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To determine the optimum regimen for giving recombinant human erythropoietin (EPO) to patients on continuous ambulatory peritoneal dialysis (CAPD), the pharmacokinetics of single-dose EPO administered intravenously (120 U/kg), intraperitoneally (50,000 U), and subcutaneously (120 U/kg) was investigated. After intravenous administration serum EPO levels decayed exponentially from a peak of 3959 mU/ml, with a half-life of 8.2 h. 2.3% of the total intravenous dose was lost in the dialysate during the first 24 h. Peak serum EPO levels of 375 mU/ml at 12 h and 176 mU/ml at 18 h were attained following intraperitoneal and subcutaneous administration, respectively. The bioavailability of subcutaneous EPO (21.5%) was seven times greater than that of intraperitoneal EPO (2.9%). These results suggest that subcutaneous EPO represents the most satisfactory route of administration for CAPD patients. [ABSTRACT FROM AUTHOR]

The article focuses on the application of therapy with iron and erythropoiesis-stimulating agents (ESA) in treating chronic kidney disease (CKD). It mentions that the serum ferritin levels in patient receiving iron supplementation must be quantitated every three months. It states that iron therapy in CKD patients should be discontinued during acute bacterial infections.

Summary: In the intravenous iron therapy to treat iron deficiency anaemia in patients undergoing major abdominal surgery (PREVENTT) trial, the use of intravenous iron did not reduce the need for blood transfusion or reduce patient complications or length of hospital stay. As part of the trial protocol, serum was collected at randomisation and on the day of surgery. These samples were analysed in a central laboratory for markers of iron deficiency. We performed a secondary analysis to explore the potential interactions between pre‐operative markers of iron deficiency and intervention status on the trial outcome measures. Absolute iron deficiency was defined as ferritin <30 μg.l−1; functional iron deficiency as ferritin 30–100 μg.l−1 or transferrin saturation < 20%; and the remainder as non‐iron deficient. Interactions were estimated using generalised linear models that included different subgroup indicators of baseline iron status. Co‐primary endpoints were blood transfusion or death and number of blood transfusions, from randomisation to 30 days postoperatively. Secondary endpoints included peri‐operative change in haemoglobin, postoperative complications and length of hospital stay. Most patients had iron deficiency (369/452 [82%]) at randomisation; one‐third had absolute iron deficiency (144/452 [32%]) and half had functional iron deficiency (225/452 [50%]). The change in pre‐operative haemoglobin with intravenous iron compared with placebo was greatest in patients with absolute iron deficiency, mean difference 8.9 g.l−1, 95%CI 5.3–12.5; moderate in functional iron deficiency, mean difference 2.8 g.l−1, 95%CI −0.1 to 5.7; and with little change seen in those patients who were non‐iron deficient. Subgroup analyses did not suggest that intravenous iron compared with placebo reduced the likelihood of death or blood transfusion at 30 days differentially across subgroups according to baseline ferritin (p = 0.33 for interaction), transferrin saturation (p = 0.13) or in combination (p = 0.45), or for the number of blood transfusions (p = 0.06, 0.29, and 0.39, respectively). There was no beneficial effect of the use of intravenous iron compared with placebo, regardless of the metrics to diagnose iron deficiency, on postoperative complications or length of hospital stay. [ABSTRACT FROM AUTHOR]

Deals with a study which established the dose of iron sucrose that can be administered as a single IV infusion in patients with renal failure. Methodology used in the study; Results and conclusion.

Abstract Aims An erythropoietin (EPO)-deficient anaemia is recognized in Type 1 diabetic patients with early nephropathy and symptomatic autonomic neuropathy (DN). The aim of this study was to determine whether the EPO response to hypoxia was deficient in order to clarify the mechanisms involved in this process. Methods Five Type 1 diabetic patients DN (age 39 (28–48) years (mean (range))) with EPO-deficient anaemia (haemoglobin, Hb 10.6 (9.5–12.0) g/dl, EPO 5.0 (3.2–6.5) IU/l) and early diabetic nephropathy (persistent proteinuria 1161.6 (130–2835) mg/day, serum creatinine 97.6 (63–123) µmol/l)) were compared with nine normal subjects (age 31 (24–39) years, Hb 13.4 (11.8–15.7) g/dl, EPO 7.6 (5.6–10.3) IU/l) and four patients with non-diabetic advanced chronic renal failure RF (proteinuria 2157.5 (571–4578) mg/day, serum creatinine 490.2 (406–659) µmol/l, Hb 10.3 (9.0–11.3) g/dl, EPO 4.6 (2.9–8.5) IU/l). The subjects were exposed to 6 h of hypoxia (inspired oxygen 11.6–12.6%) by breathing a gas mixture via a hood. Hourly serum EPO levels were measured. Results All groups showed a rise in EPO production after 2 h. The diabetic DN group achieved a similar maximal response to the normal subjects at 6 h (EPO 17.3 ± 5.4 vs. 17.8 ± 7.9 IU/l). The renal failure patients mounted an EPO response to hypoxia but at lower EPO levels. Conclusions Although the DN patients have inappropriately low EPO levels for the severity of their anaemia, they can mount an appropriate EPO response to moderate hypoxia. The mechanism underlying the EPO-deficient anaemia present in some diabetic patients remains unclear. [ABSTRACT FROM AUTHOR]

Objective: The normochromic normocytic anemia of erythropoietin (EPO) deficiency is recognized in advanced renal failure but not in early renal disease. The aim of this study was to determine whether anemia with EPO deficiency is found in type 1 diabetic patients with diabetic nephropathy in the absence of advanced renal failure and to compare them with patients with nondiabetic renal disease of similar severity.Research Design and Methods: A total of 27 type 1 diabetic patients with diabetic nephropathy (DN), defined as having persistent proteinuria (mean 1,086 mg/day [CI 120-5,1901), a serum creatinine < or = 180 micromol/l, and retinopathy, were compared with 26 nondiabetic patients with glomerulonephritis (GN) and persistent proteinuria (1,874 mg/day [349-5,005]). The Hb concentration, red cell indexes, and serum EPO levels were measured, and other causes for the anemia were excluded. The EPO values were compared with a normal reference range obtained from nondiabetic patients with a microcytic anemia. The DN patients were tested for signs of diabetic peripheral and autonomic neuropathy.Results: We found that 13 of the 27 DN patients were anemic (Hb 10.6 +/- 0.9 g/dl) in marked contrast to none of the GN patients (Hb 13.7 +/- 1.4 g/dl, P < 0.005). In the DN group, serum EPO concentrations failed to increase in response to anemia compared with the response seen in patients with microcytic anemia. Thus, the anemia of the DN group was associated with EPO deficiency. The anemic DN patients showed evidence of more severe proteinuria and diabetic neuropathy than the nonanemic DN patients.Conclusions: Anemia associated with EPO deficiency can occur early in DN before the onset of advanced renal failure, but does not normally occur in nondiabetic renal disease of similar severity. The pathogenesis requires elucidation. [ABSTRACT FROM AUTHOR]