SERUM FROM CONTINUOUS AMBULATORY PERITONEAL-DIALYSIS PATIENTS WITH ACUTE BACTERIAL PERITONITIS INHIBITS IN-VITRO ERYTHROID COLONY FORMATION

Citation
Jm. Stevens et Cg. Winearls, SERUM FROM CONTINUOUS AMBULATORY PERITONEAL-DIALYSIS PATIENTS WITH ACUTE BACTERIAL PERITONITIS INHIBITS IN-VITRO ERYTHROID COLONY FORMATION, American journal of kidney diseases, 24(4), 1994, pp. 569-574
Citations number
26
Categorie Soggetti
Urology & Nephrology
ISSN journal
02726386
Volume
24
Issue
4
Year of publication
1994
Pages
569 - 574
Database
ISI
SICI code
0272-6386(1994)24:4<569:SFCAPP>2.0.ZU;2-I
Abstract
During episodes of acute infection there is a reduced response to epoe tin therapy. It is well known that ''endogenous pyrogens,'' such as in terleukin-1 (IL-1) and tumor necrosis factor, inhibit erythropoiesis w hen administered exogenously. To determine whether there is a relation ship between these observations, serum samples were obtained from nine patients with chronic renal failure maintained by continuous ambulato ry peritoneal dialysis, during and after recovery from bacterial perit onitis, to study the effect of circulating factors on erythropoiesis. Normal human bone marrow-derived erythroid progenitors were cultured i n vitro in 5% and 10% patient serum. Depression of the growth of rate progenitors, colony-forming units-erythroid (at 10% serum, P = 0.005; 95% confidence intervals, 6.2 and 24.4, respectively), was observed bu t there was no effect on the earlier progenitors, burst-forming units- erythroid (at 10% serum, P = 0.7; 95% confidence intervals, -18.5 and 13, respectively). The effect was not prevented by antisera to IL-1. S imilarly, when added to cultures, IL-1 inhibited the colony-forming un its-erythroid and the effect was abrogated by IL-1 antisera. These fin dings suggest that a circulating soluble factor that is inhibitory to erythropoiesis and may contribute to loss of response to epoetin thera py, is present in cases of peritonitis in continuous ambulatory perito neal dialysis patients. (C) 1994 by the National Kidney Foundation, in c.