Peritoneal dialysis effluent, cytokine levels, and peritoneal mesothelial cell viability in CAPD: a possible relationship.

Recent studies have emphasized the role of peritoneal mesothelial cell (PMC) in peritoneal immune defense mechanisms in continuous ambulatory peritoneal dialysis (CAPD). The aim of this study was to evaluate a possible relationship between peritoneal dialysis effluent (PDE), cytokine (Cy) levels, and PMC viability and their impact on peritonitis morbidity. Fifteen patients initiating CAPD for end-stage renal failure participated in the study.

Bone marrow erythroid precursor Ca++ regulates the response to human recombinant erythropoietin (rHuEPO) in hemodialysis patients.

The modulation of erythropoiesis by erythropoietin is conditioned by the concentration of Ca++ in the cytoplasm of the bone marrow erythroid precursors. We evaluated in vitro erythroid colony development from bone marrow erythroid precursors incubated with increasing concentrations of Ca++ or Ca++ plus 1,25 (OH)2 D3, and bone marrow erythroid precursor cytoplasmic Ca++ concentrations in 10 anemic hemodialysis (HD) patients before and during rHuEPO therapy. Results showed that: a) in vitro: in uremics patients before rHuEPO therapy, bone marrow erythroid precursor cytoplasmic Ca++ was lower than in normal subjects; the addition of Ca++ to the bone marrow erythroid precursors induced a dose-dependent Ca++ and erythroid colony development increase; 1,25 (OH)2 D3 potentiated this effect; b) in vivo: rHuEPO normalized bone marrow erythroid precursor Ca++ and erythroid colony development.

Ca++ and 1,25(OH)2D3 regulate in vitro and in vivo the response to human recombinant erythropoietin in CAPD patients.

In vitro studies indicate that the culture medium Ca++ concentration conditions the response to erythropoietin of bone marrow erythropoietic cells which also have specific receptors for 1,25(OH)2D3. We therefore evaluated in 12 anemic CAPD patients: 1) in vitro with increasing concentrations of Ca++ alone or Ca++ plus 1,25(OH)2D3 a) Ca++ in the bone marrow erythroid cell cytoplasm; b) colony (BFU-E and CFU-E) growth from bone marrow erythroid cells. 2) in vivo before and after 24 weeks of i.

Effect of monophosphoryl lipid A on the in vitro function of peritoneal leukocytes from uremic patients on continuous ambulatory peritoneal dialysis.

We analyzed the effects of monophosphoryl lipid A (MPL), a relatively nontoxic immunostimulant derived from bacterial endotoxin, on the depressed in vitro immune function of leukocytes derived from six patients undergoing continuous ambulatory peritoneal dialysis and who had histories of recurrent bacterial peritonitis. MPL was also tested for its capacity to stimulate the proliferation of peritoneal fibroblasts, as determined by [3H]thymidine incorporation. In vitro incubation of peritoneal lymphocytes and macrophages (PM phi) with increasing amounts of MPL, up to 5 micrograms/ml, resulted in a dose-dependent enhancement of gamma interferon and interleukin-2 production by peritoneal lymphocytes and interleukin-1 release by PM phi.

Intraperitoneal therapy with interferon-alpha in CAPD patients with relapsing bacterial peritonitis.

In CAPD patients with relapsing bacterial peritonitis who do not benefit from intraperitoneal therapy with IgG (IgG nonresponders), the authors demonstrated that peritoneal macrophages are deficient in IgG Fc receptors (FcR) and, therefore, unable to kill bacteria, independent of the levels of the opsonic molecule IgG in the peritoneal dialysis effluent (PDE). Because previous studies showed that interferon-alpha (IFN-alpha) is able to increase in vitro the number of PM0 IgG FcR in CAPD patients with relapsing bacterial peritonitis, the authors studied the in vivo effects of IP administration of IFN-alpha (1,000 IU daily in the overnight exchange for 12 months) on: PM0 superoxide generation; PM0 bacterial killing; PM0 IgG FcR; the number of bacteria in the PM0 cytoplasm; and peritonitis relapses in these patients. By the 10th day, IFN-alpha induced a progressive rise in all of the previously depressed PM0 functions tested, the disappearance of bacteria from the PM0 cytoplasm, and no further episodes of bacterial peritonitis were detected during 12 months.