Avaliação do acesso vascular para hemodiálise em crianças e adolescentes: um estudo de coorte retrospectivo de 10 anos

INTRODUÇÃO: As intercorrências do acesso vascular têm sido a maior causa de internação entre os pacientes com estágio V da doença renal crônica (DRC) em hemodiálise (HD). Apesar de campanhas para a diminuição do uso de cateter venoso central (CVC) como via de acesso para HD, este ainda representa a principal via de acesso para crianças e adolescentes que iniciam HD. OBJETIVOS E MÉTODOS: Este estudo tem o objetivo de avaliar, por meio de um coorte retrospectivo, o tipo de acesso vascular inicial, a incidência de complicações dos acessos vasculares e as razões de falência dos acessos em crianças e adolescentes com idade entre 0 e 18 anos que iniciaram HD no período de 1997 a 2007. RESULTADOS: Foram estudados 251 acessos em 61 pacientes, sendo 97 fístulas arteriovenosas (FAV) e 154 CVC de curta permanência. Dos pacientes do estudo 51 % iniciaram HD pelo CVC. A média de idade dos pacientes no início da HD foi de 12,5 anos. A doença de base predominante foi glomerulopatia (46%). A principal causa de retirada de CVC foi infecção, em 35%. A sobrevida média do CVC foi de 40 dias. A falência primária da FAV foi detectada em 37,8% das FAV confeccionadas. Para as FAV funcionantes, a principal causa de falência foi a trombose (84%). A infecção não foi a causa de nenhuma falência de FAV. Comparando-se os tipos de acesso, constatou-se risco de infecção 34 vezes maior para os pacientes em uso de CVC em relação aos em uso de FAV. CONCLUSÃO: A infecção foi a maior causa de retirada de CVC temporário. Esse estudo sugere que o CVC temporário deve ser evitado, e, sempre que possível, substituído por FAV ou CVC de longa permanência. A trombose foi a principal causa de perda da FAV, reforçando a importância de um programa para a detecção precoce da disfunção do acesso.

Calcificação vascular em doença renal crônica: uma revisão

Pacientes com doença renal crônica (DRC) frequentemente apresentam calcificação vascular (CV) - um forte e independente fator preditor de risco cardiovascular. O grau da CV tem proporcionado maior valor prognóstico quando comparado a outros marcadores mais tradicionais de risco. Há muito interesse em aprimorar nosso conhecimento sobre os mecanismos, estabelecer métodos diagnósticos e desenvolver modalidades mais eficazes de prevenção e tratamento. Sabe-se que a anormalidade metabólica encontrada na DRC facilita a progressão da CV juntamente com alterações nas atividades dos inibidores da CV. Possíveis medidas para se evitar a CV incluem o controle do cálcio e fosfato séricos, assim como outros fatores envolvidos em sua progressão, incluindo ésteres da vitamina D, hormônio da paratireoide, fator 23 de crescimento de fibroblastos, klotho e inibidores da CV. Além disso, discutimos novas abordagens terapêuticas para interromper a progressão da CV e reverter sua ação. O principal objetivo dessa revisão é proporcionar uma atualização sobre a CV em pacientes com DRC, concentrando-se mais especificamente em sua fisiopatologia, diagnóstico, prevenção e tratamento.

Distúrbio mineral ósseo e calcificação vascular em pacientes renais crônicos

Calcificações vasculares têm sido associadas aos distúrbios minerais e ósseos. As alterações nas concentrações séricas de cálcio e fosfato são fatores importantes implicados no processo da calcificação arterial na doença renal crônica. A patogênese da calcificação vascular é um mecanismo complexo e não completamente claro, podendo corresponder a um processo ativo de transformação celular e ossificação heterotópica. Além da hipercalcemia e hiperfosfatemia, estão envolvidos neste processo alterações no metabolismo de substâncias inibidoras e promotoras de calcificação como a fetuína A, osteopontina, osteoprotegerina e proteína de matriz gla. Para o diagnóstico da lesão arterial calcificada, estão disponíveis diversos métodos, um método de estimativa do risco cardiovascular baseado em radiografias simples de coluna lombar e outro método baseado em radiografias simples da pelve e das mãos. Apresentamos, a seguir, uma revisão abordando a relação entre calcificações vasculares e os distúrbios minerais.

Erythropoietin resistance in end-stage renal disease patient with gastric antral vascular ectasia

AbstractWe observed a case of recombinant human erythropoietin resistance caused by Gastric Antral Vascular Ectasia in a 40-year-old female with ESRD on hemodialysis. Some associated factors such as autoimmune disease, hemolysis, heart and liver disease were discarded on physical examination and complementary tests. The diagnosis is based on the clinical history and endoscopic appearance of watermelon stomach. The histologic findings are fibromuscular proliferation and capillary ectasia with microvascular thrombosis of the lamina propria. However, these histologic findings are not necessary to confirm the diagnosis. Gastric Antral Vascular Ectasia is a serious condition and should be considered in ESRD patients on hemodialysis with anemia and resistance to recombinant human erythropoietin because GAVE is potentially curable with specific endoscopic treatment method or through surgical procedure.

Erythropoietin resistance in end-stage renal disease patient with gastric antral vascular ectasia

AbstractWe observed a case of recombinant human erythropoietin resistance caused by Gastric Antral Vascular Ectasia in a 40-year-old female with ESRD on hemodialysis. Some associated factors such as autoimmune disease, hemolysis, heart and liver disease were discarded on physical examination and complementary tests. The diagnosis is based on the clinical history and endoscopic appearance of watermelon stomach. The histologic findings are fibromuscular proliferation and capillary ectasia with microvascular thrombosis of the lamina propria. However, these histologic findings are not necessary to confirm the diagnosis. Gastric Antral Vascular Ectasia is a serious condition and should be considered in ESRD patients on hemodialysis with anemia and resistance to recombinant human erythropoietin because GAVE is potentially curable with specific endoscopic treatment method or through surgical procedure.

Expression and function of endothelin and its receptors in vascular adventitial fibroblasts

Objective: The adventitia has been recognized to play important roles in vascular oxidative stress, remodelling and contraction. We recently demonstrated that adventitial fibroblasts are able to express endothelin-1 (ET-1) in response to angiotensin II (ANG II). However, the mechanisms by which ANG II induces ET-1 expression are unknown. It is also unclear whether the ET-1 receptors are expressed in the adventitia. We therefore examined the role of oxidative stress in the regulation of ET-1. We also investigated the expression of both the ETA and ETB receptors and the roles of these two types of receptors in collagen synthesis and ET-1 clearance in adventitial fibroblasts. Methods and Results: Adventitial fibroblasts were isolated and cultured from the thoracic mouse aorta. Cells were treated with ANG II (lOOnM), ET-1 (lOpM), NADPH oxidase inhibitor apocynin (lOOfiM), the superoxide anion scavenger tempol (lOOfiM), the ANG II receptor antagonists (100[aM), losartan (AT| receptor) and PD 1233 19 (AT2 receptor), the ET-1 receptor antagonists (lOOuM), BQ123 (ETA receptor) and BQ788 (ETB receptor), and the ETB receptor agonist (lOOnM) Sarafotoxin 6C. ET-1 peptide levels were determined by ELISA, while ETA ,ETB and collagen levels were determined by Western blot. ANG II increased ET-1 peptide levels in a time-dependent manner reaching significance when incubated for 24 hours. NAD(P)H oxidase inhibitor, apocynin, as well as the superoxide scanverger, tempol, significantly reduced ANG Il-induced ET-1 peptide levels while over-expression of SOD1 (endogenous antioxidant enzyme) significantly decreased ANG Il-induced collagen I expression, therefore implicating reactive oxygen species in the mediation of ET-1. ANG II increased ETA receptor protein as well as collagen in a similar fashion, reaching significance after 4, 6, and 24 hours treatment. ANG II induced collagen was reduced while in the presence of the ETA receptor antagonist suggesting the role of the ETa receptor in the regulation of the extracellular matrix. ANG II treatment also increased ETB receptor protein levels in a time-dependent manner. ANG II treatment in the presence of the ETB receptor antagonist significantly increased ET-1 peptide levels. On another hand, the ETB receptor agonist, Sarafotoxin 6C, significantly decreased ET-1 peptide levels. These data implicate the role of the ETb receptor in the clearance of the ET-1 peptide. Conclusion: ANG II-induced increases of ET-1 peptide appears to be mediated by reactive oxygen species derived from NAD(P)H oxidase. Both the ETA and ETB receptors are expressed in adventitial fibroblasts. The ETA receptor subtype mediates collagen I expression, while the ETB receptor may play a protective role through increasing the clearance of the ET- 1 peptide.

Mechanisms of endothelin-1 induced reactive oxygen species production in vascular adventitial fibroblasts

With the relationship between endothelin-1 (ET-1) stimulation and reactive oxygen species (ROS) production unknown in adventitial fibroblasts, I examined the ROS response to ET-1 and angiotensin (Ang II). ET-1 -induced ROS peaked following 4 hrs of ET-1 stimulation and was inhibited by an ETA receptor antagonist (BQ 123, 1 uM) an extracellular signal-regulated kinase (ERK) 1/2 inhibitor (PD98059, 10 uM), and by both a specific, apocynin (10 uM), and non-specific, diphenyleneiodonium (10 uM), NAD(P)H oxidase inhibitor. NOX2 knockout fibroblasts did not produce an ET-1 induced change in ROS levels. Ang II treatment increased ROS levels in a biphasic manner, with the second peak occurring 6 hrs following stimulation. The secondary phase of Ang II induced ROS was inhibited by an ATi receptor antagonist, Losartan (100 uM) and BQ 123. In conclusion, ET-1 induces ROS production primarily through an ETA-ERKl/2 NOX2 pathway, additionally, Ang II-induced ROS production also involves an ETa pathway.

The roles of ERK1/2 and PI3K in abnormal vascular functions in angiotensin II-infused hypertensive rats

Background: Ang II plays a major role in cardiovascular regulation. Recently, it has become apparent that vascular superoxide anion may play an important role in hypertension development. Treatment with antisense NAD(P)H oxidase or SOD decreased BP in Ang II-infused rats. Wang et al recently reported mice which lack one of the subunits of NAD(P)H oxidase developed hypertension at a much lower extent when compared to the wild type animals infused with Ang II, indicating that superoxide anion contributes to elevation in BP in the Ang II-infused hypertensive model. In the Ang II-infused hypertensive model, altered reactivity of blood vessels is often associated with the elevation of systolic blood pressure. We have observed abnormal tension development and impaired endothelium-dependent relaxation in the isolated aorta of Ang II-infused and DOCA-salt hypertensive rats. Recently, several other cellular signal molecules, including ERK1I2 and PI3K, have been determined to play important roles in the regulation of smooth muscle contraction and relaxation. ERKl/2 and PI3K pathways are also reported to contribute to Ang II induced cell growth, hypertrophy, remodeling and contraction. Moreover, these signaling pathways have shown ROS-sensitive properties. Therefore, the aim of the present study is to investigate the roles of ERKl12 and PI3K in vascular oxidative stress, spontaneous tone and impaired endothelium relaxation in Ang II-infused hypertensive model. Hypothesis: We hypothesize that the activation of ERKl12 and PI3K are elevated in response to an Ang II infusion for 6 days. The elevated activation of phospho-ERKl/2 and PI3K mediated the increased level of vascular superoxide anion, the abnormal vascular contraction and impaired endothelium-dependent vascular relaxation in Ang II-infused hypertensive rats. Methods: Vascular superoxide anion level is measured by lucigenin chemiluminescence. Spontaneous tone and ACh-induced endothelium-dependent relaxation was measured by isometric tension recording in organ chamber. The activity of ERK pathway will be measured by its Western blot of phosphorylation of ERK. PI3K activity was evaluated indirectly by Western blot of the phosphorylation of PDKl, a downstream protein of PI3K signaling pathway. The role of each pathway was also addressed via comparing the responses to the specific inhibitors. Results: Superoxide anion was markedly increased in the isolated thoracic aorta from Ang II-infused rats. There was spontaneous tone developed in rings from Ang II-induced hypertensive but not sham-operated normotensive rats. ACh-induced endothelium-dependent relaxation function is impaired in Ang II-infused hypertensive rats. Superoxide dismutase and NAD(P)H oxidase inhibitor, apocynin, inhibited the abnormal spontaneous tone and ameliorated impaired endothelium-dependent relaxation. The expression of phopho-ERKII2 was enhanced in Ang II-infused rats, indicating the activity of ERK1I2 could be increased. MEK1I2 inhibitors, PD98059 and U126, but not their inactive analogues, SB203580 and U124, significantly reduced the vascular superoxide anion in aortas from Ang II-infused rats. The MEK1I2 inhibitors reduced the spontaneous tone and improved the impaired endothelium-dependent relaxation in aorta of hypertension. These findings supported the role of ERKII2 signaling pathway in vascular oxidative stress, spontaneous tone and impaired endothelium-dependent relaxation in Ang II-infused hypertensive rats. The amount of phospho-PDK, a downstream protein of PI3K was increased in Ang II rats indicating the activity of PI3K activity was elevated. Strikingly, PI3K significantly inhibited the increase of superoxide anion level, abnormal spontaneous tone and restored endothelium-dependent relaxation in Ang II-infused hypertensive rats. These findings indicated the important role of PI3K in Ang II-infused hypertensive rats. Conclusion: ERKII2 and PI3K signaling pathways are sustained activated in Ang II-infused hypertensive rats. The activated ERKII2 and PI3K mediate the increase of vascular superoxide anion level, vascular abnormal spontaneous tone and impaired endothelium-dependent relaxation.

Persons who served more than six months in the War of 1812 : letter from the Secretary of War, transmitting in compliance with a resolution of the House calling for a statement of the number of officers, non-commissioned officers, privates, &c., who served for a period of six months and upwards in the War of 1812.--

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The association between blood pressure and vascular characteristics in children

Hypertension is thought to exist in up to five percent of children. A select number of studies have investigated the role elevated blood pressure plays in pediatric atherosclerotic progression. However these studies contain significant methodological flaws and fail to recognize important confounding factors. Therefore, the influence of elevated blood pressure on arterial health in children remains to be clearly understood. The purpose of this study was to investigate the association between blood pressure (BP) and arterial thickness and stiffuess in children. Common carotid artery (CCA) intima-media thickness (IMT) and distensibility (Dist), as well as systemic pulse wave velocity (PWV) were measured in 21 elevated blood pressure (EBP; BP ~ 95th percentile) and 83 normal blood pressure (NBP; BP < 90th percentile) children 11-14 years of age. Both EBP and NBP groups demonstrated BP within the normal clinical range, but EBP showed significantly elevated BP as compared to the NBP group. Independent t-tests failed to show significant differences between the EBP and NBP groups for CCA IMT (0.43 ± 0.05 mm and 0.42 ± 0.06 mm, respectively) and Dist (0.0058 ± 0.0024 mmHg-1 and 0.0064 ± 0.0019 mmHil respectively). In contrast, a significantly elevated PWV (p

Message from the President of the United States, communicating, in compliance with a resolutión of the Senate, the proceedings of thetwo courts of inquiry in the case of Major General Pillow.

UANL

Report of the Secretary of War, communicating; in compliance witha resolution of the Senate, a map showing the operations of the army of the United States in Texas and the adjacent Mexican Stateson the Rio Grande, accompanied by astronomical observations, and descriptive and military memoirs of the country.

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The Compliance Costs of Taxes on Businesses and Individuals a Review of the Evidence

This Paper Reviews the Literature on the Compliance Costs Incurred by Businesses and Individuals Because of One Or More Taxes. It Presents Both the Main Characteristics, Such As Sample Size, Interview Techniques and So On, and the Key Findings of the Nineteen Studies Reviewed. in General, One Can Conclude That Simpler Taxes Lead to Lower Compliance Costs.