Anaemia correction--does the mode of dialysis matter?

associated inhibitors of erythropoiesis has remained The enormous success of treating renal anaemia with unclear. When canine or murine erythroid progenitor recombinant human erythropoietin (rhEpo) during the cells were cultured in vitro with Epo, the addition of last 15 years easily lets one forget that the discussion uraemic human serum was found to inhibit the growth about the pathogenesis of renal anaemia was dominof erythroid colonies [6 ]. However, the clinical relevated for decades by the question whether it is primarily ance of this inhibition is questionable, since it is not due to relative Epo deficiency or uraemic inhibition of specific for red cell production and also affects granuloerythropoiesis. Although it has so far not been possible and megakaryopoiesis [7], which are both not supto identify or isolate a substance retained in uraemia pressed in chronic renal failure. Moreover, inhibition with a suppressive action directed specifically against of erythropoiesis was not observed in cultures of red cell production, dialysis therapy can improve the marrow cells from uraemic patients incubated with effect of both residual endogenous and exogenous autologous sera [8]. Among the polyamines, spermine rhEpo. To which extent mode and/or dose of dialysis was considered as an inhibitor of erythropoiesis that influence Epo efficacy is yet poorly understood. In this accumulates in patients with renal failure [9], but its issue Locatelli et al. report the results of a prospective effect also appears to be non-specific [10]. Parathyroid multicentre trial that provides some new evidence hormone was found to impair erythroid colony growth related to this question and the potential role of [11], but these results could not be reproduced in other uraemic inhibitors of red cell production [1]. experiments [12]. Probably the adverse effect of hyperparathyroidism on red cell production is at least partially due to marrow fibrosis [13]. Albumin bound Uraemic toxins as inhibitors of erythropoiesis? metabolites such as furancarboxylic acid were reported to have some inhibitory effect on marrow cultures [14], Plasma Epo levels in patients with chronic renal failure but their role has also not been clarified. Moreover, in do not rise appropriately for the degree of their anaeferrokinetic studies the acute response to rhEpo was mia. Instead they remain within or only slightly above not found to be significantly different in normal the normal range of non-anaemic individuals. This and uraemic subjects [15], which argues against the relative deficiency in Epo is considered as the main general importance of uraemic inhibitors of red cell cause of renal anaemia [2]. In addition, however, the production. rates of red cell production in haemodialysis patients Although direct proof for the existence of substances were estimated to be only about one half of the rate specifically inhibiting red cell formation in uraemia is in normal individuals despite the same or even higher lacking, this does not exclude that a variety of different Epo titres [3]. Conversely, serum Epo levels achieved molecules accumulating in the uraemic state may conwith s.c. administration of 100 IU rhEpo/kg b.w.—a tribute to an impairment of erythropoiesis. In support dose which many patients require to maintain a subnorof this it has been observed since several decades that mal haemoglobin level—are higher than serum concenhaemoglobin levels can increase following the onset or trations that have been measured during the correction a change of dialysis therapy. phase of anaemia after kidney transplantation [4,5]. Thus factors other than Epo deficiency seem to blunt