982 resultados para Renal vascular conductance


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OBJETIVO: Demonstrar os acessos vasculares para hemodiálise mais utilizados em 23 unidades de hemodiálise, distribuídas em sete estados brasileiros. MÉTODO: Entre outubro de 1999 a agosto de 2000, foram avaliados 2559 pacientes em 23 unidades de hemodiálise distribuídas em 23 estados brasileiros onde foi observado: A - A freqüência da utilização do acesso vascular, se externo através de cateteres ou se interno através de fístula arteriovenosa (FAV). B - Os tipos de cateteres, se de curta permanência ou de longa permanência, assim como os locais anatômicos utilizados para sua inserção. C - Os tipos de FAV, se direta ou com interposição de algum tipo de prótese e os locais anatômicos onde foram construídas, se distais ou proximais. D - O custo financeiro com os acessos vasculares. RESULTADOS: Constatou-se que 93,4% dos pacientes tinham um acesso vascular através de FAV e 6,6% através de cateter. As FAV diretas distais foram as mais utilizadas em 74,8% dos pacientes; as FAV diretas proximais foram construídas em 21,7% das vezes; as FAV com politetrafluoretileno expandido (PTFE) 3,2% da totalidade; a veia safena foi utilizada em 0,1% e as FAV consideradas como outras em 0,2%. Os cateteres de longa permanência foram utilizados em 8,7% da totalidade dos cateteres e os de curta permanência em 91,3%. Como via de acesso a veia jugular foi utilizada em 42,4%, a veia subclávia em 42,4% e a veia femoral em 6,5%. O custo financeiro com acesso para hemodiálise foi de 1% do custo total das unidades. CONCLUSÕES: O acesso vascular no Brasil tem características próprias. O acesso mais utilizado é a FAV distal e o uso do PTFE é baixo.

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OBJETIVO: Avaliar as características e os efeitos de um agente embólico, disponível comercialmente, consistindo de Polivinil Álcool (PVA) de morfologia flocular, e comparar com um agente esférico, de tecnologia nacional, consistindo de Polivinil Álcool e Polivinil Acetato (PVA + PVAc). MÉTODO: Foram utilizadas fêmeas de coelho albino "New Zealand", submetidas à embolização arterial renal. PVA-flocular foi usado em 24 animais, assim como PVA+PVAc-esférico. Seis animais foram utilizados como controle. Todos foram mantidos em cativeiro até a morte, por períodos pós-operatórios de 48 horas, cinco dias, 10 dias e 30 dias. RESULTADOS: Ambos os agentes promoveram oclusão do vaso e infarto do órgão. O estudo microscópico inicial das artérias embolizadas com PVA-flocular, mostra oclusão com trombo e PVA. Os vasos embolizados com PVA+PVAc-esférico, mostram os agentes ocupando praticamente todo o lúmen. No estudo de 30 dias, observa-se absorção do trombo e retração dos agentes de PVAflocular, criando espaços. E com PVA+PVAc-esférico, pode-se observar os agentes circundados por intensa fibrose. CONCLUSÕES: Ambas as partículas foram efetivas para causar isquemia tecidual. A reação inflamatória foi mais intensa com PVA+PVAc-esférico que também apresentou grau de penetração maior no sistema vascular.

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OBJETIVO: Relacionar as alterações morfológicas renais sob microscopia de luz, de ratos submetidos à oclusão de aorta, em modelo que simule a condição clínica de reparação cirúrgica de um aneurisma de aorta abdominal. MÉTODO: Ratos Wistar (N = 60), machos pesando entre 200 e 250g, foram distribuídos em três grupos: I (simulado); II (isquemia); III (isquemia + reperfusão); e cada grupo redistribuído em dois subgrupos: A (30 min); B (60 min). Foi realizada isquemia utilizando clamp vascular (8mm) na aorta abdominal infra-renal de acordo com o grupo estudado. Ao final de cada experimento os animais foram mortos e realizada análise histológica renal cortical e medular (descritiva e morfométrica) através de metodologia convencional (parafina-hematoxilinaeosina). A análise semiquantitativa de lesão tubular e intersticial foi realizada de acordo com o índice de lesão tubular e índice de lesão intersticial. Para a análise estatística foram aplicados os seguintes testes: Mann-Whitney, Kruskal-Wallis, Comparações múltiplas (p < 0,001). RESULTADOS: Observou-se no grupo III alterações histológicas tubulares e intersticiais significantes com relação aos outros grupos (p < 0,001). CONCLUSÕES: A oclusão da aorta abdominal infra-renal em ratos está associada a lesões estruturais renais tanto tubulares quanto intersticiais principalmente na fase de reperfusão.

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Vascular complications after kidney transplantation have been described and pseudoaneurysms represent a well-recognized vascular complication. Although the incidence of pseudoaneurysm is low, it may potentially cause graft loss or may even be fatal for the patients if it is not diagnosed and treated quickly. The authors report a case of renal artery pseudoaneurysm diagnosed two months posttransplantation with cadaveric graft, the treatment and literature data.

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Intravascular papillary endothelial hyperplasia is a benign and rare intravascular process thought to arise from an organizing thrombus. Involvement of the adrenal gland is extremely rare, with only one case reported in the literature. We report a case of this vascular lesion in the adrenal gland, treated with laparoscopic adrenalectomy.

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Resumo: Meios de contraste iodado podem promover efeitos hemodinâmicos relacionados à vasoconstrição intrarrenal prolongada e redução da perfusão, predispondo à hipóxia e isquemia medular. Alterações de resistência vascular renal podem representar os primeiros sinais de mudança funcional desse órgão. A técnica Doppler pulsado é considerada acessível, não invasiva e permite avaliar a dinâmica vascular dos rins, por meio da aferição dos índices de resistividade (IR) e pulsatilidade (IP). Contudo, na espécie canina, a aquisição de traçados espectrais pode ser penosa devido às dificuldades de varredura e captação de sinal Doppler, sobretudo em relação ao rim direito, devido à sua localização dorsocranial na cavidade abdominal, o que prolonga substancialmente a realização do exame. O objetivo deste estudo é comprovar que a avaliação Doppler pulsado das artérias intrarrenais do rim esquerdo de cães representa a repercussão hemodinâmica renal da administração intravenosa de meios de contraste iodado não sendo necessária a realização do exame nos dois rins. Foram avaliados ambos os rins de seis cadelas adultas em quatro momentos distintos: antes da infusão intravenosa do contraste radiológico e após 1,5 horas, 24 horas e 48 horas, por meio da análise subjetiva da morfologia, ecogenicidade cortical e grau de perfusão renais e análise objetiva do comprimento, volume e resistência vascular intrarrenais (IR e IP). Os parâmetros avaliados ao modo B e Doppler dos rins direito e esquerdo não apresentaram diferenças estatisticamente significativas entre si em cada momento avaliado. Assim, constatou-se que o exame ultrassonográfico Doppler pulsado do rim esquerdo representou a repercussão hemodinâmica renal da aplicação intravenosa de meios de contraste iodado, desde que morfometria, morfologia, ecogenicidade cortical e perfusão de ambos os rins fossem consideradas semelhantes na abordagem ultrassonográfica inicial.

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We assessed a kallikrein-like amidase activity probably related to the kallikrein-kinin system, as well as the participation of leukocyte infiltration in renal ischemia and reperfusion. Male C57BL/KSJmdb mice were subjected to 20 or 60 min of ischemia and to different periods of reperfusion. A control group consisted of sham-operated mice, under similar conditions, except for ischemia induction. Kallikrein-like amidase activity, Evans blue extravasation and myeloperoxidase activity were measured in kidney homogenates, previously perfused with 0.9% NaCl. Plasma creatinine concentration increased only in the 60-min ischemic group. After 20 min of ischemia and 1 or 24 h of reperfusion, no change in kallikrein-like amidase activity or Evans blue extravasation was observed. In the mice subjected to 20 min of ischemia, edema was evident at 1 h of reperfusion, but kidney water content returned to basal levels after 24 h of reperfusion. In the 60-min ischemic group, kallikrein-like amidase activity and Evans blue extravasation showed a similar significant increase along reperfusion time. Kallikrein-like amidase activity increased from 4 nmol PNA mg protein-1 min-1 in the basal condition to 15 nmol PNA mg protein-1 min-1 at 10 h of reperfusion. For dye extravasation the concentration measured was near 200 µg of Evans blue/g dry tissue in the basal condition and 1750 µg of Evans blue/g dry tissue at 10 h of reperfusion. No variation could be detected in the control group. A significant increase from 5 to 40 units of DAbs 655 nm g wet tissue-1 min-1 in the activity of the enzyme myeloperoxidase was observed in the 60-min ischemic group, when it was evaluated after 24 h of reperfusion. Histological analysis of the kidneys showed migration of polymorphonuclear leukocytes from the vascular bed to the interstitial tissue in the 60-min ischemic group after 24 h of reperfusion. We conclude that the duration of ischemia is critical for the development of damage during reperfusion and that the increase in renal cortex kallikrein-like amidase activity probably released from both the kidney and leukocytes may be responsible, at least in part, for the observed effects, probably through direct induction of increased vascular permeability.

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To determine if radiocontrast impairs vascular relaxation of the renal artery, segments (4-5 mm in length) of canine renal artery were suspended in vitro in organ chambers to measure isometric force (95% O2/5% CO2, at 37ºC). Arterial segments with and without endothelium were placed at the optimal point of their length-tension relation and incubated with 10 µM indomethacin to prevent synthesis of endogenous prostanoids. The presence of nonionic radiocontrast (iohexol, Omnipaque 350, 1 ml in 25 ml control solution, 4% (v/v)) did not alter endothelium-dependent relaxation to acetylcholine in rings precontracted with both norepinephrine and prostaglandin F2alpha (N = 6). When the rings were precontracted with prostaglandin F2alpha, the presence of ionic contrast did not inhibit the relaxation of the arteries. However, in canine renal arteries contracted with norepinephrine, the presence of ionic radiocontrast (diatrizoate meglumine and diatrizoate sodium, MD-76, 1 ml in 25 ml control solution, 4% (v/v)) inhibited relaxation in response to acetylcholine, sodium nitroprusside (N = 6 in each group), and isoproterenol (N = 5; P < 0.05). Rings were relaxed less than 50% of norepinephrine contraction. Following removal of the contrast, vascular relaxation in response to the agonists returned to normal. These results indicate that ionic radiocontrast nonspecifically inhibits vasodilation (both cAMP-mediated and cGMP-mediated) of canine renal arteries contracted with norepinephrine. This reversible impairment of vasodilation could inhibit normal renal perfusion and act as a mechanism of renal failure following radiocontrast infusion. In the adopted experimental protocol the isoproterenol-induced relaxation of renal arteries precontracted with norepinephrine was more affected, suggesting a pivotal role of the cAMP system.

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Acid-base homeostasis maintains systemic arterial pH within a narrow range. Whereas the normal range of pH for clinical laboratories is 7.35-7.45, in vivo pH is maintained within a much narrower range. In clinical and experimental settings, blood pH can vary in response to respiratory or renal impairment. This altered pH promotes changes in vascular smooth muscle tone with impact on circulation and blood pressure control. Changes in pH can be divided into those occurring in the extracellular space (pHo) and those occurring within the intracellular space (pHi), although, extracellular and intracellular compartments influence each other. Consistent with the multiple events involved in the changes in tone produced by altered pHo, including type of vascular bed, several factors and mechanisms, in addition to hydrogen ion concentration, have been suggested to be involved. The scientific literature has many reports concerning acid-base balance and endothelium function, but these concepts are not clear about acid-base disorders and their relations with the three known mechanisms of endothelium-dependent vascular reactivity: nitric oxide (NO/cGMP-dependent), prostacyclin (PGI2/cAMP-dependent) and hyperpolarization. During the last decades, many studies have been published and have given rise to confronting data on acid-base disorder and endothelial function. Therefore, the main proposal of this review is to provide a critical analysis of the state of art and incentivate researchers to develop more studies about these issues.

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The objective of the present study was to determine the acute effect of hemodialysis on endothelial venous function and oxidative stress. We studied 9 patients with end-stage renal disease (ESRD), 36.8 ± 3.0 years old, arterial pressure 133.8 ± 6.8/80.0 ± 5.0 mmHg, time on dialysis 55.0 ± 16.6 months, immediately before and after a hemodialysis session, and 10 healthy controls matched for age and gender. Endothelial function was assessed by the dorsal hand vein technique using graded local infusion of acetylcholine (endothelium-dependent venodilation, EDV) and sodium nitroprusside (endothelium-independent venodilation). Oxidative stress was evaluated by measuring protein oxidative damage (carbonyls) and antioxidant defense (total radical trapping antioxidant potential - TRAP) in blood samples. All patients were receiving recombinant human erythropoietin for at least 3 months and were not taking nitrates or a-receptor antagonists. EDV was significantly lower in ESRD patients before hemodialysis (65.6 ± 10.5) vs controls (109.6 ± 10.8; P = 0.010) and after hemodialysis (106.6 ± 15.7; P = 0.045). Endothelium-independent venodilation was similar in all comparisons performed. The hemodialysis session significantly decreased TRAP (402.0 ± 53.5 vs 157.1 ± 28.3 U Trolox/µL plasma; P = 0.001). There was no difference in protein damage comparing ESRD patients before and after hemodialysis. The magnitude of change in the EDV was correlated negatively with the magnitude of change in TRAP (r = -0.70; P = 0.037). These results suggest that a hemodialysis session improves endothelial venous function, in association with an antioxidant effect.

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Ethnicity has been shown to be associated with micro- and macrovascular complications of diabetes in European and North American populations. We analyzed the contribution of ethnicity to the prevalence of micro- and macrovascular complications in Brazilian subjects with type 2 diabetes attending the national public health system. Data from 1810 subjects with type 2 diabetes (1512 whites and 298 blacks) were analyzed cross-sectionally. The rates of ischemic heart disease, peripheral vascular disease, stroke, distal sensory neuropathy, and diabetic retinopathy were assessed according to self-reported ethnicity using multiple logistic regression models. Compared to whites, black subjects [odds ratio = 1.72 (95%CI = 1.14-2.6)] were more likely to have ischemic heart disease when data were adjusted for age, sex, fasting plasma glucose, HDL cholesterol, hypertension, smoking habit, and serum creatinine. Blacks were also more likely to have end-stage renal disease [3.2 (1.7-6.0)] and proliferative diabetic retinopathy [1.9 (1.1-3.2)] compared to whites when data were adjusted for age, sex, fasting plasma glucose, HDL cholesterol, hypertension, and smoking habit. The rates of peripheral vascular disease, stroke and distal sensory neuropathy did not differ between groups. The higher rates of ischemic heart disease, end-stage renal disease and proliferative diabetic retinopathy in black rather than in white Brazilians were not explained by differences in conventional risk factors. Identifying which aspects of ethnicity confer a higher risk for these complications in black patients is crucial in order to understand why such differences exist and to develop more effective strategies to reduce the onset and progression of these complications.

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A major problem in renal transplantation is identifying a grading system that can predict long-term graft survival. The present study determined the extent to which the two existing grading systems (Banff 97 and chronic allograft damage index, CADI) correlate with each other and with graft loss. A total of 161 transplant patient biopsies with chronic allograft nephropathy (CAN) were studied. The samples were coded and evaluated blindly by two pathologists using the two grading systems. Logistic regression analyses were used to evaluate the best predictor index for renal allograft loss. Patients with higher Banff 97 and CADI scores had higher rates of graft loss. Moreover, these measures also correlated with worse renal function and higher proteinuria levels at the time of CAN diagnosis. Logistic regression analyses showed that the use of angiotensin-converting enzyme inhibitor (ACEI), hepatitis C virus (HCV), tubular atrophy, and the use of mycophenolate mofetil (MMF) were associated with graft loss in the CADI, while the use of ACEI, HCV, moderate interstitial fibrosis and tubular atrophy and the use of MMF were associated in the Banff 97 index. Although Banff 97 and CADI analyze different parameters in different renal compartments, only some isolated parameters correlated with graft loss. This suggests that we need to review the CAN grading systems in order to devise a system that includes all parameters able to predict long-term graft survival, including chronic glomerulopathy, glomerular sclerosis, vascular changes, and severity of chronic interstitial fibrosis and tubular atrophy.

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Acute renal failure (ARF) is a frequent complication of Gram-negative sepsis, with a high risk of mortality. Lipopolysaccharide (LPS)-induced ARF is associated with hemodynamic changes that are strongly influenced by the overproduction of nitric oxide (NO) through the cytokine-mediated up-regulation of inducible NO synthase. LPS-induced reductions in systemic vascular resistance paradoxically culminate in renal vasoconstriction. Collagen XVIII is an important component of the extracellular matrix expressed in basement membranes. Its degradation by matrix metalloproteases, cathepsins and elastases results in the formation of endostatin, claimed to have antiangiogenic activity and to be a prominent vasorelaxing agent. We evaluated the expression of endostatin/collagen XVIII in an endotoxemic ARF model. ARF was induced in C57BL/6 mice by intraperitoneal injection of LPS (10 mg/kg) followed by sacrifice 4 and 12 h later. Kidney tissue was the source of RNA and protein and the subject of histological analysis. As early as 4 h after LPS administration, blood urea, creatinine and NO levels were significantly increased compared to control. Endostatin/collagen XVIII mRNA levels were 0.71 times lower than sham-inoculated mice 4 h after LPS inoculation, returning to normal levels 12 h after LPS inoculation. Immunohistological examination revealed that acute injury caused by LPS leads to an increase of endostatin basement membrane staining in association with the decrease of CD31 endothelial basement membrane staining. These results indicate that in the early phase of endotoxemic ARF the endostatin levels were not regulated by gene expression, but by the metabolism of collagen XVIII.

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It has been recently shown that calcium channel blockers might have a protective effect on cardiac fibrogenesis induced by aldosterone. The objective of this study was to evaluate the protective effect of felodipine, a dihydropyridine calcium channel blocker, against heart and kidney damage caused by aldosterone-high sodium intake in uninephrectomized rats. Wistar rats were divided into three groups: CNEP (uninephrectomized + 1% NaCl in the drinking water, N = 9); ALDO (same as CNEP group plus continuous infusion of 0.75 µg/h aldosterone, N = 12); ALDOF (same as ALDO group plus 30 mg·kg-1·day-1 felodipine in the drinking water, N = 10). All results were compared with those of age-matched, untreated rats (CTL group, N = 10). After 6 weeks, tail cuff blood pressure was recorded and the rats were killed for histological analysis. Blood pressure (mmHg) was significantly elevated (P < 0.05) in ALDO (180 ± 20) and ALDOF (168 ± 13) compared to CTL (123 ± 12) and CNEP (134 ± 13). Heart damage (lesion scores - median and interquartile range) was 7.0 (5.5-8.0) in ALDO and was fully prevented in ALDOF (1.5; 1.0-2.0). Also, left ventricular collagen volume fraction (%) in ALDOF (2.9 ± 0.5) was similar to CTL (2.9 ± 0.5) and CNEP (3.4 ± 0.4) and decreased compared to ALDO (5.1 ± 1.6). Felodipine partially prevented kidney injury since the damage score for ALDOF (2.0; 2.0-3.0) was significantly decreased compared to ALDO (7.5; 4.0-10.5), although higher than CTL (null score). Felodipine has a protective effect on the myocardium and kidney as evidenced by decreased perivascular inflammation, myocardial necrosis and fibrosis.

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Circulating microRNAs (miRNAs) may represent a potential noninvasive molecular biomarker for various pathological conditions. Moreover, the detection of circulating miRNAs can provide important novel disease-related information. In particular, inflammation-associated miR-155 and endothelial-enriched miR-126 are reported to be associated with vascular homeostasis. Vascular damage is a common event described in end-stage renal disease (ESRD). We hypothesized that miR-155 and miR-126 may be detectable in the circulation and serve as potential biomarkers for risk stratification. In this study, we assessed miR-155 and miR-126 in the plasma of 30 ESRD patients and 20 healthy controls using real-time quantification RT-PCR. The circulating levels of miR-155 and miR-126 were significantly reduced in patients with ESRD compared to healthy controls. However, there was no significant difference of circulating miR-155 and miR-126 levels between prehemodialysis and posthemodialysis patients. Furthermore, both circulating miR-126 and miR-155 correlated positively with estimated glomerular filtration rate (miR-126: r = 0.383, P = 0.037; miR-155: r = 0.494, P = 0.006) and hemoglobin (miR-126: r = 0.515, P = 0.004; miR-155: r = 0.598, P < 0.001) and correlated inversely with phosphate level (miR-126: r = -0.675, P < 0.001; miR-155: r = -0.399, P = 0.029). Pearson’s correlation was used to compare circulating levels of miRNAs with clinical parameters. These results suggested that circulating miR-155 and miR-126 might be involved in the development of ESRD. Further studies are needed to demonstrate the role of circulating miR-155 and miR-126 as candidate biomarkers for risk estimation.