibodies in atypical hemolytic uremic syndrome (aHUS)." Thesis, Open University, 2018. http://oro.open.ac.uk/55853/.
Atypical hemolytic uremic syndrome (aHUS) is a rare form of thrombotic microangiopathy characterized by renal failure and determined by genetic and acquired defects of alternative pathway (AP) of the complement system. Autoantibodies against factor H (anti-FHs), a regulator of the AP, were reported in 10% of patients, and are associated with the deficiency of factor H related 1 (FHR1), a FH homologous protein. The aim of this thesis was to evaluate the contribution of genetics to the development of anti-FHs in aHUS. Thirty patients affected by aHUS resulted positive for anti-FHs (9.8%) and FHR1 deficiency was present in 83.3% of them. A healthy control also showed anti-FHs in concomitance with FHR1 deficiency documenting that the lack of FHR1 strongly predisposed to anti-FH development also in healthy subjects although this condition was not sufficient for the disease manifestation. The presence of infectious prodromal signs and an age at the disease onset around 8 years indicated that common infections may trigger the development of autoantibodies in subjects with at risk genetic background. Likely pathogenetic variants in complement genes were observed in 37% of our patients with anti-FHs. At variance, common variants in complement genes did not seem to contribute to the disease, as documented by comparing patients with super controls, unaffected subjects carrying FHR1 deficiency. Finally, I report that the HLA-DRB1*11:04 allele could be a predisposing genetic variant for anti-FH associated aHUS. Further works will be necessary to confirm this finding and to explore the presence of other genetic susceptibility factors that, in combination with the HLA-DRB1*11:04 allele and the FHR1 deficiency, could increase the risk for anti-FHs.
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Morigi, Marina. "Unravelling molecular and biochemical dysfunction by Shiga toxin: implication for thrombotic microangiopathy in Hemolytic Uremic Syndrome." Maastricht : Maastricht : Universiteit Maastricht ; University Library, Maastricht University [Host], 2006. http://arno.unimaas.nl/show.cgi?fid=7590.
Marinozzi, Maria Chiara. "Characterization of the complement hereditary and acquired abnormalities in atypical Hemolytic Uremic Syndrome and C3 Glomerulopathy." Thesis, Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCB037/document.
McGannon, Colleen M. "Antibiotic Therapy in the Treatment of E. coli O157:H7." University of Cincinnati / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1230919332.
Books on the topic "Hemolytic uremic syndrome Prevention":
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Parker, James N., and Philip M. Parker. The official patient's sourcebook on hemolytic uremic syndrome. Edited by Icon Group International Inc and NetLibrary Inc. San Diego, Calif: Icon Health Publications, 2002.
Rotman, Tamara Avril. Role of verocytotoxin-1 in the pathogenesis of hemorrhagic colitis and hemolytic uremic syndrome. Ottawa: National Library of Canada, 1992.
1941-, Kaplan Bernard S., Trompeter Richard S, and Moake Joel L. 1940-, eds. Hemolytic uremic syndrome and thrombotic thrombocytopenic purpura. New York: Marcel Dekker, Inc., 1992.
Globotriaosylceramide (Gb3) expression and membrane presentation: Implications for the hemolytic uremic syndrome and human immunodeficiency virus infection. Ottawa: National Library of Canada, 2003.
Publications, ICON Health. The Official Patient's Sourcebook on Hemolytic Uremic Syndrome: A Revised and Updated Directory for the Internet Age. Icon Health Publications, 2002.
Ali, Uma, and Bradley P. Dixon. "Hemolytic Uremic Syndrome." In Critical Care Nephrology and Renal Replacement Therapy in Children, 129–44. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-90281-4_9.
Metze, Dieter, Vanessa F. Cury, Ricardo S. Gomez, Luiz Marco, Dror Robinson, Eitan Melamed, Alexander K. C. Leung, et al. "Hemolytic Uremic Syndrome." In Encyclopedia of Molecular Mechanisms of Disease, 801–2. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_763.
Clark, Elaine, and Scott Orme. "Hemolytic-uremic syndrome." In Health-related disorders in children and adolescents: A guidebook for understanding and educating., 309–14. Washington: American Psychological Association, 1998. http://dx.doi.org/10.1037/10300-042.
Vercellone, Antonio, Piero Stratta, and Caterine Canavese. "Hemolytic Uremic Syndrome." In Advances in Experimental Medicine and Biology, 185–98. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-8240-9_24.
Johnson, S., and C. Mark Taylor. "Hemolytic Uremic Syndrome." In Pediatric Nephrology, 1155–80. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-76341-3_48.
Watkins, Sandra L. "Hemolytic Uremic Syndrome." In Textbook of Clinical Pediatrics, 2769–72. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-02202-9_297.
Conference papers on the topic "Hemolytic uremic syndrome Prevention":
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Bahlavouni, Alina, and Aleena Paul. "Hemolytic Uremic Syndrome Associated with Entamoeba Histolytica." In AAP National Conference & Exhibition Meeting Abstracts. American Academy of Pediatrics, 2021. http://dx.doi.org/10.1542/peds.147.3_meetingabstract.866.
Selvam, M. Masilamani, Divya Sasitharan, and W. Manohar Paul. "Clinical validation of vaccines against hemolytic uremic syndrome." In 2014 International Conference on Science Engineering and Management Research (ICSEMR). IEEE, 2014. http://dx.doi.org/10.1109/icsemr.2014.7043626.
Pankratenko, T. E., O. V. Moskalec, and T. Yu Abaseeva T. "Cell adhesion molecules in childrenwith diarrhea-associated hemolytic uremic syndrome." In General question of world science. "Л-Журнал", 2018. http://dx.doi.org/10.18411/gq-31-03-2018-13.
Moskalec, O. V., T. E. Pankratenko, and T. Yu Abaseeva. "Soluble adhesion molecules in children with typical hemolytic uremic syndrome." In Scientific achievements of the third millennium. SPC "LJournal", 2018. http://dx.doi.org/10.18411/scc-05-2018-06.
Abdou, M., M. Alsharif, T. Naguib, and M. L. Patel. "Eculizumab: A Life Saver in Postpartum Atypical Hemolytic Uremic Syndrome." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a6530.
ROMERO LEGRO, IVAN, Sadia Shah, and Vaidehi Kaza. "Tacrolimus Induced Hemolytic Uremic Syndrome In A Lung Transplant Patient." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a5834.
Moskalets, O. V., T. E. Pankratenko, and T. Yu Abaseeva. "Biomarkers of endothelial disfunction in children with atypical hemolytic uremic syndrome." In Scientific achievements of the third millennium. SPC "LJournal", 2018. http://dx.doi.org/10.18411/scc-09-2018-08.
Cruz, Pedro Costa e., Patrícia Mendes, Marisol Anselmo, and Luís Gonçalves. "P102 Typical vs atypical hemolytic-uremic syndrome: eculizumab, a difficult decision." In 8th Europaediatrics Congress jointly held with, The 13th National Congress of Romanian Pediatrics Society, 7–10 June 2017, Palace of Parliament, Romania, Paediatrics building bridges across Europe. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2017. http://dx.doi.org/10.1136/archdischild-2017-313273.190.
Moskalets, O. V. "Prognostic value of sICAM-1 and sVCAM-1 in hemolytic uremic syndrome." In Global science. Development and novelty. НИЦ «Л-Журнал», 2018. http://dx.doi.org/10.18411/gdsn-25-12-2018-04.
Pankratenko, T. E., and O. V. Moskalec. "sICAM-1 and sVCAM-1 in children with typical hemolytic uremic syndrome." In Global science. Development and novelty. НИЦ «Л-Журнал», 2018. http://dx.doi.org/10.18411/gdsn-28-02-2018-07.
