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NDT Advance Access published online on February 13, 2007
Nephrology Dialysis Transplantation, doi:10.1093/ndt/gfm005
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© The Author [2007]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Two different modalities of iron gluconate i.v. administration: effects on iron, oxidative and inflammatory status in peritoneal dialysis patients

Amedeo F. de Vecchi1, Cristina Novembrino2, Silvia Lonati2, Silvia Ippolito2 and Fabrizia Bamonti2

1UO Nefrologia, Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena, Fondazione IRCCS, Milano and 2Department Scienze Mediche, Università degli Studi, Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena, Fondazione IRCCS, Milano, Italy

Correspondence and offprint requests to: Dr De Vecchi, Amedeo, Divisione di Nefrologia e Dialisi, Milano 20122, Italy. Email: deveccpd{at}policlinico.mi.it



   Abstract
Top
 Abstract
Introduction
 Subjects and methods
 Results
 Discussion
 Acknowledgements
 References
 
Background. Iron deficiency represents an important problem for dialysis patients. Oral iron administration is frequently ineffective, requiring parenteral administration, which may trigger severe side effects due to inflammation and/or peroxidation. The aim of the present study was to clarify the effects of parenteral iron administration on iron, inflammatory and oxidative status in peritoneal dialysis patients and compare two different modalities of injecting ferric gluconate intravenously.

Methods. Twenty peritoneal dialysis patients (10M/10F, mean age 60 ± 16 years) were given i.v. iron gluconate (62.5 mg) both concentrated (1–2 min, PULSE) and diluted in 100 ml of glucose solution (30 min, SLOW). The interval between the first and second administration was 15–60 days. Blood cell count, serum iron, total iron binding capacity (TIBC), ferritin, C-reactive protein (CRP), reactive oxygen species (ROS) concentrations and total antioxidant capacity (TAC) were measured before iron infusion (T0), after 30 min (T1) and after 24 h (T2).

Results. No patient had clinical symptoms during or within an hour of iron administration. Serum transferrin was oversaturated in 25% of cases, no matter how iron was injected. Oxidative and inflammatory status parameters were not affected by iron administration: no difference in CRP, ROS concentrations or TAC was found at any time between PULSE and SLOW group.

Conclusions. Our findings showed that neither inflammation nor peroxidation in peritoneal dialysis patients was clinically triggered by 62.5 mg i.v. iron infusion. Both modalities were equally safe. Therefore, in the absence of clinical side effects, PULSE intravenous administration, being cheaper and not so problematic for outpatients, is preferable to SLOW.

Keywords: inflammation; intravenous iron; oxidative stress; peritoneal dialysis



   Introduction
Top
 Abstract
 Introduction
Subjects and methods
 Results
 Discussion
 Acknowledgements
 References
 
Iron deficiency is a common problem occurring in chronic renal insufficiency and in dialysis patients. When oral iron replacement is inadequate, parenteral iron administration is unavoidable. Different iron compounds are available for parenteral administration [1]. In particular, iron sucrose and ferric gluconate are the most frequently used iron compounds [2–4].

The iron preparations are effective, but not free from side effects and potential long term toxicity: anaphylactic shock is the most serious and life-threatening complication, but other symptoms may occur such as hypotension, gastrointestinal disorders, malaise, flushing, loin pain and paraesthesia [3–5]. High molecular weight iron dextrane is associated with a higher incidence of side effects [6,7]. However, some authors reported serious adverse events related to i.v. administration of iron gluconate or saccarate [3,4,8,9].

Low serum concentrations of transferrin are often observed in dialysis patients, perhaps as a consequence of inadequate protein intake and/or protein loss [10]. Intravenous iron administration may therefore lead to oversaturation and release of molecular iron which, when present in large amounts, may trigger inflammation cascade, hyperoxidative mechanisms and endothelial damage [11]. In addition, chronic iron infusion and the presence of free iron molecules have been reported to increase oxidation and inflammation and worsen cardiovascular prognosis [11,12].

In the last few years, however, few studies have been performed to assess the mechanisms and risk of these complications in patients with chronic renal failure. The majority of authors investigated the acute effect of an iron injection immediately after a haemodialysis session [12,13]. It is known that haemodialysis itself tends to trigger several proinflammatory and prooxidative mechanisms [14] thus masking the possible effect of iron administration on oxidation and inflammation.

In peritoneal dialysis patients, the attention was focused on the effects of high doses of intravenous iron, in order to reduce the number of injections [15,16], while other authors suggested frequent administration of low iron doses [17].

Iron can be administered intravenously either in a single ‘bolus’ of undiluted drug (2–10 min) or diluted in 100 ml of saline (approximately 30 min). The latter is more expensive and troublesome for the patient, but it is supposed to be the safer way even if this is not established and there are not enough, convincing data on this subject. In fact, at present it is unclear which approach is safer. The pros and cons of each modality, therefore, need to be compared and carefully weighed before deciding which is the more suitable method of the two.

The aim of the present study was to clarify the effects of parenteral iron administration on iron, inflammatory and oxidative status in peritoneal dialysis patients and compare two different modalities of injecting standard dose (62.5 mg) ferric gluconate intravenously.



   Subjects and methods
Top
 Abstract
 Introduction
 Subjects and methods
Results
 Discussion
 Acknowledgements
 References
 
Eligibility criteria
Continuous peritoneal dialysis (CAPD) as first treatment and for over 3 months, age 18–80 years, plasma haemoglobin <12 g/dl, no active immunological disease or neoplasm, and previous treatment with intravenous iron infusions were the inclusion criteria for this study.

Exclusion criteria
Excluded from the study were those with anaemia requiring blood transfusions, known hypersensitivity to iron gluconate, local or systemic infection during the 2 months preceding the study, and aluminium intoxication (>80 µg/dl after desferrioxamine test).

Out of 60 patients, 20 (10 men and 10 women), on CAPD for 31.3 ± 33.9 months at the Nephrology Unit of Ospedale Policlinico of Milan (mean age 60 ± 16 years, range 22–80), accepted to participate in the present study and signed their informed consent. Peritoneal dialysis was performed with 2–4 daily exchanges 2–2.5 l each. Fourteen patients were given intravenous or subcutaneous alpha or beta erythropoietin shots (2000–6000 U/week, mean 3800 ± 2200 U/week).

Patients were randomly divided into two groups: the first one (PULSE: 10 patients) was assigned to receive as the first treatment a single i.v. iron gluconate injection (62.5 mg) as a rapid undiluted push in 1–2 min. The second group (SLOW: 10 patients) was given iron first as a 30-min infusion after dilution of iron into 100 ml of saline. Then the study followed a crossover design and each patient received another iron i.v. injection by the other modality, 15–60 days after the first injection, according to need and standard intervals between visits.

Peripheral venous blood samples were drawn before iron administration (baseline, T0) and 30 min (T1) and 24 h (T2) after iron infusion. Two blood specimens from each subject were collected each time into pre-evacuated tubes, either plain for serum determinations or containing EDTA. Serum aliquots were used for measuring iron concentrations, total iron binding capacity (TIBC), ferritin (Ferr), C-reactive protein (CRP) and reactive oxygen species (ROS) concentrations and total antioxidant capacity (TAC). EDTA whole blood was used for a complete blood count (Coulter counter model STKS). All the aliquots, except the one for blood count, were frozen after separation and stored at –20°C until assayed.

Serum iron and TIBC concentrations were measured with colorimetric tests, SERA-PAK Iron and SERA-PAK Iron-Binding Capacity (Bayer Corporation, Tarrytown, NY, USA), respectively. The percentage of transferrin saturation (TSAT) was calculated as follows: TSAT = serum iron/TIBC x 100%. Serum ferritin concentrations were determined by immunoenzymatic method using a commercial kit (IMx Ferritin, Abbott Laboratories, Abbott Park, IL, USA) on IMx analyser (Abbott). Serum ROS concentrations and TAC were measured by spectrophotometric method using commercial kits (dROMs and OXY-Adsorbent test, respectively, Diacron, Grosseto, Italy) on F.R.E.E. analyser (Diacron) [18]. Briefly, the dROMs test measures serum ROS levels taking advantage of the ability of these molecules to generate free radicals in the presence of transition metals (Fe, Cu, etc.) acting as catalyser. When free radicals react with a correctly buffered chromogenic substance, they develop a coloured complex that can be measured photometrically. The concentration of the coloured complex is proportional to ROS concentration. CRP levels were determined by means of a highly sensitive ELISA test on microtitre (Zymutest CRP, Hyphen BioMed, France) on EASIA Reader (Medgenix Diagnostic, Belgium).

Data are reported as mean ± SD. Statistical evaluation was performed by Student's t-test for paired data.



   Results
Top
 Abstract
 Introduction
 Subjects and methods
 Results
Discussion
 Acknowledgements
 References
 
No patient complained of any clinical side effect during or after i.v. iron administration, regardless of administration method, either slow i.v. infusion of diluted iron or rapid i.v. bolus of undiluted compound.

As shown in Table 1, serum iron and TSAT increased significantly 30 min after i.v. iron infusion, irrespective of injection modality. In 25% of patients from each group, TSAT increased to more than 100%. Twenty-four hours after infusion, serum iron concentrations did not differ significantly from baseline in either group. TSAT returned to basal values after a rapid iron injection in the PULSE group, while it maintained slightly higher values (P < 0.05) than baseline in the SLOW group. No significant changes were observed in Ferr and haemoglobin levels after either method of administration (Table 1).


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  		Table 1. Comparison between two different modalities of iron injection (PULSE and SLOW infusion). Markers of iron status and haemoglobin concentrations in 20 patients on peritoneal dialysis, before (T0) and 30 min (T1) and 24 h (T2) after a 62.5 mg i.v. injection of iron gluconate (results are expressed as mean ± SD).

 
The effects of both modalities of iron administration on oxidative and inflammatory status markers are reported in Table 2. Mean ROS concentrations and TAC, at baseline, were almost within reference interval in both groups. In both groups, mean concentrations of ROS and TAC were almost unchanged both immediately after iron infusion and 24 h later. The percentage of patients with abnormally high ROS and lower TAC values did not increase after rapid iron injection, while the percentage of those with low TAC values increased slightly after slow iron infusion (from 30 to 40% at T2).


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  		Table 2. Comparison between two different modalities of iron injection (PULSE and SLOW infusion). Markers of oxidative (ROS and TAC) and inflammation (CRP) status in 20 patients on peritoneal dialysis, before (T0) and 30 min (T1) and 24 h (T2) after a 62.5 mg i.v. injection of iron gluconate (results are expressed as mean ± SD).

 
Mean CRP concentrations, at T0, were within the reference interval, even if CRP values were above reference interval in 20% of PULSE and 15% of SLOW patients. No changes in CRP levels were observed after either modality of iron infusion.

In order to increase statistical power and exclude possible effects of i.v. iron on inflammation and oxidation, we reanalysed ROS, TAC and CRP in all patients irrespective of iron infusion modality and again no significant difference was evaluated at any time. Mean ROS concentrations were: 309 ± 112 UCarr at T0, 307 ± 112 UCarr at T1 and 299 ± 90 UCarr at T2; mean TAC was: 364 ± 84 µmolHClO/ml at T0, 351 ± 82 µmolHClO/ml at T1 and 347 ± 77 µmolHClO/ml at T2; mean CRP levels were 4.3 ± 4.3 mg/l at T0, 4.2 ± 4.2 mg/l at T1 and 4.1 ± 4.2 mg/l at T2.



   Discussion
Top
 Abstract
 Introduction
 Subjects and methods
 Results
 Discussion
Acknowledgements
 References
 
Intravenous iron administration might affect inflammation and oxidation in pre-dialysis or haemodialysis patients [12,19]. However, most data relate to the effects of iron dextrane but, as far as we know, there are not many data on the effects of iron gluconate or saccharate on peritoneal dialysis patients, who frequently need i.v. iron administration.

In our study, peritoneal dialysis patients proved to be useful ‘models’ for investigating iron prooxidant and inflammatory effects because they are free from the possible influence of haemodialysis sessions on endothelial function and/or inflammation. We gave our patients ferric gluconate (the only available i.v. iron compound in our hospital). We decided to give a relatively small iron dose as PD patients do not lose any blood during dialysis and therefore require small amounts of parenteral iron. Based on our experience, we consider 62.5 mg every 1–2 weeks a suitable dose to maintain adequate iron balance. After iron infusion, TSAT increased to >100% in 25% of patients. Considering that available methods are unable to discriminate between drug-bound and free iron [20], these data are probably overestimated. In our unpublished experience in PD, the use of high-dose iron gluconate (250 mg given in 2-h i.v. infusion after dilution in 250 ml with isotonic glucose solution) caused large oversaturation of transferrin in all patients, with frequent and severe side effects, such as hypotension, gastrointestinal disturbances and dizziness. We therefore consider 62.5 mg every 1–2 weeks a suitable dose to maintain adequate iron balance with few side effects.

The balance between ROS and TAC was evaluated in order to find out whether parenteral iron administration had caused oxidative stress. These parameters were chosen instead of a specific oxidation marker or a single antioxidant, in order to obtain a more comprehensive ‘view’ of oxidative status in all patients. Even if at the beginning of the study the markers analysed were altered in a number of patients, CAPD patients did not present important changes in their oxidative status. Moreover, our results showed that oxidative status did not change after iron infusion.

A high-sensitivity test was used to detect any small variation in CRP levels in order to evaluate inflammatory status, which, in the majority of patients, was within the reference interval and unaltered by i.v. iron administration.

A review by Himmelfarb [21] suggests that, in uraemic patients, i.v. iron exposure contributes to increased oxidative stress. Increased albumin oxidation was observed by Anraku et al. [22] in haemodialysis patients after ferric saccharate injections at the end of dialysis sessions. Similar to what occurs after dialysis sessions without iron administration, no transferrin oversaturation or any increased peroxide activity in haemodialysis patients treated with 100 mg iron saccharate injection was reported by Scheiber-Mojdehkar et al. [23]. An additional increase in total DNA damage and malondialdehyde concentrations was observed by Muller et al. in patients receiving 62.5 mg ferric gluconate infusion during haemodialysis sessions [24], while an improvement in erythrocyte deformability and no prooxidant effect was reported by Cavdar et al. [13] after iron saccharate injections at the end of haemodialysis sessions. No change in markers of endothelial injury after i.v. iron saccharate injections was observed by Borawski et al. in patients with chronic renal failure [25]. In HD patients [26], no changes in carbonylated fibrinogen were observed after 62.5 mg ferric gluconate injection, while plasma carbonylated fibrinogen significantly increased in the same patients after the injection of 125 mg iron.

It is difficult to explain these differences, which might be caused by differences in iron doses, in oxidative stress markers and in sensitivity and specificity of the laboratory methods used. Moreover, different degrees of inflammation and oxidation may be caused by different dialysis techniques.

The other aim of our study was to compare the effects of the two different modalities of injecting iron. Both techniques rapidly increased iron and transferrin saturation, which decreased to pre-injection levels after 24 h, when transferrin saturation was still significantly higher than at baseline only in the SLOW group. Statistical significance is borderline and difference is minimal, thus minimizing the possible clinical relevance of this result. Oxidative balance was not in any way impaired either by rapid pulse or slow infusion. No differences in CRP levels, ROS concentrations and TAC were reported between the two groups at any time. A similar protocol of both slow and pulse iron saccharate injections was performed in haemodialysis patients; the results showed no changes in malondialdehyde levels when evaluated as thiobarbituric acid-reactive substances [27]. Interestingly, a similar incidence of transferrin oversaturation and free iron level was observed by these authors in both rapid and slow infusion groups. Two other articles reported clinical effects of iron in non-dialysis-dependent patients with chronic renal insufficiency. Prospective evaluation of 2297 pulse injections of 200 mg iron sucrose highlighted seven reversible anaphylactoid reactions and other mild undesired side effects (lethargy, gastrointestinal disturbances, light headedness) [4]. In another study, van Wyck et al. [3] observed severe side effects in 2/30 patients after slow 500 mg iron sucrose injection over 4 h and in 1/60 after 200 mg pulse injection.

In conclusion, neither rapid pulse nor slow i.v. iron gluconate injections were found to have any negative effects on inflammatory and oxidative status. According to our results, it is reasonable to assume that both methods of i.v. iron administration (62.5 mg of iron gluconate) are equally safe, at least with regard to the effects on oxidation and inflammation. Pulse i.v. administration is cheaper and not so problematic for outpatients and could therefore be chosen for peritoneal dialysis patients instead of slow administration.



   Acknowledgements
Top
 Abstract
 Introduction
 Subjects and methods
 Results
 Discussion
 Acknowledgements
References
 
The authors are very grateful to Mrs Mary Coduri for linguistic consultation and to Dr Anita Boddie for helpful advice.

Conflict of interest statement. The authors have declared no conflict of interest and the sole support was a grant to F.B. from the Ministero Università e Ricerca Scientifica Tecnologica, Rome, Italy.



   References
Top
 Abstract
 Introduction
 Subjects and methods
 Results
 Discussion
 Acknowledgements
 References
 

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Received for publication: 27. 6.06
Accepted in revised form: 4. 1.07


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