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Introduction: Hemolytic uremic syndrome (HUS) is a condition that results in acute kidney failure mainly in children, which is caused by Shiga toxin-producing Escherichia coli and inflammatory response. Although anti-inflammatory mechanisms are triggered, studies on the implication in HUS are scarce. Interleukin-10 (IL-10) regulates inflammation in vivo, and the interindividual differences in its expression are related to genetic variants. Notably, the single nucleotide polymorphism (SNP) rs1800896 -1082 (A/G), located in the IL-10 promoter, regulates cytokine expression. Methods: Plasma and peripheral blood mononuclear cells (PBMC) were collected from healthy children and HUS patients exhibiting hemolytic anemia, thrombocytopenia, and kidney damage. Monocytes identified as CD14+ cells were analyzed within PBMC by flow cytometry. IL-10 levels were quantified by ELISA, and SNP -1082 (A/G) was analyzed by allele-specific PCR. Results: Circulating IL-10 levels were increased in HUS patients, but PBMC from these patients exhibited a lower capacity to secrete this cytokine compared with those from healthy children. Interestingly, there was a negative association between the circulating levels of IL-10 and inflammatory cytokine IL-8. We observed that circulating IL-10 levels were threefold higher in HUS patients with -1082G allele in comparison to AA genotype. Moreover, there was relative enrichment of GG/AG genotypes in HUS patients with severe kidney failure. Discussion: Our results suggest a possible contribution of SNP -1082 (A/G) to the severity of kidney failure in HUS patients that should be further evaluated in a larger cohort.
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Purpose of Review: Compared with high-income countries, healthcare disparities and inequities are more evident in low, lower-middle, and upper-middle-income countries with poorer housing and nutrition conditions. At least 20% of Latin America and the Caribbean are low and lower-middle-income countries. Despite the majority of the other countries being upper-middle income, the United Nations Children's Fund had classified all the regions as "less developed," with limited access to health care for the most vulnerable, the children. Latin America and the Caribbean regions represent an extensive territory with communication limitations and an unstable socio-political and economic environment. After considering the vast population affected by poverty worldwide and the long-term impact of kidney disease starting in childhood, it is crucial to better understand and analyze the multifactorial limiting conditions in accessing specialized care such as pediatric nephrology in disadvantaged areas. Recent Findings: Constraints in accessing basic healthcare in rural areas make it impossible to receive specialized pediatric nephrology care including dialysis and transplantation. Disturbingly, incidence and prevalence figures of acute kidney injury, chronic and end-stage kidney disease in some Latin American and the Caribbean countries are unknown, and these conditions still represent a death sentence for underprivileged populations. However, the monumental efforts of the dedicated healthcare providers and stakeholders that pioneered the actions in the past 50 years have shown remarkable progress in developing pediatric nephology services across the continent. Summary: In this review, we compile some of the latest evidence about the care of children and adolescents with kidney conditions in Latin America and the Caribbean, along with the experiences from the field in the care of these patients facing adverse conditions. We also highlight recommendations to address inequities and disparities.
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BACKGROUND: Hemolytic uremic syndrome (HUS) is characterized by microangiopathic hemolysis, thrombocytopenia, and thrombus formation leading to tissue injury. HUS is classified according to its etiology as post-diarrheal or atypical HUS. Differential diagnosis of both entities continues to be a challenge for pediatric physicians. METHODS: The aim was to improve the rapid etiological diagnosis of post-diarrheal HUS cases based on the detection of Shiga toxin (Stx)-producing Escherichia coli (STEC) infection by screening of stx1/stx2 and rfbO157 in cultured stools by multiplex PCR, and the additional detection of anti-lipopolysaccharide (anti-LPS) O157, O145, and O121 antibodies by Glyco-iELISA test. In addition, we studied patients' relatives to detect circulating pathogenic strains that could contribute to HUS diagnosis and/or lead to the implementation of measures to prevent dissemination of familial outbreaks. This study describes the diagnosis of 31 HUS patients admitted to Hospital Municipal de Niños Prof Dr Ramón Exeni during the 2017-2020 period. RESULTS: Stool PCR confirmed the diagnosis of STEC associated with HUS in 38.7% of patients (12/31), while anti-LPS serology did in 88.9% (24/27). In those patients in which both methods were carried out (n = 27), a strong association between the results obtained was found. We found that 30.4% of HUS patients had at least one relative positive for STEC. CONCLUSIONS: We could identify 96.3% (26/27) of HUS cases as secondary to STEC infections when both methods (genotyping and serology) were used. The results demonstrated a high circulation of STEC in HUS families and the prevalence of the STEC O157 serotype (83%) in our pediatric cohort. A higher-resolution version of the Graphical abstract is available as Supplementary information.
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Síndrome Hemolítico Urémico Atípico , Infecciones por Escherichia coli , Escherichia coli Shiga-Toxigénica , Niño , Humanos , Diarrea/diagnóstico , Diarrea/etiología , Diarrea/epidemiología , Serogrupo , Lipopolisacáridos , Anticuerpos Antibacterianos , Infecciones por Escherichia coli/complicaciones , Infecciones por Escherichia coli/diagnóstico , Infecciones por Escherichia coli/epidemiologíaRESUMEN
Hemolytic uremic syndrome (HUS) is defined as a triad of noninmune microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury. The most frequent presentation is secondary to Shiga toxin (Stx)-producing Escherichia coli (STEC) infections, which is termed postdiarrheal, epidemiologic or Stx-HUS, considering that Stx is the necessary etiological factor. After ingestion, STEC colonize the intestine and produce Stx, which translocates across the intestinal epithelium. Once Stx enters the bloodstream, it interacts with renal endothelial and epithelial cells, and leukocytes. This review summarizes the current evidence about the involvement of inflammatory components as central pathogenic factors that could determine outcome of STEC infections. Intestinal inflammation may favor epithelial leakage and subsequent passage of Stx to the systemic circulation. Vascular damage triggered by Stx promotes not only release of thrombin and increased fibrin concentration but also production of cytokines and chemokines by endothelial cells. Recent evidence from animal models and patients strongly indicate that several immune cells types may participate in HUS physiopathology: neutrophils, through release of proteases and reactive oxygen species (ROS); monocytes/macrophages through secretion of cytokines and chemokines. In addition, high levels of Bb factor and soluble C5b-9 (sC5b-9) in plasma as well as complement factors adhered to platelet-leukocyte complexes, microparticles and microvesicles, suggest activation of the alternative pathway of complement. Thus, acute immune response secondary to STEC infection, the Stx stimulatory effect on different immune cells, and inflammatory stimulus secondary to endothelial damage all together converge to define a strong inflammatory status that worsens Stx toxicity and disease.
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Infecciones por Escherichia coli/inmunología , Síndrome Hemolítico-Urémico/inmunología , Microvasos/patología , Escherichia coli Shiga-Toxigénica/inmunología , Animales , Vía Alternativa del Complemento/inmunología , Citocinas/inmunología , Citocinas/metabolismo , Modelos Animales de Enfermedad , Células Endoteliales/inmunología , Células Endoteliales/patología , Endotelio Vascular/citología , Endotelio Vascular/inmunología , Endotelio Vascular/patología , Células Epiteliales/inmunología , Células Epiteliales/patología , Infecciones por Escherichia coli/sangre , Infecciones por Escherichia coli/microbiología , Infecciones por Escherichia coli/patología , Síndrome Hemolítico-Urémico/sangre , Síndrome Hemolítico-Urémico/microbiología , Síndrome Hemolítico-Urémico/patología , Humanos , Mucosa Intestinal/microbiología , Riñón/irrigación sanguínea , Riñón/inmunología , Riñón/patología , Microvasos/citología , Microvasos/inmunología , Escherichia coli Shiga-Toxigénica/aislamiento & purificaciónRESUMEN
Shiga toxin (Stx), produced by Escherichia coli, is the main pathogenic factor of diarrhea-associated hemolytic uremic syndrome (HUS), which is characterized by the obstruction of renal microvasculature by platelet-fibrin thrombi. It is well known that the oxidative imbalance generated by Stx induces platelet activation, contributing to thrombus formation. Moreover, activated platelets release soluble CD40 ligand (sCD40L), which in turn contributes to oxidative imbalance, triggering the release of reactive oxidative species (ROS) on various cellular types. The aim of this work was to determine if the interaction between the oxidative response and platelet-derived sCD40L, as consequence of Stx-induced endothelium damage, participates in the pathogenic mechanism during HUS. Activated human glomerular endothelial cells (HGEC) by Stx2 induced platelets to adhere to them. Although platelet adhesion did not contribute to endothelial damage, high levels of sCD40L were released to the medium. The release of sCD40L by activated platelets was inhibited by antioxidant treatment. Furthermore, we found increased levels of sCD40L in plasma from HUS patients, which were also able to trigger the respiratory burst in monocytes in a sCD40L-dependent manner. Thus, we concluded that platelet-derived sCD40L and the oxidative response are reciprocally stimulated during Stx2-associated HUS. This process may contribute to the evolution of glomerular occlusion and the microangiopathic lesions.
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Ligando de CD40/sangre , Células Endoteliales/efectos de los fármacos , Síndrome Hemolítico-Urémico/sangre , Toxina Shiga/toxicidad , Células Cultivadas , Niño , Preescolar , Células Endoteliales/patología , Femenino , Síndrome Hemolítico-Urémico/inducido químicamente , Humanos , Lactante , Riñón/metabolismo , Riñón/patología , Masculino , Microvasos , Monocitos/metabolismo , Estrés Oxidativo , Activación Plaquetaria/efectos de los fármacos , Especies Reactivas de Oxígeno/metabolismoRESUMEN
Hemolytic uremic syndrome (HUS), a vascular disease characterized by hemolytic anemia, thrombocytopenia, and acute renal failure, is caused by enterohemorrhagic Shiga toxin (Stx)-producing bacteria, which mainly affect children. Besides Stx, the inflammatory response mediated by neutrophils (PMN) is essential to HUS evolution. PMN can release neutrophil extracellular traps (NET) composed of DNA, histones, and other proteins. Since NET are involved in infectious and inflammatory diseases, the aim of this work was to investigate the contribution of NET to HUS. Plasma from HUS patients contained increased levels of circulating free-DNA and nucleosomes in comparison to plasma from healthy children. Neutrophils from HUS patients exhibited a greater capacity to undergo spontaneous NETosis. NET activated human glomerular endothelial cells, stimulating secretion of the proinflammatory cytokines IL-6 and IL-8. Stx induced PMN activation as judged by its ability to trigger reactive oxygen species production, increase CD11b and CD66b expression, and induce NETosis in PMN from healthy donors. During HUS, NET can contribute to the inflammatory response and thrombosis in the microvasculature and thus to renal failure. Intervention strategies to inhibit inflammatory mechanisms mediated by PMN, such as NETosis, could have a potential therapeutic impact towards amelioration of the severity of HUS.
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Infecciones Bacterianas/inmunología , Células Endoteliales/inmunología , Trampas Extracelulares/inmunología , Síndrome Hemolítico-Urémico/inmunología , Riñón/patología , Neutrófilos/inmunología , Toxina Shiga/inmunología , Lesión Renal Aguda , Anemia Hemolítica , Apoptosis , Células Cultivadas , Niño , Humanos , Interleucina-6/metabolismo , Interleucina-8/metabolismo , Activación Neutrófila , Neutrófilos/microbiología , Especies Reactivas de Oxígeno/metabolismo , TrombocitopeniaRESUMEN
Haemolytic uraemic syndrome (HUS) is the major complication of Escherichia coli gastrointestinal infections that are Shiga toxin (Stx) producing. Monocytes contribute to HUS evolution by producing cytokines that sensitize endothelial cells to Stx action and migration to the injured kidney. As CC chemokine receptors (CCRs) are involved in monocyte recruitment to injured tissue, we analysed the contribution of these receptors to the pathogenesis of HUS. We analysed CCR1, CCR2 and CCR5 expression in peripheral monocytes from HUS patients during the acute period, with healthy children as controls. We observed an increased expression of CCRs per cell in monocytes from HUS patients, accompanied by an increase in the absolute number of monocytes CCR1+, CCR2+ and CCR5+. It is interesting that prospective analysis confirmed that CCR1 expression positively correlated with HUS severity. The evaluation of chemokine levels in plasma showed that regulated on activation of normal T-cell-expressed and -secreted (RANTES) protein was reduced in plasma from patients with severe HUS, and this decrease correlated with thrombocytopenia. Finally, the expression of the higher CCRs was accompanied by a loss of functionality which could be due to a mechanism for desensitization to compensate for altered receptor expression. The increase in CCR expression correlates with HUS severity, suggesting that the dysregulation of these receptors might contribute to an increased risk of renal damage. Activated monocytes could be recruited by chemokines and then receptors could be dysregulated. The dysregulation of CCRs and their ligands observed during the acute period suggests that a chemokine pathway would participate in HUS development.
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Quimiocinas/inmunología , Síndrome Hemolítico-Urémico/metabolismo , Monocitos/metabolismo , Receptores de Quimiocina/metabolismo , Movimiento Celular , Niño , Preescolar , Femenino , Expresión Génica/fisiología , Síndrome Hemolítico-Urémico/inmunología , Humanos , Riñón/metabolismo , Masculino , Monocitos/citología , Estudios ProspectivosRESUMEN
PURPOSE: The interaction of Shiga toxin (Stx) and/or lipopolysaccharide (LPS) with monocytes (Mo) may be central to the pathogenesis of hemolytic uremic syndrome (HUS), providing the cytokines necessary to sensitize endothelial cells to Stx action. We have previously demonstrated phenotypical alterations in Mo from HUS patients, including increased number of CD16+ Mo. Our aim was to investigate cytokine production in Mo from HUS patients. METHODS: We evaluated TNF-α and IL-10 intracellular contents and secretion in the different Mo subsets in mild (HUS 1) and moderate/severe (HUS 2 + 3) patients. As controls, we studied healthy (HC) and infected children (IC). We also studied Mo responsive capacity towards LPS, measuring the modulation of Mo surface molecules and cytokine production. RESULTS: In basal conditions, the intracellular measurement of TNF-α and IL-10 revealed that the highest number of cytokine-producing Mo was found in HUS 2 + 3 and IC, whereas LPS caused a similar increase in TNF-α and IL-10-producing Mo for all groups. However, when evaluating the release of TNF-α and IL-10, we found a diminished secretion capacity in the entire HUS group and IC compared to HC in basal and LPS conditions. Similarly, a lower Mo response to LPS in HUS 2 + 3 and IC groups was observed when surface markers were studied. CONCLUSION: These results indicate that Mo from severe cases of HUS, similar to IC but different to mild HUS cases, present functional changes in Mo subpopulations and abnormal responses to LPS.
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Síndrome Hemolítico-Urémico/inmunología , Interleucina-10/inmunología , Monocitos/inmunología , Factor de Necrosis Tumoral alfa/inmunología , Niño , Preescolar , Femenino , Humanos , Lactante , Interleucina-10/sangre , Lipopolisacáridos/inmunología , Masculino , Factor de Necrosis Tumoral alfa/sangreRESUMEN
The typical form of hemolytic uremic syndrome (HUS) is the major complication of Shiga toxin-producing Escherichia coli (STEC) infections. HUS is a critical health problem in Argentina since it is the main cause of acute renal failure in children and the second cause of chronic renal failure, giving account for 20% of renal transplants in children and adolescents in our country. In spite of the extensive research in the field, the mainstay of treatment for patients with HUS is supportive therapy, and there are no specific therapies preventing or ameliorating the disease course. In this review, we present the current knowledge about pathogenic mechanisms and discuss traditional and innovative therapeutic approaches, with special focus in national status and contributions made by Argentinean groups.
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Síndrome Hemolítico-Urémico , Escherichia coli Shiga-Toxigénica , Argentina/epidemiología , Síndrome Hemolítico-Urémico/epidemiología , Síndrome Hemolítico-Urémico/microbiología , Síndrome Hemolítico-Urémico/terapia , Humanos , Escherichia coli Shiga-Toxigénica/patogenicidadRESUMEN
La forma típica o post-diarreica del síndrome urémico hemolítico (SUH) es la complicación más grave de las infecciones por cepas de Escherichia coli productoras de toxina Shiga (STEC). En la Argentina el SUH es un problema crítico de salud pública, ya que representa la principal causa de falla renal aguda en la infancia, la segunda causa de falla renal crónica, y aporta el 20% de los casos de transplante renal durante la infancia y la adolescencia. A pesar de los avances en el conocimiento de su patogénesis, el único tratamiento actual de los pacientes con SUH es de sostén, y no existen terapias específicas ni preventivas. En la presente revisión expondremos los conocimientos básicos de los mecanismos patogénicos y discutiremos los enfoques terapéuticos tradicionales e innovadores, con especial foco en la situación nacional y los aportes hechos por grupos de la Argentina.
The typical form of hemolytic uremic syndrome (HUS) is the major complication of Shiga toxin-producing Escherichia coli (STEC) infections. HUS is a critical health problem in Argentina since it is the main cause of acute renal failure in children and the second cause of chronic renal failure, giving account for 20% of renal transplants in children and adolescents in our country. In spite of the extensive research in the field, the mainstay of treatment for patients with HUS is supportive therapy, and there are no specific therapies preventing or ameliorating the disease course. In this review, we present the current knowledge about pathogenic mechanisms and discuss traditional and innovative therapeutic approaches, with special focus in national status and contributions made by Argentinean groups.
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Humanos , Síndrome Hemolítico-Urémico , Escherichia coli Shiga-Toxigénica , Argentina/epidemiología , Síndrome Hemolítico-Urémico/epidemiología , Síndrome Hemolítico-Urémico/microbiología , Síndrome Hemolítico-Urémico/terapia , Escherichia coli Shiga-Toxigénica/patogenicidadRESUMEN
Proteinuria is the main indicator of renal disease progression in many chronic conditions. There is currently little information available on the efficacy, safety, and individual tolerance of patients with post-diarrheal hemolytic uremic syndrome (D+ HUS) nephropathy to therapies involving diet, enalapril, or losartan. A multicenter, double-blind, randomized controlled trail was conducted to evaluate the effect of a normosodic-normoproteic diet (Phase I) and the effect of normosodic-normoproteic diet plus enalapril (0.18-0.27 mg/kg/day) or losartan (0.89-1.34 mg/kg/day) (Phase II) on children with D+ HUS, normal renal function, and persistent, mild (5.1-49.9 mg/kg/day) proteinuria. Dietary intervention reduced the mean protein intake from 3.4 to 2.2 mg/kg/day. Of 137 children, proteinuria normalized in 91 (66.4 %) within 23-45 days; the remaining 46 patients were randomized to diet plus placebo (group 1, n = 16), plus losartan (group 2, n = 16), or enalapril (group 3, n = 14). In groups 1, 2, and 3, proteinuria was reduced by 30.0, 82.0, and 66.3%, respectively, and normalized in six (37.5%), three (81.3%), and 11 (78.6%) patients, respectively (χ(2)= 8.9, p = 0.015). These results suggest that: (1) a normosodic-normoproteic diet can normalize proteinuria in the majority of children with D+ HUS with mild sequelae, (2) the addition of enalapril or losartan to such dietary restrictions of protein further reduces proteinuria, and (3) these therapeutic interventions are safe and well tolerated. Whether these short-term effects can be extended to the long-term remains to be demonstrated.
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Inhibidores de la Enzima Convertidora de Angiotensina/uso terapéutico , Dietoterapia/métodos , Enalapril/uso terapéutico , Síndrome Hemolítico-Urémico/terapia , Losartán/uso terapéutico , Adulto , Niño , Preescolar , Diarrea/complicaciones , Método Doble Ciego , Femenino , Humanos , Fallo Renal Crónico/prevención & control , Masculino , Proteinuria/terapiaRESUMEN
Shiga toxin (Stx)-producing Escherichia coli (STEC) infection is associated with a broad spectrum of clinical manifestations that include diarrhea, hemorrhagic colitis, and hemolytic uremic syndrome (HUS). Systemic Stx toxemia is considered to be central to the genesis of HUS. Distinct methods have been used to evaluate anti-Stx response for immunodiagnostic or epidemiological analysis of HUS cases. The development of enzyme-linked immunosorbent assay (ELISA) and western blot (WB) assay to detect the presence of specific antibodies to Stx has introduced important advantages for serodiagnosis of HUS. However, application of these methods for seroepidemiological studies in Argentina has been limited. The aim of this work was to develop an ELISA to detect antibodies against the B subunit of Stx2, and a WB to evaluate antibodies against both subunits of Stx2 and Stx1, in order to analyze the pertinence and effectiveness of these techniques in the Argentinean population. We studied 72 normal healthy children (NHC) and 105 HUS patients of the urban pediatric population from the surrounding area of Buenos Aires city. Using the WB method we detected 67% of plasma from NHC reactive for Stx2, but only 8% for Stx1. These results are in agreement with the broad circulation of Stx2-expressing STEC in Argentina and the endemic behavior of HUS in this country. Moreover, the simultaneous evaluation by the two methods allowed us to differentiate acute HUS patients from NHC with a great specificity and accuracy, in order to confirm the HUS etiology when pathogenic bacteria were not isolated from stools.
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Síndrome Hemolítico-Urémico/inmunología , Síndrome Hemolítico-Urémico/microbiología , Toxinas Shiga/inmunología , Anticuerpos/inmunología , Argentina , Estudios de Casos y Controles , Niño , Preescolar , Ensayo de Inmunoadsorción Enzimática/métodos , Femenino , Estudios de Seguimiento , Síndrome Hemolítico-Urémico/tratamiento farmacológico , Humanos , Masculino , Pruebas Serológicas , Toxinas Shiga/química , Factores de Tiempo , Resultado del TratamientoRESUMEN
The typical form of hemolytic uremic syndrome (HUS) is the major complication of Shiga toxin-producing Escherichia coli infections. HUS is a critical health problem in Argentina since it is the main cause of acute renal failure in children and the second cause of chronic renal failure, accounting for 20% of renal transplants in children and adolescents in Argentina. Despite extensive research in the field, the mainstay of treatment for patients with HUS is supportive therapy, and there are no specific therapies preventing or ameliorating the disease course. In this review, we present the current knowledge about pathogenic mechanisms and discuss traditional and innovative therapeutic approaches, with special focus in Argentinean contribution. The hope that a better understanding of transmission dynamics and pathogenesis of this disease will produce better therapies to prevent the acute mortality and the long-term morbidity of HUS is the driving force for intensified research.
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Escherichia coli O157/patogenicidad , Síndrome Hemolítico-Urémico/fisiopatología , Síndrome Hemolítico-Urémico/terapia , Toxina Shiga/toxicidad , Adolescente , Anticoagulantes/uso terapéutico , Argentina/epidemiología , Niño , Infecciones por Escherichia coli/epidemiología , Infecciones por Escherichia coli/microbiología , Infecciones por Escherichia coli/fisiopatología , Infecciones por Escherichia coli/terapia , Fluidoterapia , Síndrome Hemolítico-Urémico/epidemiología , Síndrome Hemolítico-Urémico/microbiología , Humanos , Ensayos Clínicos Controlados Aleatorios como Asunto , Diálisis Renal , Insuficiencia Renal/etiología , Toxina Shiga/metabolismo , Resultado del TratamientoRESUMEN
OBJECTIVE: To examine the interrelationships of body composition variables derived from simple anthropometry, bioelectrical impedance (BIA) and dualenergy X-ray absorptiometry (DXA). POPULATION, MATERIAL AND METHODS: A total of 230 healthy preschool children (118 males and 112 females) age 4-6 years, attending a day care center, were examined to determine body mass index (BMI) and waist circumference (WC). Percentage of body fat content (%BF) was predicted by BIA (Maltron BF- 900) and DXA (Lunar DPX-L, pediatric software). RESULTS: BMI and WC did not show significant differences among sex, while %BF by BIA or DXA did. BIA measures were lower than DXA s (p <0.0001). Correlation between BIA vs. anthropometric methods and WC vs. DXA were moderate (Pearson r= 0.43 to 0.53), whereas the other correlations were strong (r= 0.71 to 0.83). However Bland Altman comparison showed wide limits of agreement between BIA and DXA; BIA significantly underestimated %BF as determined by DXA (p <0.0001). CONCLUSION: The methods used to estimate body composition in healthy preschool children highly correlated. However, the Bland Altman procedure suggests that BIA and DXA should not be used interchangeably.
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Absorciometría de Fotón , Antropometría , Composición Corporal , Impedancia Eléctrica , Niño , Preescolar , Estudios Transversales , Femenino , Humanos , MasculinoRESUMEN
Objetivo. Comparar la composición corporal estimadapor dos métodos antropométricos simples ypor impedanciometría (BIA, por sus siglas en inglés)y absorciometría de doble haz de rayos X(DXA, por sus siglas en inglés) y estudiar las correlacionesexistentes entre ellos, en una poblaciónpreescolar de Argentina.Población, material y métodos. Se estudió transversalmenteuna población clínicamente sana, deedad comprendida entre 4 y 6 años, de 230 niños(118 varones y 112 niñas), que concurrían a JardinesIntegrales de La Matanza, Argentina. Se determinóel índice de masa corporal (IMC), la circunferenciade cintura (Cci) y el contenido de grasa corporal,expresado como porcentaje, por BIA (Maltron BF-900) y por DXA (densitómetro Lunar DPX-L, softwarepediátrico).Resultados. En IMC y Cci no se observaron diferenciasestadísticamente significativas entre ambossexos, pero sí en el porcentaje de grasa corporal porBIA o DXA. La correlación entre BIA y ambos métodosantropométricos fue moderada (r de Pearson=0,43-0,53), al igual que entre DXA y Cci (r= 0,66),mientras que las demás correlaciones fueron fuertes(r= 0,71-0,83). Las medidas obtenidas por BIA yDXA no concordaron (prueba de Bland Altman); sinembargo, las diferencias se distribuyeron en formahomogénea a lo largo del eje horizontal e independientementede las medias. BIA reprodujo valoresmás bajos de porcentaje de grasa corporal que DXA(p <0,0001).Conclusiones. Existe buena correlación entre losmétodos antropométricos sencillos y la bioimpedanciay DXA. Sin embargo, los resultados no sonintercambiables, incluso entre BIA y DXA
Objective. To examine the interrelationships of body composition variables derived from simple anthropometry, bioelectrical impedance (BIA) and dualenergy X-ray absorptiometry (DXA). Population, material and methods. A total of 230 healthy preschool children (118 males and 112 females) age 4-6 years, attending a day care center, were examined to determine body mass index (BMI) and waist circumference (WC). Percentage of body fat content (%BF) was predicted by BIA (Maltron BF- 900) and DXA (Lunar DPX-L, pediatric software). Results. BMI and WC did not show significant differences among sex, while %BF by BIA or DXA did. BIA measures were lower than DXA´s (p <0.0001). Correlation between BIA vs. anthropometric methods and WC vs. DXA were moderate (Pearson r= 0.43 to 0.53), whereas the other correlations were strong (r= 0.71 to 0.83). However Bland Altman comparison showed wide limits of agreementbetween BIA and DXA; BIA significantly underestimated %BF as determined by DXA (p <0.0001). Conclusion. The methods used to estimate body composition in healthy preschool children highly correlated. However, the Bland Altman procedure suggests that BIA and DXA should not be used interchangeably.
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Preescolar , Niño , Absorciometría de Fotón , Antropometría , Composición Corporal , Índice de Masa Corporal , Peso por Edad , Peso por Estatura , Estudio Comparativo , Estudios Transversales , Epidemiología Descriptiva , Estudios Observacionales como Asunto , Interpretación Estadística de DatosAsunto(s)
Humanos , Masculino , Adulto , Persona de Mediana Edad , Femenino , Congreso , Educación Médica , Nefrología , PediatríaAsunto(s)
Humanos , Masculino , Niño , Femenino , Argentina , Discusiones Bioéticas , Trasplante/ética , Trasplante/legislación & jurisprudencia , TrasplanteRESUMEN
Thrombotic microangiopathy and acute renal failure are cardinal features of post-diarrheal hemolytic uremic syndrome (HUS). These conditions are related to endothelial and epithelial cell damage induced by Shiga toxin (Stx), through an interaction with its globotriaosylceramide (Gb3) receptor. Although, Stx is the main pathogenic factor and necessary for HUS development, clinical and experimental evidence suggest that the inflammatory response is able to potentiate Stx toxicity. Lipopolysaccharides (LPS) and neutrophils (PMN) represent two central components of inflammation during a Gram-negative infection. In this regard, patients with high peripheral PMN counts at presentation have a poor prognosis. In the present review, we discuss the contribution of experimental models and patient's studies in an attempt to elucidate the pathogenic mechanisms of HUS.