Kidney international. Supplement最新文献

In 1966 two research groups, one in the United States and the other in Germany, were independently evaluating new membranes for renal replacement techniques. These filters were characterized by high filtration rates, where solutes up to a certain molecular weight were filtered by convection. At the same time the understanding of the transport mechanisms through membranes was improving. In 1976 Burton created the term "hemofiltration" for this new convective technique, and the first multicenter trial was initiated to evaluate its effectiveness for treating chronic renal failure. In 1977 Kramer in Göttingen (Germany) developed the continuous arteriovenous hemofiltration (CAVH) technique, which used a systemic arteriovenous pressure difference in an extracorporeal circuit to continuously produce an ultrafiltrate. The advantages of this effective method for elimination of fluid and solutes were its technical simplicity and the hemodynamic stability of even critically ill patients. Therefore, it soon became a widely used method for treating acute renal failure in intensive care patients. However, its limited capacity to remove nephrotoxins in the presence of high catabolism and complications connected to the arterial access lead to the development of a venovenous pump-driven technique (CVVH) in order to become independent from the systemic circulation and the arterial access. Further progress to improve solute clearance was made by combining the convective principle of hemofiltration with the diffusive transport of dialysis (continuous arteriovenous hemodialysis or hemodiafiltration). Today this combination has become the most effective renal replacement technique for treating acute renal failure in critically ill patients.

We describe our experience with continuous renal replacement therapy (CRRT) in critically ill neonates. From June 1995 to June 1997 36 critically ill oliguric or anuric infants and children underwent continuous arterio-venous (N = 17) or veno-venous (N = 15) renal support. In addition, four neonates were treated with continuous ultrafiltration (CUF) during extracorporeal membrane oxygenation (ECMO) because of severe diuretic-resistant hypervolemia. Their mean age was 9.8 +/- 1.5 days, their mean body weight 3.0 +/- 0.1 kg. The membrane surface area of the hemofilters ranged from 0.015 m2 to 0.2 m2 and the priming volume from 3.7 to 15 ml. For pump-driven hemofiltration a roller pump with pressure alarms, an air trap, an air bubble detector, and small blood lines was used. Fluid balance was controlled by a microprocessor controlled unit. The ultrafiltrate substitution fluid was based on bicarbonate in the majority of the patients and was partially or totally replaced according to the clinical situation. The mean duration of renal support was 97 +/- 20 hours, ranging from 14 to 720 hours. During arterio-venous and veno-venous hemofiltration the mean blood flow rates were 7.0 +/- 1.2 ml/min and 23.1 +/- 2.4 ml/min (P < 0.01), respectively, and the mean ultrafiltration rates 3.3 +/- 0.4 and 9.5 +/- 1.9 ml/min/m2 (P < 0.01), respectively. During continuous hemodiafiltration urea clearances increased by 300%. Overall survival rate was 66%. CRRT related complications included local bleeding at the catheter entrance site, partial thrombosis of the inferior or superior caval veins and transient ischemia due to femoral artery catheters. Continuous hemofiltration either driven in the arterio-venous or veno-venous mode is a very effective method of renal support for critically ill neonates to control fluid balance and metabolic derangement. Urea clearance can be improved by adding some dialysate fluid in a countercurrent direction to blood flow.

Recovery from ischemic and nephrotoxic acute renal failure (ARF) requires the replacement of damaged tubular cells with new ones that restore the continuity of the renal epithelium. The repair process involves a number of growth factors produced in renal tissue that participate as autocrine or paracrine regulators in the repair process. The aim of this review is threefold: (1) to focus on the role of local growth factors such as EGF, TGF-alpha, IGF-1, HGF and TGF-beta in renal regeneration immediately after an acute renal insult. Receptors for these growth factors have been found in renal epithelial cells, medullary interstitial cells and glomeruli. These mediators play an important role in renal repair by promoting tubular cell proliferation. (2) A review the data supporting the administration of these growth factors in animal models of ARF, and the possibility of using these mediators in humans for the purpose of accelerating renal recovery and decreasing the morbidity and mortality rates, and the costs of multidisciplinary medical care, is presented. (3) Finally, the possibilities of introducing supportive therapy aimed at specific targets such as RGD peptides to reduce intratubular obstruction, atrial natriuretic factor to improve altered glomerular hemodynamics, and cell therapy such as bioartificial renal tubule in association with dialysis are discussed.

The decision to initiate renal replacement therapy is usually based on a careful assessment of conflicting priorities in the care of critically ill patients. It is particularly difficult because of the lack of information on what are the optimal criteria and indications for the application of renal replacement therapy (RRT) in the intensive care unit (ICU). As we will discuss in this paper, even though there are several time-honored indications for initiating dialytic therapy in patients with near end-stage renal failure, such indications may not apply to the management of acute renal failure (ARF). In fact, there are several reasons why a more aggressive approach and an earlier intervention may be justified in the ICU.

Several factors combine to facilitate the evolution towards heart and multi-organ failure following cardiac surgery. Some of these factors are related to pure cardiac aspects, for example, the existence of a preoperative heart disease, the use of aortic cross clamping or performance of cardiotomy. Cardiopulmonary bypass (CPB) also plays an important role in the occurrence of postoperative organ dysfunctions by two principal means. It induces a profound hemodilution, which impairs oxygen transport through tissues. This phenomenon becomes obvious in the postoperative period by the existence of increased transpulmonary O2 gradients, extravascular lung water volume and subsequent impairments of O2 transport. (2) Cardiopulmonary bypass is deleterious by triggering an important inflammatory reaction. This reaction is largely related to the ratio of the circuit area to the patient's body surface area and is therefore maximal in children. It has been widely demonstrated that the very early paths of this reaction imply several humoral factors including kinins, coagulation factor XII and complement fragments. The activation of these factors is self-amplified and triggers both expression and release of numerous mediators by endothelial cells and leukocytes. Finally, these mediators are responsible for the well described "post-bypass syndrome," which is, from a clinical viewpoint, very close to hyperkinetic septic shock. Several methods have been proposed to reduce the deleterious effects of both cardiac surgery and CPB. The older one is hypothermia that considerably reduces the triggering of the inflammatory mediator network. Heparin-coated circuits may also reduce this reaction to some extent. Hemofiltration has been introduced in the 1990s in CPB management. Because of its very high tolerance in patients with compromised circulatory status this technique was already used in the postoperative period to treat patients with acute renal failure. Initially hemofiltration was intended to correct the accumulation of extravascular water during or immediately following the surgical procedure. Nevertheless, several of its side-effects appeared to be useful, such as the reduction of postoperative blood loss and immediate improvement in hemodynamics. Several studies attempted to point out the mechanism of action of hemofiltration and although removal of inflammatory mediator occurs, there is currently no proof that this removal is the actual mechanism by which this technique acts.

To evaluate plasma dopamine concentration and the effects of low doses infusion on urinary output after abdominal vascular surgery in patients with renal function impairment we performed a prospective clinical study. Twenty hemodynamically stable patients (mean age 66.6 years), with serum creatinine concentration < 2 mg %, who undergoing general anesthesia for major vascular surgery participated. A low dose of dopamine (3 micrograms/kg/min) was administrated to patients with postoperative protracted urinary output < 0.5 ml/kg/hr for at least eight hours. Plasmatic determinations were taken at T0 (no dopamine administration), when urinary output began to increase, or if not, after two hours (T1), at eight (T2), and 24 (T3) hours after the beginning of infusion. After 24 hours the dopamine infusion was stopped and the patient's plasmatic level was measured four hours later (T4). Dopamine plasma concentrations were measured using high-performance liquid chromatography. Plasma dopamine concentration increased in all patients and reached a steady state at T2 (T2 = 76.41 +/- 16.84 ng/ml). Dopamine induced a concentration-dependent increase in urinary output (T0 = 0.45 +/- 0.14; T1 = 1.49 +/- 1.11; T2 = 2.34 +/- 1.44; T3 = 1.57 +/- 0.57; T4 = 0.85 +/- 0.7 ml/kg/hr). Three patients did not have an enhanced urinary output after dopamine infusion; they did have a prolonged clamping time and operation time (162 +/- 24 and 570 +/ 30 min, respectively). We conclude that low dose dopamine induces a dose-dependent increase of urinary output. This phenomenon also has been found in patients when their plasma concentration had not yet reached the steady-state. Lack of responsiveness to dopamine suggests a renal function impairment probably due to the prolonged aortic clamping time.