Growth and shape of a laboratory alluvial fan.

Using laboratory experiments, we investigate the influence of water and sediment discharges on the morphology of an alluvial fan. In our flume, a single-thread laminar river deposits corundum sand into a conical fan. We record the fan progradation with top-view images and measure its shape using the deformation of a Moiré pattern. The fan remains virtually self-affine as it grows, with a nearly constant slope. We find that, when the sediment discharge is small, the longitudinal slope of the fan remains close to that of a river at the threshold for sediment transport. Consequently the slope depends on the water discharge only. A higher sediment discharge causes the fan's slope to depart from the threshold value. Due to the downstream decrease of the sediment load, this slope gets shallower towards the fan's toe. This mechanism generates a concave fan profile. This suggests that we could infer the sediment flux that feeds a fan based on its proximal slope.

Estimating ecosystem metabolism from continuous multi-sensor measurements in the Seine River.

Large rivers are important components of the global C cycle. While they are facing an overall degradation of their water quality, little remains known about the dynamics of their metabolism. In the present study, we used continuous multi-sensors measurements to assess the temporal variability of gross primary production (GPP) and ecosystem respiration (ER) rates of the anthropized Seine River over an annual cycle. Downstream from the Paris urban area, the Seine River is net heterotrophic at the annual scale (-226 gO2 m-2 year-1 or -264 gC m-2 year-1). Yet, it displays a net autotrophy at the daily and seasonal scales during phytoplankton blooms occurring from late winter to early summer. Multivariate analyses were performed to identify the drivers of river metabolism. Daily GPP is best predicted by chlorophyll a (Chla), water temperature (T), light, and rainfalls, and the coupling of daily GPP and Chla allows for the estimation of the productivity rates of the different phytoplankton communities. ER rates are mainly controlled by T and, to a lesser extent, by Chla. The increase of combined sewer overflows related to storm events during the second half of the year stimulates ER and the net heterotrophy of the river. River metabolism is, thus, controlled at different timescales by factors that are affected by human pressures. Continuous monitoring of river metabolism must, therefore, be pursued to deepen our understanding about the responses of ecosystem processes to changing human pressures and climate.

Laboratory alluvial fans in one dimension.

When they reach a flat plain, rivers often deposit their sediment load into a cone-shaped structure called alluvial fan. We present a simplified experimental setup that reproduces, in one dimension, basic features of alluvial fans. A mixture of water and glycerol transports and deposits glass beads between two transparent panels separated by a narrow gap. As the beads, which mimic natural sediments, get deposited in this gap, they form an almost one-dimensional fan. At a moderate sediment discharge, the fan grows quasistatically and maintains its slope just above the threshold for sediment transport. The water discharge determines this critical slope. At leading order, the sediment discharge only controls the velocity at which the fan grows. A more detailed analysis reveals a slight curvature of the fan profile, which relates directly to the rate at which sediments are transported.

Width of laminar laboratory rivers.

A viscous fluid flowing over plastic grains spontaneously generates single-thread channels. With time, these laminar analogues of alluvial rivers reach a reproducible steady state, showing a well-defined width and cross section. In the absence of sediment transport, their shape conforms with the threshold hypothesis which states that, at equilibrium, the combined effects of gravity and flow-induced stress maintain the bed surface at the threshold of motion. This theory explains how the channel selects its size and slope for a given discharge. In this light, laboratory rivers illustrate the similarity between the avalanche angle of granular materials and Shields's criterion for sediment transport.

[Arterial hypertension, chronic renal insufficiency and dialysis]. / Hypertension arterielle, insuffisance renale chronique et dialyse.

The principal characteristic of hypertension in chronic kidney disease (CKD), especially at CKD stage 5. Is an increased systolic pressure, with normal or even low diastolic pressure. This isolated systolic hypertension is also characterized by ab abnormal increase in pulse pressure which is by itself an independent cardiovascular risk factor. The principal reason for these abnormalities is accelerated ageing of arterial system, principally the aorta and large central arteries. This ageing is characterized by stiffening of arteritis whose natural history is not clearly understood. One of the principal pathogenic factor associated with stiffening is extensive calcification of arterial walls, mainly the medial layer (media-calcinosis). Mineral metabolism disorders such as hyperphosphatemia, play a major role in pathophysiology of calcifications. Arterial stiffness is characterized by very steep volume-pressure relationship and for this reason is associated with hemodynamic instability. Small blood volume increase producing abnormally high pressure while small decrease in blood volume could be associated with deep hypotension.

Continuous Erythropoietin Receptor Activator (C.E.R.A.) administered at extended administration intervals corrects anaemia in patients with chronic kidney disease on dialysis: a randomised, multicentre, multiple-dose, phase II study.

This dose-finding, open-label study examined the potential of subcutaneous Continuous Erythropoietin Receptor Activator (C.E.R.A.) to correct anaemia at extended administration intervals in 61 erythropoiesis-stimulating agent-naïve patients with chronic kidney disease (CKD) on dialysis. After a 4-week run-in, patients were randomised to C.E.R.A. 0.15, 0.30 and 0.45 microg/kg/week. Within these dose groups, patients were further randomised to once weekly, once every 2 weeks or once every 3 weeks treatment. Mean changes in haemoglobin (Hb) increased with increasing C.E.R.A. dose during a period of 6 weeks where no dose adjustments were permitted. The effect was independent of administration schedule. Erythropoietic responses were sustained until the end of the study (12 weeks) in all groups. In total, 90% of patients in the 0.30 microg/kg/week group and 79% in the 0.45 microg/kg/week group responded to treatment (Hb increase > or =1.0 g/dl), compared with 72% in the 0.15 microg/kg/week group. Faster median response time was associated with increasing dose (51, 38 and 31 days, respectively) and response was unrelated to administration frequency. C.E.R.A. was generally well tolerated. Our results suggest that 0.60 microg/kg twice monthly would be a suitable starting dose of C.E.R.A. for the initiation of anaemia correction in patients with CKD on dialysis. Phase III studies will confirm the feasibility of using C.E.R.A. at extended administration intervals in patients with CKD and anaemia.

Arterial structural and functional alterations in uraemia.

Epidemiological and clinical studies have shown that cardiovascular disease in patients with end-stage renal disease (ESRD) is frequently related to damage of large conduit arteries. Arterial disease is responsible for the high incidence of ischaemic heart disease, peripheral artery diseases, left ventricular hypertrophy and congestive heart failure. The vascular complications in ESRD are ascribed to two different but associated mechanisms, namely atherosclerosis and arteriosclerosis. Whereas the former principally affects the conduit function with ischaemic lesions being the most characteristic consequence, the latter primarily disturbs the dampening function of large arteries. Arteriosclerosis in ESRD patients is characterized by diffuse dilation and wall hypertrophy of large conduit arteries and stiffening of arterial walls. These changes represent a clinical form of an accelerated ageing process. The main clinical characteristics due to arterial stiffening are isolated increase in systolic blood pressure with normal or lower diastolic pressure resulting in an increased pulse pressure. The consequences of these alterations are: (i) an increased left ventricular afterload with development of left ventricular hypertrophy and increased myocardial oxygen demand; and (ii) altered coronary perfusion and subendocardial blood flow distribution. Epidemiological studies have identified arterial remodelling and stiffening as independent predictors of overall and cardiac mortality in ESRD patients.

Iodine-131 ablation therapy for a patient receiving peritoneal dialysis.

The authors describe a patient with follicular thyroid carcinoma who was receiving continuous ambulatory peritoneal dialysis to manage end-stage renal disease. To deliver radioiodine therapy to ablate thyroid remnants safely and under optimal conditions, the behavior of 37 MBq (1 mCi) I-131 was followed daily for 3 days. Blood activity and total body count decreased with a half-life of 100 hours (4.17 days). The daily iodide removal rate, estimated as a percentage of the total administrated activity, was low: 5.3% to 8.6% in peritoneal dialysate and 1.3% to 2.2% in urine. The thyroid uptake, measured using a probe, was 2.4% to 2.1% from day 1 to day 3 and 1.9% later at day 8. The volume of thyroid remnants was determined by ultrasonography to be 0.6 g. The patient received a reduced ablative I-131 dose of 814 MBq (22 mCi). Radiation emitted from the patient after I-131 therapy, monitored using a radiation monitor probe located at a distance of 1 meter, decreased with an effective half-life of 70 hours (2.9 days). The integration of the curve from t = 0 showed a level always less than 25 microSv/hour as early as 24 hours after treatment. Because the iodine removal rate is continuous but low in a case of peritoneal dialysis, smaller therapeutic doses must be administered to deliver maximal radiation to residual thyroid tissue while minimizing excessive radiation exposure to patients, their families, and medical staff.

Pathophysiology of anaemia: focus on the heart and blood vessels.

The amount of oxygen delivered to an organ depends on three factors: blood flow and its distribution; the oxygen-carrying capacity of the blood, i.e. haemoglobin concentration; and oxygen extraction. Non-haemodynamic and haemodynamic mechanisms operate to compensate for anaemia. Non-haemodynamic mechanisms include increased erythropoietin production to stimulate erythropoiesis, and increased oxygen extraction (displacement of the haemoglobin oxygen dissociation curve). This decreased affinity of oxygen for haemoglobin is mediated by increased 2,3-diphosphoglycerate concentrations. Increased cardiac output is the main haemodynamic factor, mediated by lower afterload, increased preload, and positive inotropic and chronotropic effects. Decreased afterload is due to vasodilatation and reduced vascular resistance as a consequence of lower blood viscosity, hypoxia-induced vasodilatation, and enhanced nitric oxide activity. Vasodilatation also involves recruitment of microvessels and, in the case of chronic anaemia, stimulation of angiogenesis. With decreased afterload, the venous return (preload) and left ventricular (LV) filling increase, leading to increased LV end-diastolic volume and maintenance of a high stroke volume and high stroke work. High stroke work is also due to enhanced LV contractility attributed to increased concentrations of catecholamines and non-catecholamine inotropic factors. In addition, heart rate is increased in anaemia, due to hypoxia-stimulated chemoreceptors and increased sympathetic activity. In the long term, these haemodynamic alterations lead to gradual development of cardiac enlargement and LV hypertrophy (LVH). The LVH is eccentric, characterized by increased LV internal dimensions and a normal ratio of wall thickness to cavity diameter, as occurs in other forms of volume overload. When anaemia-related LVH develops in an otherwise 'healthy' humoral environment, the lesions are reversible and the type of LVH is primarily physiological and is not associated with impaired diastolic function. In the absence of underlying cardiovascular disorders, severe anaemia (Haemoglobin concentration < 4-5 g/dl) leads to congestive heart failure. In the presence of heart disease, especially coronary artery disease, anaemia intensifies angina and contributes to a high incidence of cardiovascular complications. In end-stage renal disease (ESRD), LVH is influenced by many other factors, leading to intense interstitial fibrosis, to alterations in diastolic function, and usually to poor reversibility. The chronic increase in cardiac output contributes to arterial remodelling of central elastic arteries such as the aorta and common carotid artery. This remodelling consists principally of arterial enlargement and compensatory arterial intima--media thickening. In ESRD, these geometric changes are accompanied by arterial stiffening. The principal consequences of arterial alterations are increased systolic pressure and high inertia due to higher blood mass in the dilated arterial system. These alterations contribute to the development of LVH and abnormal coronary perfusion.

Arterial stiffening and vascular calcifications in end-stage renal disease.

BACKGROUND: Epidemiological studies have identified aortic stiffness as an independent predictor of cardiovascular mortality in end-stage renal disease (ESRD) patients. In these patients, aortic pulse wave velocity (PWV) was associated with mediacalcosis, but the influence of arterial calcifications on the viscoelastic properties of large arteries was not well characterized. The purpose of the present study was to analyse the influence of arterial calcifications on arterial stiffness in stable haemodialysed patients. METHODS: We studied 120 stable ESRD patients on haemodialysis. All patients underwent B-mode ultrasonography of common carotid artery (CCA), aorta, and femoral arteries to determine CCA distensibility, the elastic incremental modulus (Einc), and the presence of vascular calcifications. All patients underwent measurement of aortic PWV and echocardiogram. The presence of calcifications was analysed semiquantitatively as a score (0 to 4) according to the number of arterial sites with calcifications. RESULTS: Our observations indicate that arterial and aortic stiffness is significantly influenced by the presence and extent of arterial calcifications. The extent of arterial calcifications is in part responsible for increased left ventricular afterload, and is inversely correlated with stroke volume. The influence of calcifications is independent of the role of ageing and blood pressure. Arterial calcifications density increases with age, duration of haemodialysis, the fibrinogen level, and the prescribed dose of calcium-based phosphate binders. CONCLUSIONS: The results of this study showed that the presence of vascular calcifications in ESRD patients was associated with increased stiffness of large capacity, elastic-type arteries, like the aorta and CCA. The extent of arterial calcifications increased with the use of calcium-based phosphate-binders.

Postischemic vasodilation, endothelial activation, and cardiovascular remodeling in end-stage renal disease.

BACKGROUND: Cardiovascular complications are the major cause of death in end-stage renal disease (ESRD) patients. These complications are associated with concomitant cardiac and vascular remodeling, including left ventricular (LV) hypertrophy and hypertrophy of arterial walls. The endothelium influences the process of arterial remodeling. ESRD patients are characterized by the development of both cardiovascular remodeling and endothelial dysfunction. METHODS: Common carotid artery (CCA) intima-media thickness (IMT), CCA diameter, CCA distensibility, LV mass, and function were determined in 60 stable ESRD patients on hemodialysis and 34 age-, sex-, and blood pressure (BP)-matched controls, and their relationships with endothelial alterations were estimated by forearm postischemic vasodilation [flow debt repayment (FDR)] measured by venous plethysmography. We also evaluated the relationships between FDR and several cardiovascular risk factors or markers of inflammatory response or endothelial activation, for example, duration of dialysis, BP, smoking habits, cholesterol, parathormone (PTH), serum albumin, plasma fibrinogen, C-reactive protein (CRP), plasma homocysteine, plasminogen activator inhibitor (PAI-1), and von Willebrand factor (vWF). RESULTS: ESRD patients had increased LV mass, CCA diameter and CCA IMT, and had decreased CCA distensibility (P < 0.05). While the postischemic peak flow was comparable in controls and ESRD patients (29.2 +/- 9.1 vs. 27.9 +/- 0.2 mL/100 mL/min), FDR was lower in ESRD patients (116 +/- 31 vs. 88 +/- 32%, P < 0.001) because of the shorter duration of vasodilation (127 +/- 36 vs. 96 +/- 32 s, P < 0.001). The time to complete FDR was longer in ESRD patients (110 +/- 54 vs. 162 +/- 72 s, P < 0.001). ESRD patients had lower high-density lipoprotein cholesterol and serum albumin (P < 0.01) and higher triglycerides, fibrinogen, plasma homocysteine, vWF (P < 0.01), and PAI-1 (P < 0.05). For ESRD patients, significant negative age- and pressure-independent correlations were established between FDR and CCA diameter, duration of dialysis, and PAI-1. FDR was positively correlated with serum albumin. FDR and time to FDR were negatively correlated with CCA IMT and LV mass. CCA distensibility was positively associated with FDR (P < 0.001) and negatively with time to FDR (P < 0.001). The PAI-1 concentration was positively correlated with CCA IMT (P < 0.01) and negatively with CCA distensibility (P < 0.001). CONCLUSIONS: Our data provide the first evidence that cardiac and arterial remodeling in ESRD patients are inversely related to forearm reactive hyperemia. The diminished hyperemic response is due to the shorter duration of hyperemia and is associated with higher concentrations of serum markers of endothelial activation, suggesting that, in ESRD patients, endothelial dysfunction may be a factor influencing cardiovascular changes.

Association of hyperphosphataemia with haemodynamic disturbances in end-stage renal disease.

BACKGROUND: Because recent data demonstrated that the shortened survival and excess cardiovascular death of end-stage renal disease (ESRD) patients are predicted by hyperphosphataemia, we examined the haemodynamic alterations associated with high serum phosphorus levels in ESRD patients on haemodialysis. METHODS: Sixty-six ESRD patients were studied. Patients were separated arbitrarily into two groups, i.e. with predialysis serum phosphate <2 mmol/l ('normal' phosphate) and, serum phosphate >2 mmol/l ('high' phosphate). Cardiac and arterial function and structure were analysed by computer-assisted ultrasonography. RESULTS: Hyperphosphataemic patients were characterized by higher diastolic and mean blood pressures (P<0.05), and higher cardiac index (P<0.001) caused by an increased stroke index (P<0.05) and higher heart rate (P<0.01). The cardiac work index was significantly increased in patients with higher phosphate levels (P<0.01). Hyperphosphataemic patients tended to have a higher common carotid artery diameter (P=0.07), but similar carotid artery intima-media thickness, and lower carotid wall-to-lumen ratio (P<0.05) than patients with 'normal' serum phosphorus. As a result of lower wall-to-lumen ratio in the presence of higher mean blood pressure, the carotid tensile stress was higher in hyperphosphataemic ESRD patients (P<0.05). CONCLUSION: These findings suggest that, in stable ESRD patients, hyperphosphataemia is associated with increased BP, hyperkinetic circulation, increased cardiac work, and high arterial tensile stress. These haemodynamic abnormalities could favour the development of cardiovascular complications and contribute to high cardiovascular morbidity and mortality.

Diffusivelike buffering and saturation of large rivers.

We use mass balance data from Asian rivers together with a first-order diffusive simplification of the St. Venant-Exner equations to characterize river flood plain processes and discuss the reaction of a large model river to a hill slope supply of eroded masses. The simple analytical solution derived for the long-term profile of the river bed shows that (i) the system converges towards a state in which it reacts to perturbations in erosion of the landscape by small-amplitude oscillations around an average "stationary" state, (ii) to have an effective influence on the river plain profile, the perturbations need to have frequencies smaller than the characteristic frequencies of the river system, and (iii) this river buffering might be linked with a possible long-term saturation of the system carrying capacity.

Cardiac and arterial interactions in end-stage renal disease.

Although cardiac hypertrophy is a frequent complication of end-stage renal disease (ESRD), relatively little is known about large arterial geometry and function in vivo in these patients, and the relationship between arterial changes and cardiac hypertrophy is unknown. Common carotid artery (CCA) intima-media thickness and internal diameter and left ventricular geometry and function were determined by ultrasound imaging in 70 uncomplicated ESRD patients and in 50 age-, sex-, and blood pressure-matched controls. Arterial distensibility and compliance were determined from simultaneously recorded CCA diameter and stroke changes in diameter and CCA pressure waveforms, obtained by applanation tonometry, and also by the measurement of carotid-femoral pulse wave velocity. Compared with control subjects, ESRD patients had greater left ventricular diameter (P < 0.01), wall thicknesses and mass (P < 0.001), increased CCA diameter (6.25 +/- 0.87 vs. 5.55 +/- 0.65 mm; P < 0.001), larger CCA intima-media thickness (777 +/- 115 vs. 678 +/- 105 microns; P < 0.001) and intima-media cross-sectional area (17.5 +/- 4.5 vs. 13.4 +/- 3.3 mm2; P < 0.001). In uremic patients, arterial hypertrophy was associated with decreased CCA distensibility (17.8 +/- 8.8 vs. 24.0 +/- 12.7 kPa-1.10(-3); P < 0.001) and compliance (5.15 +/- 2 vs. 6.0 +/- 2.5 m2.kPa-1.10(-7); P < 0.05), accelerated carotid-femoral pulse wave velocity (1055 +/- 290 vs. 957 +/- 180 cm/seconds; P < 0.001), early return and increased effect of arterial wave reflections (20.5 +/- 15.4 vs. 9.2 +/- 18.4%; P < 0.001). The latter phenomenons were responsible for increased pulsatile pressure load in CCA (58.3 +/- 21 vs. 48 +/- 17 mm Hg; P < 0.01) and were associated with a decreased subendocardial viability index (157 +/- 31 vs. 173 +/- 30%; P < 0.001). The CCA diameter was correlated with the left ventricular diameter (P < 0.01), and a significant correlations existed between CCA wall thickness or CCA intima-media cross-sectional area and left ventricular wall thicknesses and/or left ventricular mass (P < 0.01). In multivariate analysis, these relationships were independent regarding age, sex, blood pressure and body surface area. The present study documents parallel cardiac and vascular adaptation in ESRD, and demonstrates the potential contribution of structural and functional large artery alterations to the pathogenesis of left ventricular hypertrophy and functional alterations.