Disfunción endotelial en niños con enfermedad renal crónica / Endothelial dysfunction in children with chronic kidney disease

Antecedentes y objetivo: La enfermedad cardiovascular es la principal causa de muerte en niños con enfermedad renal crónica. La inflamación y la disfunción endotelial se presenta en la mayoría de estos pacientes y son factores asociados a enfermedad cardiovascular. La dilatación mediada por flujo (DMF)<7% es un marcador subrogado validado en la evaluación de la disfunción endotelial. Nuestro objetivo fue identificar los factores de riesgo asociados a disfunción endotelial en niños con enfermedad renal crónica. Materiales y métodos: Se estudió a niños de 2-16 años de edad. Se recopiló su información clínica y variables bioquímicas, incluidos hormona paratiroidea intacta (iPTH), interleucinas 6 y 1β, proteína C reactiva de alta sensibilidad (hsCRP), glutatión reducido, óxido nítrico, malondialdehído y homocisteína. Se consideró DMF alterada<7%. Resultados: Se incluyó a 129 pacientes con edad de 13,1±2,6 años. Tuvieron DMF<7% 69 (52,7%). Los pacientes con DMF<7% tuvieron niveles más altos de triglicéridos y de hsCRP que aquellos con DMF≥7% (145,5 vs. 120,0mg/dl, p=0,042, y 1,24 vs. 0,55U/l, p=0,007, respectivamente), así como una mayor frecuencia de iPTH baja (19,1 vs. 4,9%, p=0,036). Los niveles de hsCRP se correlacionaron significativamente con la DMF (Rho=−0,28, p=0,003). Los pacientes con iPTH baja (OR 4,41, IC 95% 1,13-17,27, p=0,033) y con hsCRP incrementada (OR 2,89, IC 95% 1,16-7,17, p=0,022) tuvieron un riesgo ajustado mayor de DMF<7%. Conclusiones: La hipertrigliceridemia, la inflamación y una iPTH baja se asociaron significativamente a una DMF alterada. Son factores de riesgo de enfermedad cardiovascular frecuentes y tratables. (AU)

Background and objective: Cardiovascular disease is the main cause of death in children with chronic kidney disease. Inflammation and endothelial dysfunction are found in the majority of these patients and are factors associated to cardiovascular disease. Flow mediated dilatation (FMD) is a surrogate marker validated for evaluating endothelial dysfunction. Our objective was to identify risk factors associated to endothelial dysfunction in children with chronic kidney disease. Materials and methods: Children 2-16 years of age were studied. Clinical information and biochemical variables were gathered, including intact parathyroid hormone (iPTH), interleukins 6 and 1β, high sensitivity C reactive protein (hsCRP), reduced glutathione, nitric oxide, malondialdehyde and homocysteine. FMD was measured, and considered altered if<7%. Results: Included were 129 patients aged 13.1±2.6 years. FMD<7% was found in 69 (52.7%). Patients with altered FMD had higher levels of triglycerides and hsCRP than those with normal FMD (145.5 vs. 120.0mg/dL, P=.042, and 1.24 vs. 0.55U/L, P=.007, respectively), as well as higher frequency of low iPTH (19.1 vs. 4.9%, P=.036). Levels of hsCRP correlated significantly with FMD (Rho=−0.28, P=.003). Patients with low iPTH (OR 4.41, 95% CI 1.13-17.27, P=.033) and increased hsCRP (OR 2.89, 95% CI 1.16-7.17, P=.022) had higher adjusted risk of having FMD<7%. Conclusions: Hypertriglyceridemia, inflammation and low iPTH associated significantly with altered FMD. They are frequent, treatable risk factors for cardiovascular disease. (AU)

Endothelial dysfunction in children with chronic kidney disease.

BACKGROUND AND OBJECTIVE: Cardiovascular disease (CVD) is the main cause of death in children with chronic kidney disease (CKD). Inflammation and endothelial dysfunction (ED) are found in the majority of these patients and are factors associated to CVD. Flow mediated dilatation (FMD) is a surrogate marker validated for evaluating ED. Our objective was to identify risk factors associated to ED in children with CKD. MATERIALS AND METHODS: Children 2-16 years of age were studied. Clinical information and biochemical variables were gathered, including intact parathyroid hormone (iPTH), interleukins 6 and 1b, high sensitivity C reactive protein (hsCRP), reduced glutathione, nitric oxide, malondialdehyde and homocysteine. FMD was measured, and considered altered if <7%. RESULTS: Included were 129 patients aged 13.1 ±â€¯2.6 years. FMD < 7% was found in 69 (52.7%). Patients with altered FMD had higher levels of triglycerides and hsCRP than those with normal FMD (145.5 mg/dl vs. 120.0 mg/dl, P = .042, y 1.24 U/L vs. 0.55 U/L, P = .007, respectively), as well as higher frequency of low iPTH (19.1% vs. 4.9%, P = .036). Levels of hsCRP correlated significantly with FMD (Rho = -0.28, P = .003). Patients with low iPTH (OR = 4.41, 95%CI 1.13-17.27, P = .033) and increased hsCRP (OR = 2.89, 95%CI 1.16-7.17, P = .022) had higher adjusted risk of having FMD < 7%. CONCLUSIONS: Hypertriglyceridemia, inflammation and low iPTH associated significantly with altered FMD. They are frequent, treatable risk factors for CVD.

Endothelial Dysfunction and Pentraxin-3 in Clinically Stable Adult Asthma Patients

Background: Asthma is associated with low-grade systemic inflammation, prothrombotic state, and premature atherosclerosis. Objective: To evaluate the relationships between asthma, inflammatory biomarkers, and parameters of endothelial dysfunction. Material and Methods: We analyzed flow-mediated dilatation (FMD) of the brachial artery and intima-media thickness (IMT) of the common carotid artery using ultrasound in 92 clinically stable adult asthmatics and 62 well-matched controls. We also measured blood levels of selected inflammatory and asthma-specific biomarkers, including interleukin (IL) 4, IL-5, IL-6, IL-10, IL-12 (p70), IL-17A, IL-23, and interferon γ, as well as a disintegrin and metalloproteinase domain–containing protein 33 (ADAM-33). In addition, we assessed endothelial damage using 2 laboratory biomarkers: circulating von Willebrand factor (vWF) and pentraxin-3. We analyzed relationships between the study variables and asthma severity, lung function abnormalities, airway remodeling indices on computed tomography, and transthoracic echocardiography parameters. Results: Asthmatics had higher IL-6, IL-10, and ADAM-33 levels. They were also characterized by 23% lower FMD% and 15% thicker IMT, as compared with controls (P<.001, both). In asthma, vWF was related to age (ß=0.28 [95%CI, 0.15-0.41]) and remained inversely associated with FEV1 (ß=–0.2 [95%CI, –0.05 to –0.35]). Surprisingly, a negative correlation was revealed between vWF and pentraxin-3 (ß=–0.17 [95%CI, –0.3 to –0.04]). Pentraxin-3 remained positively associated with airway remodeling indices. Conclusions: Asthma is characterized by endothelial dysfunction associated with airway obstruction. The biological role of pentraxin-3 is unknown, although our data suggest a protective role against endothelial damage and atherosclerosis (AU)

Antecedentes: El asma se asocia con inflamación sistémica de bajo grado, con un estado protrombótico y la existencia de aterosclerosisprematura.Objetivo: Evaluar las relaciones entre asma, biomarcadores inflamatorios y parámetros de disfunción endotelial.Material y métodos: Se ha analizado la dilatación mediada por flujo (DMF) de la arteria braquial y el grosor íntima-media (GIM) dela arteria carótida común mediante ecografía, en 92 adultos asmáticos clínicamente estables y 62 controles. También se midieron losniveles sanguíneos de determinados biomarcadores inflamatorios específicos de asma, incluyendo interleucina (IL) -4, IL-5, IL-6, IL-10,IL-12 (p70), IL-17A, IL-23, interferón γ, así como desintegrina y la metaloproteinasa que contiene el dominio proteína 33 (ADAM-33),junto con marcadores de laboratorio de daño endotelial: pentraxina-3 circulante y actividad plasmática del factor von Willebrand (vWF).Analizamos las relaciones de las variables estudiadas con la gravedad del asma, las anomalías de la función pulmonar, los índices detomografía computarizada (TC) pulmonar de remodelación de las vías respiratorias y los parámetros de ecocardiografía transtorácica.Resultados: Los asmáticos tuvieron mayores niveles de IL-6, IL-10 y ADAM-33. También se caracterizaron por tener un 23% menos deDMF y un 15% más grueso el GIM, en comparación con los controles (p <0,001, ambos). En el asma, vWF se relacionó con la edad (ß =0,28 [IC 95%: 0,15 a 0,41]) y se mantuvo en una relación inversa con FEV1 (ß = -0,2 [IC 95%: -0,05 a -0,35]). Sorprendentemente, seobservó una correlación negativa entre vWF y pentraxina-3 (ß = -0,17 [IC 95%: -0,3 a -0,04]). La pentraxin-3 se asoció positivamentecon los índices CT de remodelación de la vía aérea...(AU)

Uric acid and gamma-glutamyl transferase activity are associated with left ventricular remodeling indices in patients with chronic heart failure.

INTRODUCTION AND OBJECTIVES: Uric acid and gamma-glutamyl transferase are prognostic indicators in chronic heart failure. Nevertheless, the mechanism underlying the association between uric acid, gamma-glutamyl transferase, and chronic heart failure progression and prognosis remains largely unknown. METHODS: The association of uric acid and gamma-glutamyl transferase with flow-mediated dilation and echocardiographic indices of cardiac remodeling was addressed in 120 patients with chronic ischemic heart failure. To determine the independent contribution of uric acid and gamma-glutamyl transferase to the flow-mediated dilation and echocardiographic indices of remodeling, a series of multiple linear regression models, based on traditional and nontraditional risk factors impacting upon these parameters, were constructed. RESULTS: Uric acid, but not gamma-glutamyl transferase, was an independent predictor of flow-mediated dilation. Uric acid was associated with all the echocardiographic indices of left ventricular dysfunction tested in 3 multiple-regression models. Uric acid correlated with left ventricular end-systolic diameter, left ventricular end-diastolic diameter, left ventricular end-systolic volume, and left ventricular end-diastolic volume (r = 0.337; r = 0.340; r = 0.321; r = 0.294; P = .001, respectively). Gamma-glutamyl transferase was an independent predictor of left ventricular end-systolic volume and left ventricular end-diastolic volume, after adjustment for all variables. Gamma-glutamyl transferase correlated with left ventricular end-systolic diameter, left ventricular end-diastolic diameter, left ventricular end-systolic volume, and left ventricular end-diastolic volume (r = 0.238, P = .009; r = 0.219, P = .016; r = 0.359, P < .001; r = 0.369, P = .001, respectively). CONCLUSIONS: Serum uric acid and gamma-glutamyl transferase levels are associated with left ventricular remodeling in patients with chronic ischemic heart failure.

Endothelial dysfunction in primary Sjögren syndrome / Disfunción endotelial en el síndrome de Sjögren primario

OBJECTIVE: In this study, we aimed to investigate endothelial functions in primary Sjögren syndrome. METHODS: Thirty-five patients with primary Sjögren syndrome and 20 age and sexmatched healthy volunteers were recruited to the present study. Flow mediated dilatation of brachial artery and carotid intimamedia thickness were measured in the study population. RESULTS: Carotid intimamedia thickness values were similar between groups (0.50 ± 0.10, 0.53 ± 0.08, p > 0.05). Flow mediated dilatation of the brachial artery was disrupted in the primary Sjögren syndrome group (7% vs 12%, p = 0.002). CONCLUSION: There is endothelial dysfunction in patients with primary Sjögren syndrome, although they had comparable carotid intimamedia thickness with the healthy control group.

OBJETIVO: Este estudio se encaminó a investigar las funciones endoteliales en el síndrome de Sjögren primario. MÉTODOS: Para el presente estudio, se reclutaron treinta y cinco pacientes con síndrome de Sjögren primario y 20 voluntarios sanos apareados por edad y sexo. La dilatación mediada por flujo observada en la arteria braquial, y el espesor íntimamedia carotídeo fueron medidos en la población bajo estudio. RESULTADOS: Los valores del espesor íntimamedia carotídeo fueron similares entre los grupos (0.50 ± 0.10, 0.53 ± 0.08, p > 0.05). La dilatación mediada por flujo de la arteria braquial, estaba alterada en el grupo de síndrome del Sjögren primario (7% frente a 12%, p = 0.002). CONCLUSIÓN: Hay una disfunción endotelial en los pacientes con el síndrome de Sjögren primario, aunque estos tenían un espesor íntimamedia carotídeo comparable con el grupo de control saludable.