In 2002 WAA decided to start a world-wide apheresis registry to gain insight into the extent of treatment, adverse events, and to facilitate contacts among centers when treatment indications are rare ...and experience limited. Stem cell and other blood products collections intended for therapeutic application can also be entered. The WAA planned to use the French Registry. Its translation into English has not been accomplished and the fiscal obligations for that registry has not, as yet, been determined or considered and approved by the WAA Board. From Dec 2002 the proposed registry (a merged version of the French, Canadian and Swedish registries) can be immediately implemented. We now cordially invite all centers to join that registry. Please, also inform colleagues at other centers in your country to join. E-mail and address lists of colleagues in your country who have not registered will be welcomed. The site is at:
www.iml.umu.se/medicin/ Go to World Apheresis Registry; Login code to test the Registry is: al61tms Stegmayr B, Korach JM, Norda R, Rock G, Fadel F. Is there a need for a national or a global apheresis registry? Transfus Apheresis Sci. 2003;29(2):179–85. Then apply for a specific login code for your center. We welcome you to this registry for your input of data. You will not be charged any registration fee. The registry includes a randomization system that can be used for local or multi center studies (randomization by in-center basis allows you to make your own studies). It includes a formula that increases the chance to get a more even distribution between groups also for smaller sample sizes.
Patients with chronic kidney disease (CKD) have a high burden of mortality and cardiovascular morbidity. Additional strategies to modulate cardiovascular risk in this population are needed. Data ...suggest that anemia is a potent and potentially modifiable risk factor for cardiovascular disease in patients with CKD, but these data remain unsubstantiated by any randomized controlled trial (RCT). Furthermore, the clinical practice guidelines for anemia management in patients with CKD are based on limited data. The need for new RCTs to address critical knowledge deficits, particularly with regard to the impact of anemia therapy on cardiovascular disease and survival, is recognized within the guidelines and independent comprehensive reviews of the existing published trial data.
The Trial to Reduce Cardiovascular Events with Aranesp (Amgen Inc, Thousand Oaks, Calif) (darbepoetin alfa) Therapy (TREAT) is a 4000-patient, multicenter, double-blind RCT, designed to determine the impact of anemia therapy with darbepoetin alfa on mortality and nonfatal cardiovascular events in patients with CKD and type 2 diabetes mellitus. Subjects will be randomized in a 1:1 manner to either darbepoetin alfa therapy to a target hemoglobin (Hb) of 13 g/dL or control, consisting of placebo for Hb ≥9 g/dL or darbepoetin alfa for Hb <9 g/dL until Hb is again Hb ≥9 g/dL. TREAT is event-driven and has a composite primary end point comprising time to mortality and nonfatal cardiovascular events, including myocardial infarction, myocardial ischemia, stroke, and heart failure. TREAT will provide data that are critical to evolution of the management of cardiovascular risk in this high-risk population.
The intradialytic symptoms that can be linked to components of the extracorporeal circuit of greatest clinical importance are the Type A (anaphylactoid) reactions. Most of these are IgE-mediated ...reactions due to ethylene oxide and are preventable by adequate degassing of the dialyzer by the manufacturer and by adequate rinsing of the dialyzer just prior to use. AN69-associated reactions are a second group, and are probably mediated by membrane-induced bradykinin generation coupled with ACE-inhibitor induced prolongation of bradykinin half-life. Type A reactions occur in a reuse setting, alos, and these may be related to some as yet poorly understood interaction between bleach, reuse sterilants, and certain dialyzer membranes, again, with ACE inhibitors playing an amplifier role. There is no compelling evidence linking membrane-induced complement activation to type A dialyzer reactions. However, there is a large body of evidence in animal models that exposure to complement fragment-releasing membranes can increase the pulmonary artery pressure and increase thromboxane formation. Thus, at least in principle, a case can be made for using unsubstituted cellulose membranes with caution in patients with a history of atopy or eosinophilia, particularly if acetate dialysate is to be used. Such a caution, however, must be viewed as conjectural in the absence of definitive evidence. Type B dialyzer reactions (mild back and chest pain 20-60 min into the dialysis session) is a phenomenon that is in the process of vanishing. The reason why is unclear. These reactions may have been due to some sort of dialyzer contaminant, or they may have been due to complement fragment release and required the use of acetate dialysate as a cofactor. In any event, recent well designed studies fail to find any differences in symptoms between unsubstituted cellulose and synthetic membranes. Membrane-induced complement fragment release also may play a minor role in dialysis hypoxemia, but evidence is conflicting in this area. Again, the use of acetate dialysate appears to be an important cofactor. Post-dialysis events which may be conceivably linked to the delayed effects of complement fragment releasing membranes need to be evaluated in controlled studies. Studies suggesting increased post-dialysis catabolism with use of unsubstituted cellulose membranes need to be confirmed in dialysis patients, and symptomatic correlates should be sought and evaluated.
