Local hemodynamics of the vascular access for hemodialysis.

Vascular access is called Achilles' heel of hemodialysis because it is associated with a substantial morbidity. A permanent vascular access is created either by a direct connection of the patient's own artery and vein or by the interposition of a graft. Arteriolar beds are bypassed, which leads to a substantial increase in arterial (and venous) flow and the vessels adapt to it by a complex of interesting processes. These are reviewed together with some pathophysiological mechanisms of access complications.

Mechanisms of chronic heart failure development in end-stage renal disease patients on chronic hemodialysis.

More than 50 % of end-stage renal disease (ESRD) patients treated by chronic hemodialysis die from cardiovascular diseases, including congestive heart failure (CHF). The incidence of CHF is rising in both general and ESRD population. However, the mechanisms, which lead to the development of CHF in dialyzed patients, differ considerably. First, there are several factors leading to increase of the left ventricular afterload: volume overload between dialyses, hypertension, increased arterial stiffness, anemia, vascular access flow (arteriovenous fistula) and sympathetic activation. Second, hypertension, left ventricular hypertrophy, anemia and frequently present coronary artery disease worsen myocardial oxygenation. The combination of these factors explains the high incidence of CHF in dialyzed patients and their roles are reviewed in this article.

Understanding the dialysis access steal syndrome. A review of the etiologies, diagnosis, prevention and treatment strategies.

Distal hypoperfusion ischemic syndrome (DHIS), commonly referred to as hand ischemia or 'steal' after dialysis access placement, occurs in 5-10% of cases when the brachial artery is used, or 10 times that of wrist arteriovenous fistulas (AVFs) using the radial artery. It is typically seen in elderly women with diabetes, and may carry severe morbidity including tissue or limb loss if not recognized and treated. Three distinct etiologies include (1) blood flow restriction to the hand from arterial occlusive disease either proximal or distal to the AV access anastomosis, (2) excess blood flow through the AV fistula conduit (true steal), and (3) lack of vascular (arterial) adaptation or collateral flow reserve (ie atherosclerosis) to the increased flow demand from the AV conduit. These three causes of steal may occur alone or in concert. The diagnosis of steal is based on an accurate history and physical examination and confirmed with tests including an arteriogram, duplex Doppler ultrasound (DDU) evaluation with finger pressures and waveform analysis. Treatment of steal includes observation of developing symptoms in mild cases. Balloon angioplasty is the appropriate intervention for an arterial stenosis. At least three distinct surgical corrective procedures exist to counteract the pathophysiology of steal. The ultimate treatment strategy depends on severity of symptoms, the extent of patient co-morbidity, and the local dialysis access technical team support and skills available.

The effect of adrenalectomy on exercise response of the renin-angiotensin-aldosterone system and exercise tolerance in primary aldosteronism.

Primary aldosteronism (PA) is associated with objectively measured lower physical fitness and blunted response of the renin-angiotensin-aldosterone system to exercise. The purpose of this pilot study was to objectively measure exercise response of the renin-angiotensin-aldosterone system and cardiopulmonary fitness changes after laparoscopic adrenalectomy (ADE) in patients with unilateral PA. We examined a total of 14 patients with confirmed PA before and after ADE, by means of spiroergometry and hormonal evaluation. As expected, after adrenalectomy basal aldosterone (Aldo) levels before exercise decreased significantly, with a concomitant increase in plasma renin (PR). The increase in Aldo (285.9+/-171.3 to 434.1+/-278.2 ng/l; p=0.02) and blunted increase in PR (7.1+/-0.4 to 8.9+/-10.4 pg/ml; NS) post-exercise before ADE became significant after ADE Aldo post-ADE (46.8+/-18.8 to 106.5+/-68.1 ng/l; p<0.0001) and PR post-ADE (20.1+/-14.5 to 33.9+/-30.7 pg/ml; p=0.014). After adrenalectomy, the patients had a non-significant increase in peak workload and VO(2peak). We found normalization of the renin-angiotensin-aldosterone system response to exercise with little changes in cardiopulmonary fitness six months after ADE.

Dyslipidemia and anemia in chronically hemodialyzed patients.

More than 50% of end-stage renal disease subjects treated by chronic hemodialysis die from cardiovascular events. Although there is some information regarding to anemia compensation and to the levels of biochemical risk factors of atherosclerosis in other countries, the data from the Czech Republic are missing. The aim of this study was to estimate mean cholesterol, triglyceride and hemoglobin levels in hemodialyzed subjects in the Czech Republic and to compare them with current guidelines. During the years 2001-2006, nephrologists of all subjects screened by duplex Doppler ultrasonography of our department were asked to fill in questionnaires with basic history and laboratory data. Hemoglobin concentration was calculated separately for years 2001-2004 and 2005-2006 because of the change of recommended target value from 105 to 110 g/l in 2004. A total of 258 subjects were included, aged 65 +/- 14 years, 93 of them males. Patients came from 46 different hemodialysis centers in the Czech Republic. The presence of hypertension and diabetes was in 72.5% and 39.5%, respectively. Only 13.2% of subjects had the smoking history, and another 10% currently smoked. The mean +/- SD laboratory results were as follows: total cholesterol 5.0 +/- 1.1 mmol/l, triglycerides (2.5 +/- 1.4 mmol/l). Hemoglobin concentration was 104.4 +/- 14.4 g/l (mean +/- SD) in years 2001-2004 and 110.1 +/- 16.2 g/l in years 2005-2006. Hemoglobin full blood concentration was lower than recommended 105 g/l in 55% of hemodialyzed subjects during years 2001-2004, and it was lower than 110 g/l during years 2005-2006 in 47% of patients. Hypercholesterolemia above recommended 5.17 mmol/l was present in 39% of subjects. Triglycerides were elevated above 1.69 mmol/l in 64% of patients. Only 10% of subjects were treated by lipid-lowering drugs. We can conclude that in the Czech Republic, patients treated by chronic hemodialysis frequently suffer from anemia, despite the growing evidence of erythrocyte stimulating agents treatment benefit. Similarly, considerable number of these subjects has hypercholesterolemia and hypertriglyceridemia, only rarely treated by lipid-lowering drugs. However, this therapy is still not adequately supported by clinical research evidence.

Lower physical fitness in patients with primary aldosteronism is linked to the severity of hypertension and kalemia.

Hypokalemia as a typical feature of primary aldosteronism (PA) is associated with muscle weakness and could contribute to lower cardiopulmonary fitness. The aim of this study was to describe cardiopulmonary fitness and exercise blood pressure and their determinants during a symptom-limited exercise stress test in patients with PA. We performed a cross-sectional study of patients with confirmed PA who were included before adrenal vein sampling on whom a symptom-limited exercise stress test with expired gas analysis was performed. Patients were switched to the treatment with doxazosin and verapamil at least two weeks before the study. In 27 patients (17 male) the VO(2peak) was 25.4+/-6.0 ml/kg/min which corresponds to 80.8+/-18.9 % of Czech national norm. Linear regression analysis shows that VO(2peak) depends on doxazosin dose (DX) (p=0.001) and kalemia (p=0.02): VO(2peak) = 4.2 - 1.0 * DX + 7.6 * Kalemia. Patients with higher doxazosin doses had a longer history of hypertension and had used more antihypertensives before examination, thus indicating that VO(2peak) also depends on the severity of hypertension. In patients with PA, lower cardiopulmonary fitness depends inversely on the severity of hypertension and on lower plasma potassium level.

[Wall shear stress and endothelium]. / Smykové napetí a endotel.

Blood flow influences the luminal side of vessel wall by a frictional force known as wall shear stress (WSS). This local hemodynamic factor is an important determinant of endothelial gene expression and of endothelial phenotype. The effect of WSS depends on its magnitude and direction, as well as on the characteristic of vessel geometry and blood flow. WSS seems to be a critical determinant of vessel caliber, vascular remodeling and restenosis and plays a role in intimomedial hyperplasia. Research is concentrated especially on the influence of WSS on atherosclerotic plaque formation.

Common carotid wall shear stress and carotid atherosclerosis in end-stage renal disease patients.

Decrease of arterial wall shear stress (WSS) is associated with higher probability of atherosclerotic plaque development in many disease conditions. End-stage renal diseases (ESRD) patients suffer from vascular disease frequently, but its nature differs from general population. This study was aimed at proving an association between common carotid wall shear stress and the presence of carotid bifurcation plaques in a group of ESRD patients. ESRD subjects, planned for the creation of a dialysis access and therapy were included. Wall shear rate (WSR) was used as a surrogate of WSS and was analyzed in the common carotid arteries by duplex ultrasonography. Intima media thickness (IMT) was measured at the same site. The presence/absence of carotid bifurcation plaques was recorded. The endothelial function was estimated by the levels of von Willebrand factor (vWf). 35 ESRD patients were included (19 females, 17 diabetics). Atherosclerotic plaque was present in 53 % of bifurcations. Wall shear rate was lower in arteries with plaques (349+/-148 vs. 506+/-206 s(-1), p=0.005) and was directly related to the height of IMT and inversely to the activity of vWf (r= -0.65, p=0.016). Lower wall shear rate in the common carotid arteries is linked to the endothelial dysfunction and to the presence of atherosclerotic plaques in carotid bifurcations in ESRD subjects. Faster arterial dilatation may facilitate this process in ESRD subjects.