ferric-oxide--saccharated and Inflammation

Intravenous iron is widely used to maintain adequate iron stores and prevent iron deficiency anemia in patients with chronic kidney disease, yet concerns remain about its long-term safety with respect to oxidative stress, kidney injury, and accelerated atherosclerosis, which are the subjects of this review. Three parenteral iron formulations are available for use in the United States: Iron dextran, iron gluconate, and iron sucrose. Iron dextran, especially the high molecular form, has been linked with anaphylactoid and anaphylactic reactions, and its use has been declining. A portion of intravenous iron preparations is redox-active, labile iron available for direct donation to transferrin. In vitro tests show that commonly available intravenous iron formulations have differing capacities to saturate transferrin directly: Iron gluconate > iron sucrose > iron dextran. Intravenous iron treatment produces oxidative stress, as demonstrated by increases in plasma levels of lipid peroxidation products (malondialdehyde), at a point that is much earlier than the time to peak concentration of catalytically active iron, suggesting a direct effect of iron sucrose on oxidative stress. Furthermore, iron sucrose infusion produces endothelial dysfunction that seems to peak earlier than the serum level of free iron. Intravenous iron sucrose infusion also has been shown to produce acute renal injury and inflammation as demonstrated by increased urinary albumin, enzyme (N-acetyl-beta-glucosaminidase), and cytokine (chemokine monocyte chemoattractant protein-1) excretions. Although the long-term dangers of intravenous iron are unproved, these data call for examination of effects of intravenous iron on the potential for long-term harm in patients with chronic kidney disease.

Topics: Acute Kidney Injury; Anemia, Iron-Deficiency; Animals; Atherosclerosis; Endothelium, Vascular; Ferric Compounds; Ferric Oxide, Saccharated; Glucaric Acid; Hematinics; Humans; Inflammation; Infusions, Intravenous; Iron-Dextran Complex; Oxidative Stress; Renal Dialysis; Renal Insufficiency, Chronic; Time Factors; Transferrin

Ferric iron (Fe)-carbohydrate complexes are widely used for treating Fe deficiency in patients who are unable to meet their Fe requirements with oral supplements. Intravenous Fe generally is well tolerated and effective in correcting Fe-deficient states. However, the complexing of Fe to carbohydrate polymers does not block its potent pro-oxidant effects; systemic free radical generation and, possibly, tissue damage may result. The purpose of this review is to (1) underscore the capacity of currently used parenteral Fe formulations to induce oxidative stress, (2) compare the severity of these oxidant reactions with those that result from unshielded Fe salts and with each other, and (3) speculate as to the potential of these agents to induce acute renal cell injury and augment systemic inflammatory responses. The experimental data that are reviewed should not be extrapolated to the clinical setting or be used for clinical decision making. Rather, it is hoped that the information provided herein may have utility for clinical hypothesis generation and, hence, future clinical studies. By so doing, a better understanding of Fe's potential protean effects on patients with renal disease may result.

Topics: Acute Kidney Injury; Adenosine Triphosphate; Anemia, Iron-Deficiency; Animals; Endothelial Cells; Ferric Compounds; Ferric Oxide, Saccharated; Glucaric Acid; Hematinics; Humans; Inflammation; Infusions, Intravenous; Iron Compounds; Iron-Dextran Complex; Kidney Cortex; Kidney Tubules, Proximal; Lipid Peroxidation; Mitochondria; Oxidative Stress; Renal Dialysis; Renal Insufficiency, Chronic; Tumor Necrosis Factor-alpha

Calciprotein particles (CPPs), colloidal mineral-protein nanoparticles, have emerged as potential mediators of phosphate toxicity in dialysis patients, with putative links to vascular calcification, endothelial dysfunction and inflammation. We hypothesized that phosphate binder therapy with sucroferric oxyhydroxide (SO) would reduce endogenous CPP levels and attenuate pro-calcific and pro-inflammatory effects of patient serum towards human vascular cells in vitro.. This secondary analysis of a randomised controlled crossover study compared the effect of 2-week phosphate binder washout with high-dose (2000 mg/day) and low-dose (250 mg/day) SO therapy in 28 haemodialysis patients on serum CPP levels, inflammatory cytokine/chemokine arrays and human aortic smooth muscle cell (HASMC) and coronary artery endothelial cell (HCAEC) bioassays.. In our cohort (75% male, 62 ± 12 years) high-dose SO reduced primary (amorphous) and secondary (crystalline) CPP levels {-62% [95% confidence interval (CI) -76 to -44], P < .0001 and -38% [-62 to -0.14], P < .001, respectively} compared with washout. Nine of 14 plasma cytokines/chemokines significantly decreased with high-dose SO, with consistent reductions in interleukin-6 (IL-6) and IL-8. Exposure of HASMC and HCAEC cultures to serum of SO-treated patients reduced calcification and markers of activation (IL-6, IL-8 and vascular cell adhesion protein 1) compared with washout. Serum-induced HASMC calcification and HCAEC activation was ameliorated by removal of the CPP-containing fraction from patient sera. Effects of CPP removal were confirmed in an independent cohort of chronic kidney disease patients.. High-dose SO reduced endogenous CPP formation in dialysis patients and yielded serum with attenuated pro-calcific and inflammatory effects in vitro.

Topics: Cross-Over Studies; Cytokines; Female; Humans; Inflammation; Interleukin-6; Interleukin-8; Male; Phosphates; Renal Dialysis; Vascular Calcification

Haemodialysis induces endothelial dysfunction by oxidation and inflammation. Intravenous iron administration during haemodialysis could worsen endothelial dysfunction. The aim of this study was to ascertain if iron produces endothelial dysfunction and the possible neutralizing effect of N-acetylcysteine when infused before iron. The oxidative and inflammatory effects of iron during haemodialysis were also assessed.. Forty patients undergoing haemodialysis were studied in a randomized and cross-over design with and without N-acetylcysteine infused before iron sucrose (50 or 100 mg). Plasma Von Willebrand factor (vWF), soluble intercellular adhesion molecule-1 (sICAM-1) levels, malondialdehyde, total antioxidant capacity, CD11b/CD18 expression in monocytes, interleukin (IL)-8 in monocytes and plasma IL-8 were studied at baseline and during haemodialysis.. Haemodialysis produced significant (P < 0.001) increase in plasma vWF, sICAM-1, malondialdehyde, IL-8 and CD11b/CD18 expression in monocytes, as well as decrease in total antioxidant capacity. Iron induced significant increase in plasma malondialdehyde and IL-8 in monocytes, but had no effect on total antioxidant capacity, CD11b/CD18 expression, plasma IL-8, vWF and sICAM-1. The addition of N-acetylcysteine to 50 mg of iron produced a significant (P = 0.040) decrease in malondialdehyde.. Standard (100 mg) and low (50 mg) doses of iron during haemodialysis had no effects on endothelium. Iron only had minor effects on inflammation and produced an increase in oxidative stress, which was neutralized by N-acetylcysteine at low iron dose. Haemodialysis caused a significant increase in oxidative stress, inflammation and endothelial dysfunction markers.

Topics: Acetylcysteine; Aged; Antioxidants; Biomarkers; CD11b Antigen; CD18 Antigens; Cross-Over Studies; Endothelium, Vascular; Female; Ferric Compounds; Ferric Oxide, Saccharated; Glucaric Acid; Hematinics; Humans; Inflammation; Inflammation Mediators; Infusions, Intravenous; Intercellular Adhesion Molecule-1; Interleukin-8; Male; Malondialdehyde; Middle Aged; Oxidative Stress; Prospective Studies; Renal Dialysis; Time Factors; Treatment Outcome; von Willebrand Factor

The iron-based phosphate binders, sucroferric oxyhydroxide (SFOH) and ferric citrate (FC), effectively lower serum phosphorus in clinical studies, but gastrointestinal iron absorption from these agents appears to differ. We compared iron uptake and tissue accumulation during treatment with SFOH or FC using experimental rat models.. Iron uptake was evaluated during an 8-h period following oral administration of SFOH, FC, ferrous sulphate (oral iron supplement) or control (methylcellulose vehicle) in rat models of anaemia, iron overload and inflammation. A 13-week study evaluated the effects of SFOH and FC on iron accumulation in different organs.. In the pharmacokinetic experiments, there was a minimal increase in serum iron with SFOH versus control during the 8-h post-treatment period in the iron overload and inflammation rat models, whereas a moderate increase was observed in the anaemia model. Significantly greater increases (P < 0.05) in serum iron were observed with FC versus SFOH in the rat models of anaemia and inflammation. In the 13-week iron accumulation study, total liver iron content was significantly higher in rats receiving FC versus SFOH (P < 0.01), whereas liver iron content did not differ between rats in the SFOH and control groups.. Iron uptake was higher from FC versus SFOH following a single dose in anaemia, iron overload and inflammation rat models and 13 weeks of treatment in normal rats. These observations likely relate to different physicochemical properties of SFOH and FC and suggest distinct mechanisms of iron absorption from these two phosphate binders.

Topics: Administration, Oral; Anemia; Animals; Drug Combinations; Female; Ferric Compounds; Inflammation; Iron; Iron Overload; Kinetics; Male; Rats; Rats, Sprague-Dawley; Rats, Wistar; Sucrose; Tissue Distribution

According to recent clinical trial data, correction of iron deficiency with intravenous (i.v.) iron has favorable outcomes on cardiac function. We evaluated whether i.v. iron treatment of anemic rats has favorable effect on the left ventricular (LV) performance and remodeling and the role of oxidative/nitrosative stress and inflammation in the process.. After weaning, Sprague-Dawley rats were fed low iron diet for 16weeks, after which the treatment group received five weekly doses of i.v. iron sucrose (10mg Fe/kg body weight). Echocardiography of LV was performed and hematology parameters were assessed before treatment (baseline, day 0) and at the end of the study (day 29). On day 29, rats were sacrificed and extracellular expansion and fibrosis in LV and interventricular septum were evaluated together with oxidative/nitrosative stress, pro-inflammatory, and repair process markers.. Although iron sucrose treatment did not fully correct the anemia, it reversed anemia-induced cardiac remodeling as indicated by echocardiographic and tissue Doppler parameters. Treatment with iron sucrose also prevented anemia-induced myocardial fibrosis as indicated by extracellular expansion and fibrosis markers. Anemia-induced inflammation was prevented by iron sucrose as indicated by the levels of proinflammatory (TNF-α, NF-κB65) and repair process markers (HSP27, HSP70). In addition, iron sucrose treatment significantly reduced (p<0.01) anemia-induced oxidative and nitrosative stress.. Intravenous iron sucrose treatment reversed anemia-induced remodeling of LV, prevented myocardial fibrosis, and improved cardiac function by attenuating oxidative/nitrosative stress and inflammation in the heart.

Topics: Anemia; Animals; Cardiotonic Agents; Ferric Compounds; Ferric Oxide, Saccharated; Fibrosis; Glucaric Acid; Inflammation; Infusions, Intravenous; Male; Myocardium; Oxidative Stress; Rats; Rats, Sprague-Dawley; Tyrosine; Ventricular Remodeling

The aim of this study was to determine the influence of inflammatory markers, predictive values of CRP and target hemoglobin (Hb) in patients on chronic hemodialysis.. Made is a cross-sectional study of inflammatory agents serum levels-CRP, fibrinogen and ferritin before hemodialysis in 114 patients divided into two groups according to the achieved or unachieved target hemoglobin level in the Cantonal Hospital in Zenica.. The 57 patients (test group) did not reached the target hemoglobin in the range from 10-12 g/dl and CRP values were significantly higher compared to the control group (57 patients) who had reached targeted hemoglobin values. Levels of fibrinogen and ferritin were not significantly different between the control and the test group. CRP values are in negative correlation with the Hb concentration, while fibrinogen and ferritin values had a positive correlation. Significant negative correlation was only found in case of CRP, respectively, higher CRP was at lower levels of blood Hb. It was found that the predictive value of CRP is 6.5 mg/L to achieve target Hb level. If the CRP increases by 1 mg/L, possibilities to achieve the target Hb level in dialysis patients is reduced by 7.5%, with a sensitivity of 51% and specificity of 77%. Ferritin was elevated due to iatrogenic iron saturation, because all patients received intravenous iron and was treated with erythropoietin. By identification and analysis of inflammatory agents and duration ofhemodialysis, are explored the primary influence on hematopoiesis, of course, with the primary application of erythropoietin and adjuvant agents. It has been shown that CRP alone has an impact on the target Hb level, depending on the hemodialysis duration.. The research results show how what looks as routine findings may be helpful in the timely detection of threatening complications and their treatment, and provide extended and improved quality of life for patients on hemodialysis.

Topics: Aged; Anemia; Biomarkers; C-Reactive Protein; Case-Control Studies; Cross-Sectional Studies; Erythropoietin; Female; Ferric Compounds; Ferric Oxide, Saccharated; Ferritins; Fibrinogen; Glucaric Acid; Hemoglobins; Humans; Inflammation; Kidney Failure, Chronic; Male; Middle Aged; Predictive Value of Tests; Renal Dialysis; ROC Curve; Sucrose

Iron sucrose originator (IS(ORIG)) has been used to treat iron deficiency and iron deficiency anemia for decades. Iron sucrose similars (ISSs) have recently entered the market. In this non-clinical study of non-anemic rats, five doses (40 mg iron/kg body weight) of six ISSs marketed in Asian countries, IS(ORIG) or saline solution (control) were administered intravenously over four weeks to compare their toxicologic effects. Vasodilatory effects, impaired renal function and hepatic damage were only observed in the ISS groups. Significantly elevated serum iron and transferrin saturation levels were observed in the ISS groups suggesting a higher release of iron resulting in higher amounts of non-transferrin bound (free) iron compared to IS(ORIG). This might explain the elevated oxidative stress and increased levels of inflammatory markers and antioxidant enzymes in the liver, heart and kidneys of ISS-treated animals. Physico-chemical analyses showed that the molecular structure of most of the ISSs differed greatly from that of the IS(ORIG). These differences may be responsible for the organ damage and oxidative stress observed in the ISS groups. Significant differences were also found between different lots of a single ISS product. In contrast, polarographic analyses of three different IS(ORIG) lots were identical, indicating that the molecular structure and thus the manufacturing process for IS(ORIG) is highly consistent. Data from this study suggest that ISSs and IS(ORIG) differ significantly. Therefore, before widespread use of these products it would be prudent to evaluate additional non-clinical and/or clinical data proving the safety, therapeutic equivalence and interchangeability of ISSs with IS(ORIG).

Topics: Anemia, Iron-Deficiency; Animals; Disease Models, Animal; Female; Ferric Compounds; Ferric Oxide, Saccharated; Glucaric Acid; Inflammation; Male; Oxidative Stress; Rats; Rats, Sprague-Dawley

The majority of murine models of iron sucrose-induced iron overload were carried out in adult subjects. This cannot reflect the high risk of iron overload in children who have an increased need for iron. In this study, we developed four experimental iron overload models in young rats using iron sucrose and evaluated different markers of iron overload, tissue oxidative stress and inflammation as its consequences. Iron overload was observed in all iron-treated rats, as evidenced by significant increases in serum iron indices, expression of liver hepcidin gene and total tissue iron content compared with control rats. We also showed that total tissue iron content was mainly associated with the dose of iron whereas serum iron indices depended essentially on the duration of iron administration. However, no differences in tissue inflammatory and antioxidant parameters from controls were observed. Furthermore, only rats exposed to daily iron injection at a dose of 75 mg/kg body weight for one week revealed a significant increase in lipid peroxidation in iron-treated rats compared with their controls. The present results suggest a correlation between iron overload levels and the dose of iron, as well as the duration and frequency of iron injection and confirm that iron sucrose may not play a crucial role in inflammation and oxidative stress. This study provides important information about iron sucrose-induced iron overload in rats and may be useful for iron sucrose therapy for iron deficiency anemia as well as for the prevention and diagnosis of iron sucrose-induced iron overload in pediatric patients.

Topics: Animals; Antimicrobial Cationic Peptides; Biomarkers; Disease Models, Animal; Dose-Response Relationship, Drug; Ferric Compounds; Ferric Oxide, Saccharated; Gene Expression; Glucaric Acid; Hepcidins; Humans; Inflammation; Iron; Iron Overload; Lipid Peroxidation; Liver; Oxidative Stress; Rats; Serum; Time Factors

Intravenous (i.v.) iron is associated with a risk of oxidative stress. The effects of ferumoxytol, a recently approved i.v. iron preparation, were compared with those of ferric carboxymaltose, low molecular weight iron dextran and iron sucrose in the liver, kidneys and heart of normal rats. In contrast to iron sucrose and ferric carboxymaltose, low molecular weight iron dextran and ferumoxytol caused renal and hepatic damage as demonstrated by proteinuria and increased liver enzyme levels. Higher levels of oxidative stress in these tissues were also indicated, by significantly higher levels of malondialdehyde, significantly increased antioxidant enzyme activities, and a significant reduction in the reduced to oxidized glutathione ratio. Inflammatory markers were also significantly higher with ferumoxytol and low molecular weight iron dextran rats than iron sucrose and ferric carboxymaltose. Polarographic analysis suggested that ferumoxytol contains a component with a more positive reduction potential, which may facilitate iron-catalyzed formation of reactive oxygen species and thus be responsible for the observed effects. Only low molecular weight iron dextran induced oxidative stress and inflammation in the heart.

Topics: Animals; Antioxidants; Blood Pressure; Creatinine; Female; Ferric Compounds; Ferric Oxide, Saccharated; Ferrosoferric Oxide; Glucaric Acid; Heart; Hematinics; Immunohistochemistry; Inflammation; Injections, Intravenous; Iron-Dextran Complex; Kidney; Lipid Peroxidation; Liver; Magnetite Nanoparticles; Male; Maltose; Molecular Weight; Oxidative Stress; Proteinuria; Rats; Rats, Sprague-Dawley

The physicochemical characteristics of intravenous iron complexes affect the extent of weakly-bound iron and thus the degree of oxidative stress. The new preparation iron isomaltoside 1000 (IIM) was compared to iron sucrose (IS) and a control group in terms of biochemistry, oxidative stress, inflammatory markers and iron deposition in the liver, heart and kidneys of healthy rats. Renal function was significantly impaired in the IIM group versus both IS and controls. Liver enzymes were also significantly higher in IIM-treated animals versus the other groups, indicative of hepatic injury. Systolic blood pressure was significantly lower following IIM administration compared to IS or control animals. Oxidative stress in the liver, heart and kidneys was greater in the IIM group, as indicated by significantly increased levels of malondialdehyde and antioxidant enzyme activity, accompaniedby a significantly lower ratio of reduced to oxidized glutathione. Microscopy demonstrated more extensive positive staining for iron, and a smaller area of ferritin staining, in the liver, heart and kidneys of rats treated with IIM versus IS.Levels of the inflammatory markers TNF-alpha and IL6 were both significantly higher in the IIM group versus IS in all assessed tissues. These findings indicate that IIM has a less favorable safety profile than IS in healthy rats, adversely affecting iron deposition, oxidative stress and inflammatory responses, with impaired liver and renal function.

Topics: Animals; Biomarkers; Blood Pressure; Creatinine; Disaccharides; Ferric Compounds; Ferric Oxide, Saccharated; Ferritins; Glucaric Acid; Hemoglobins; Immunohistochemistry; Inflammation; Injections, Intravenous; Iron; Iron-Dextran Complex; Kidney; Liver; Liver Function Tests; Male; Molecular Weight; Myocardium; Oxidative Stress; Rats; Rats, Sprague-Dawley

Iron sucrose (Venofer; reference) has a good safety record and is prescribed in patients with anaemia and chronic kidney disease worldwide, but various iron sucrose similar (ISS) preparations are now utilized in clinical practice. This study evaluates possible differences between iron sucrose and ISS preparations on haemodynamic and oxidative stress markers in normal rats. 60 male and 60 female Sprague Dawley rats were divided into four groups and assigned to receive commercially available ISS test 1, ISS test 2, reference or isotonic saline solution (control). A single i.v. dose of iron (40 mg/kg) or saline (equivalent volume) was administered after 24 h and every 7 days for 4 weeks. Blood samples were collected for biological assessment of haemoglobin (Hb), serum iron and percentage transferrin saturation (TSAT), and urine samples were collected to investigate creatinine clearance and proteinuria. Animals were sacrificed after receiving an i.v. dose on days 1, 7 and 28, and kidney, liver, and heart homogenates were then collected to determine antioxidant enzyme levels. Tissues were processed using Prussian blue and immmunohistochemistry techniques to identify iron deposits, tissue ferritin and pro-inflammatory markers. Systolic blood pressure was significantly reduced in the ISS groups relative to the reference and control groups after 24 h and on days 7, 14 and 21 (p < 0.05). Creatinine clearance was reduced (p < 0.01) and proteinuria marked (p < 0.01) in the ISS groups at 24 h and on days 7 and 28 relative to the reference and control groups which did not differ throughout the study. Liver enzymes were also increased in the ISS groups at 24 h and on days 7 and 28. Both ISS test 1 and ISS test 2 groups presented a significant increase in catalase, thiobarbituric reactive species, Cu, Zn-superoxide dismutase (CuZnSOD) and glutathione peroxidase activity, and a decrease in glutathione levels (p < 0.01) in the liver, heart and kidney at 24 h and on day 7 relative to the reference and control groups. Serum iron and percentage TSAT were elevated in all groups (except control) (p < 0.01) but no differences in Hb concentration were observed between them. Finally, levels of the proinflammatory markers TNF-alpha and IL6 were significantly elevated in the ISS groups (liver, heart and kidney) compared with the reference and control groups on day 28 (p < 0.01). These findings suggest significant differences between the reference and ISS test 1/ISS test 2 regarding

Topics: Animals; Biomarkers; Blood Pressure; Chemistry, Pharmaceutical; Creatinine; Female; Ferric Compounds; Ferric Oxide, Saccharated; Ferritins; Glucaric Acid; Heart; Hematinics; Hemodynamics; Immunohistochemistry; Inflammation; Injections, Intravenous; Kidney; Liver; Male; Myocardium; Oxidative Stress; Proteinuria; Rats; Rats, Sprague-Dawley

Inflammation is a central component of progressive chronic kidney disease (CKD). Iron promotes oxidative stress and inflammatory response in animals and promotes progressive CKD. Parenteral iron provokes oxidative stress in patients with CKD; however, its potential to provoke an inflammatory response is unknown. In 20 veterans with CKD, 100 mg iron sucrose was administered intravenously over 5 min and urinary excretion rate and plasma concentration of monocyte chemoattractant protein-1 (MCP-1) were measured at timed intervals over 24 h. Patients were then randomized to placebo or N-acetyl cysteine (NAC) 600 mg b.i.d. and the experiment was repeated at 1 week. Iron sucrose markedly increased plasma concentration and urinary excretion rate of MCP-1 at baseline and at 1 week visits (P < 0.0001 for time effect). Urinary excretion peaked at 30 min and plasma concentration at 15 min. Plasma MCP-1 concentration fell from 164 +/- 17.7 to 135 +/- 17.7 pg/ml with NAC, whereas it remained unchanged from 133 +/- 12.5 to 132 +/- 17.7 pg/ml with placebo (P=0.001 for visit x antioxidant drug interaction). There was a reduction in MCP-1 urinary excretion rate from visit 1 to 2. At the baseline visit, the urinary excretion rate averaged 305 +/- 66 pg/min and at the second visit 245 +/- 67 pg/min (mean difference 60 +/- 28 pg/min, P = 0.030). There was no improvement in urinary MCP-1 excretion with NAC. In conclusion, iron sucrose causes rapid and transient generation and/or release of MCP-1 plasma concentration and increases urinary excretion rate, and systemic MCP-1 level but the urinary excretion rate is not abrogated with the antioxidant NAC. These results may have implications for the progression of CKD with parenteral iron.

Topics: Aged; Chemokine CCL2; Chronic Disease; Ferric Compounds; Ferric Oxide, Saccharated; Glucaric Acid; Humans; Inflammation; Kidney Diseases; Kidney Failure, Chronic; Reproducibility of Results

Oxidative stress and inflammation contribute to the high prevalence and severity of atherosclerosis, infections, and beta2-microglobulin amyloidosis; and thus, to reduced survival rate and quality of life in hemodialysis (HD) patients. Inflammation induces oxidative stress by production of the oxidants: superoxide anion, hydrogen peroxide, and hypochlorite. Intravenous iron (IVIR), administered in HD patients to correct anemia, can release free iron, that may react with hydrogen peroxide to produce the strong oxidant hydroxyl radical. Inflammation-induced lipid and protein oxidation and IVIR-induced lipid oxidation were shown in HD patients. However, IVIR-induced protein oxidation and a relationship between inflammation and IVIR-induced oxidative stress have not been reported to date.. We examined the effect of IVIR administration on markers of protein oxidation in HD patients (advanced oxidation protein products [AOPPs], thiol, and dityrosine) in relation to such inflammatory markers as C-reactive protein (CRP) and tumor necrosis factor-alpha (TNF-alpha). Iron saccharate, 100 mg, was administered to 19 HD patients for 1 hour after 3.5 hours of high-flux dialysis. Blood samples were drawn pre-HD, pre-IVIR, and post-IVIR for iron, transferrin, TNF-alpha, AOPP, thiol, total antioxidant capacity (TEAC), and dityrosine levels and pre-HD for ferritin and CRP levels.. IVIR administration induced a 37% increase in AOPP level (P < 0.001), which correlated positively with pre-HD CRP level (r = 0.72; P < 0.05) and was greater in patients with a greater pre-HD TNF-alpha level (P < 0.05). IVIR administration did not affect TEAC, thiol, dityrosine, or TNF-alpha levels.. IVIR administration induced an increase in protein oxidation (AOPP levels) that was related to the degree of inflammation.

Topics: Aged; Aged, 80 and over; Blood Proteins; Female; Ferric Compounds; Ferric Oxide, Saccharated; Glucaric Acid; Glycation End Products, Advanced; Humans; Inflammation; Infusions, Intravenous; Male; Middle Aged; Oxidation-Reduction; Oxidative Stress; Renal Dialysis; Sodium Chloride; Sucrose