This prospective study was designed to evaluate the eventual correction of anemia and iron status in 39 iron-deficient uremics starting hemodialysis. Nine patients (control group) had no iron supplementation, 10 had oral ferrous iron, and 20 were treated with intravenous iron gluconate. Follow-up periods were 12 months for the control group and 26 months for patients treated with oral or intravenous iron. No patient was treated with erythropoietin. At zero time, all patients were anemic (Hb <78 g/l) and showed signs of severe iron deficiency, diagnosed on the basis of depleted bone marrow iron stores, reduced hemoglobin iron, and transferrin saturation <21%. The hemoglobin levels, observed in patients of the control and the oral iron groups at the end of the follow-up periods, were not significantly different from those detected at zero time. In contradistinction, patients treated with intravenous iron showed after 26 months of follow-up a significant increase of blood hemoglobin values, reaching a mean value of 126 g/l. So far, this evidence supports both the concept that iron absorption is compromised in chronic uremics and that the parenteral way is the more effective route for iron replacement in this specific group of patients.

The peritoneum has been classically considered to be an inert passive membrane. Previous studies demonstrated the presence of fixed anionic charges at the level of the peritoneal microvasculature and the subserosal interstitium. The present study describes the selective distribution of fixed anionic charges in the mesothelial cell plasmalemma and organelles as well as in the submesothelial basal lamina of rat and mice visceral, parietal and diaphragmatic peritoneum. These data support the idea that the peritoneum should be considered a negatively charged biological dialyzing membrane with selective capabilities. Therefore, transperitoneal transfer of charged solutes cannot be analyzed just on the basis of their molecular weight, size and shape.

No abstract

Previous studies showed that murine septic peritonitis induced a substantial reduction of the anionic site density distribution in mesenteric and diaphragmatic microvessels. The present study shows that acute experimental septic peritonitis induces a severe reduction of the anionic site density distribution along the submesothelial basement membrane. Five days after induction of peritonitis, there was a partial recovery of anionic sites which even at 13 days was not completed. This observation suggests that the increased protein losses observed during peritonitis are the consequence of increased microvascular and mesothelial permeability to anionic plasma proteins secondary to neutralization and/or disappearance of the anionic sites located in the microvascular wall and in the mesothelial layer.

This study shows that the luminal surface of peritoneal microvascular endothelium, coated pits and coated vesicles are all negatively charged, unlike the limiting membrane of pinocytotic vesicles and transcellular channels. Our findings suggest that these cellular organelles have different functions as well as a different chemical composition. Anionic sites were observed along the subendothelial and subperithelial basal laminae of peritoneal capillaries and post capillary venules, respectively. Electric charge is a new parameter to be considered when analyzing transperitoneal transfer of charged macromolecules.