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Query: UMLS:C0240066 (iron deficiency)
 7,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Almost all patients with end-stage renal disease suffer from renal anaemia of multifactorial pathogenesis. The use of recombinant human erythropoietin to raise the haematocrit has been a major advance in the care of patients with end-stage renal disease. The majority of these patients develop absolute or functional iron deficiency. However, the diagnosis of iron deficiency is hindered by the inaccuracy of commonly used tests. Serum ferritin and transferrin saturations are frequently used, but limitations with both parameters in end-stage renal disease patients have resulted in the development of new tests to assess iron sufficiency. The percentage of hypochromic red blood cells and particularly reticulocyte haemoglobin content are new measures of iron status in end-stage renal disease patients. An enhanced knowledge of the interpretation of available laboratory parameters will ensure that the patients receive the full benefit from their treatment with recombinant human erythropoietin and iron.
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PMID:Laboratory diagnosis of anaemia in dialysis patients: use of common laboratory tests. 937 71

Anemia in chronic renal failure is predominantly caused by diminished erythropoietin synthesis by diseased kidneys. While iron deficiency is often stated as a cause of anemia in chronic renal failure prior to end-stage renal disease, its relative contribution is debated. It is speculated that rather than frank 'iron deficiency', many patients with chronic renal failure may indeed have impaired utilization of iron. We analyzed 139 consecutive patients with chronic renal failure starting maintenance hemodialysis to determine the relationship between hematocrit, measures of renal function (blood urea nitrogen and serum creatinine concentration), and measures of iron availability (serum transferrin saturation, serum iron level and serum ferritin). The 139 study subjects (60 men, 79 women) comprised 116 blacks (83%), 15 hispanics (11%), and 8 whites (6%) of a mean age 56 +/- 15 years. Only 23 (17%) of 139 subjects had positive hemoccult stool test for blood. Their mean hematocrit was 24 +/- 4.5%, mean blood urea nitrogen concentration was 121 +/- 38, mean serum creatinine concentration was 12.6 +/- 5.2 mg/dl, mean serum transferrin saturation was 22 +/- 14%, mean serum ferritin level was 235 +/- 194 U/l, mean serum iron level was 55 +/- 40 U/l, and mean total iron binding capacity was 254 +/- 93%. Multiple regression analysis with hematocrit as the outcome variable, and blood urea nitrogen level, serum creatinine concentration, serum albumin concentration, serum transferrin saturation, and serum ferritin level as the independent variables, showed an inverse correlation between hematocrit and serum creatinine concentration (p = 0.002). We conclude that in patients with chronic renal failure starting uremia therapy, anemia does not correlate with any of the commonly measured indices of body iron stores. We infer that impaired utilization of iron may be a significant factor in the anemia of chronic renal failure.
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PMID:Relative contributions of body iron status and uremia severity to anemia in patients with advanced chronic renal failure. 937 26

To evaluate storage iron deficiency and iron-deficient erythropoiesis we determined, in a cross-sectional study of 95 patients mainly including end-stage renal disease patients (ESRD) with (32) and without rh-EPO therapy (55), the following parameters: hemoglobin, mean corpuscular red cell volume, ferritin, transferrin saturation (TS), zinc protoporphyrin (ZPP) and soluble transferrin receptor (TfR). In the dialysis group the percentage of positive samples with each marker of tissue iron supply defined as TS < 20%, ZPP > 40 mumol/mol Heme and TfR > 3.05 microgram/ml was as follows: TS 43.7% and 32.2% at a diagnostic threshold level of < 16%, ZPP 33.3% and TfR 17.2%. Manifest storage iron deficiency defined as ferritin < 30 ng/ml was observed in 5.7% of the samples while the mean ferritin concentration of the rh-Epo treated dialysis patients was 509.3 ng/ml compared to 262.5 ng/ml in the group without rh-EPO therapy. These data reflect a generous iron substitution in our series taking a TS < 20% as an intervention criterion. Looking at the different results of the three markers the best correspondence was found between ZPP and TfR resulting in a weak positive correlation (+0.64). In conclusion, we found quite different results with different assays when evaluating endogenous iron availability in our series of mainly ESRD patients in a cross-sectional study. Because a gold-standard is not defined further firm conclusions cannot be drawn from this type of study. The adequacy of the different parameters of iron metabolism including threshold levels and, consequently, the decision and route of iron substitution deserve an evaluation in a longitudinal study to characterize the best marker or marker combination in this setting.
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PMID:Transferrin receptor assay and zinc protoporphyrin as markers of iron-deficient erythropoiesis in end-stage renal disease patients. 954 1

Anemia is the most common hematologic abnormality in patients with chronic renal failure. The reasons for anemia in chronic renal failure are many and include erythropoietin and iron deficiencies, inflammation, infection, aluminum toxicity, and hyperparathyroidism. Iron deficiency alone affects more than 50% of patients on dialysis, and the estimated iron loss for these patients is 1.5 to 3 grams per year. The use of erythropoietin has also uncovered iron deficiency in a multitude of patients. Iron and erythropoietin supplementation has often restored normal or near-normal levels of hematocrit in these patients and has therefore improved some of the symptoms classically connected with chronic renal failure, such as fatigue, cold intolerance, and mental sluggishness, among others. Resistance to erythropoietin is frequently observed in the maintenance care for dialysis patients, and the most common reason is iron deficiency. It is important to understand the physiology of renal anemia, erythropoiesis and iron metabolism in order to avoid mistakes and misconceptions in the management of iron in chronic dialysis patients. In this article, we review several mistakes, misconceptions, practices, and guidelines in iron supplementation therapy. We also review the physiology of anemia in renal disease and the importance of erythropoietin and iron in causing anemia and discuss recent Dialysis Outcomes Quality Initiative (DOQI) guidelines on the topic.
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PMID:The use of iron in patients on chronic dialysis: mistake and misconceptions. 956 79

An inadequate response to recombinant human erythropoietin (rHuEPO) therapy may be attributable to many underlying causes, with the major cause being iron deficiency. Since improved rHuEPO response can improve quality of life in end-stage renal disease (ESRD) patients, rHuEPO resistance should be investigated and corrected whenever possible. This article will discuss the Winthrop-University Hospital's continuous quality improvement (CQI) initiative that was developed to improve recognition and treatment of rHuEPO resistance.
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PMID:Management of rHuEPO resistance in CRF patients: a clinical protocol at Winthrop-University Hospital. 980 89

The target organ failures associated with uremia are most often considered to be caused by processes other than uremia per se. Heart disease, for example, is considered the product of hypertension, lipid abnormalities, and so forth, rather then the uremic state. Erythropoietin deficiency, blood loss, and iron deficiency are believed to cause anemia, rather than the uremic state. Malnutrition is believed to be the product of poor nutrient intake and perhaps nutrient losses, rather than uremia per se. This article reviews evidence suggesting that anemia and malnutrition share a common cause; the acute-phase inflammatory process that is a normal host-defense mechanism. Given the high prevalence of heart disease among patients with end-stage renal disease (ESRD), data indicating activation of the acute-phase process in patients with kidney failure, and emerging evidence that the process has a significant role in the risk for cardiovascular disease among patients without kidney failure, there is a strong likelihood that heart disease will share with anemia and malnutrition the acute-phase state as a contributing cause. Thus, instead of disconnected target organ failures, each with different antecedent causes, we see emerging the likelihood of a unifying pathobiology for uremia. The antecedents of morbidity and mortality appear as a web of organ failures connected by a common pathobiology. Whereas each failure likely has contributing causes other than the acute-phase state, they probably share the state as a causative, contributing, or exacerbating factor.
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PMID:Acute-phase inflammatory process contributes to malnutrition, anemia, and possibly other abnormalities in dialysis patients. 989 76

Use of recombinant human erythropoietin in patients with end-stage renal disease has highlighted iron deficiency as the major cause of resistant anemia. The current mainstay of intravenous (i.v.) iron replacement therapy, iron dextran, has been shown in prior studies to have a risk of serious life-threatening anaphylaxis of just under 1 per 100 patients exposed. The current study assessed the safety profile of an alternative i.v. iron, sodium ferric gluconate complex in sucrose (Ferrlecit), as compared with iron dextrans. Sodium ferric gluconate complex in sucrose, a unique chemical preparation, has been in use since 1959, principally in Europe, at a rate of approximately 2.7 million i.v. doses per year (1992 to 1996) in Germany and Italy alone. For iron dextran, usage in the United States was comparable--principally renal hemodialysis--and estimated from market sources at 3.0 million doses per year (1995). From 1976 to 1996, there were 74 allergic adverse events reported for sodium ferric gluconate complex in sucrose to the World Health Organization (WHO), German Health Bureau, and the manufacturer (all combined). For the years 1992 to 1996, sodium ferric gluconate complex in sucrose had an allergy event reporting rate of 3.3 allergy episodes per million doses per year compared with a similar rate of 8.7 reported allergy events per million doses per year for iron dextran in the United States in 1995. Case fatalities for sodium ferric gluconate complex in sucrose and iron dextran within these reports were then compared. For sodium ferric gluconate complex in sucrose, there were no reports of deaths over the entire period (1976 to 1996). However, for iron dextrans, there were 31 fatalities among 196 allergy/anaphylaxis cases reported in the United States between 1976 and 1996, yielding a case-fatality rate of 15.8%. These data show that sodium ferric gluconate complex in sucrose, when compared with iron dextrans in comparably sized patient usage populations with similar total rates of reporting of allergic events, has a significantly lower reported mortality rate (P < 0.001). Thus, the data justify usage of sodium ferric gluconate complex in sucrose as the safer iron replacement therapeutic agent.
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PMID:Sodium ferric gluconate complex in sucrose: safer intravenous iron therapy than iron dextrans. 1007 Sep 26

The advent of erythropoietin (rHuEPO) has revolutionized the treatment of anemia in end-stage renal disease. While many studies indicate beneficial effects of rHuEPO in hemodialysis, peritoneal dialysis and predialysis patients, the impact of the drug in renal transplantation is less clear. Treatment with rHuEPO may reduce the degree of allosensitization produced by random blood transfusion while still allowing the possibility of the transplant survival benefit derived from deliberate transfusion. Recovery from anemia post-transplantation is hastened by treatment with rHuEPO, while patients with failing allografts respond to rHuEPO in a fashion similar to dialysis patients, despite the concomitant use of immunosuppressives. The erythropoietic response to rHuEPO is abrogated during episodes of acute rejection, and restored when successful treatment of rejection has occurred. Iron therapy is a critical factor for support of erythropoiesis and prevention of absolute iron deficiency posttransplantation. In patients presenting for renal transplant, the balance of evidence suggests that there is no increase in the rate of delayed graft function, graft loss or vascular thrombosis for patients who had received prior rHuEPO therapy.
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PMID:Erythropoietin and renal transplantation. 1008 92

Management of end-stage renal disease (ESRD) has been revolutionized by the advent of erythropoietin replacement. We briefly review its characteristics and clinical use. Also emphasized is the importance of iron deficiency in limiting the clinical response to erythropoietin therapy. Iron-replacement therapy in ESRD patients is briefly discussed.
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PMID:Anemia and cardiovascular complications: iron and EPO impact. 1020 71

A prospective randomized study of the use of recombinant human erythropoietin (rHuEPO) in children with chronic renal disease was conducted to assess dosing requirements and side effects. Forty-four children with chronic renal failure, aged 4 months to 21 years, were studied. Twenty-five patients were pre dialysis, 10 on peritoneal dialysis, and 9 on hemodialysis. Patients received either 150 U/kg per week or 450 U/kg per week divided thrice weekly of rHuEPO for 12 weeks or until target hemoglobin (Hb) was attained. Dose was then adjusted to maintain a normal Hb. Eighty-two percent of patients reached target Hb by 7.9+/-5.6 weeks (mean+/-SD); 95% of patients in the high-dose group and 66% in the low-dose group reached target Hb within 12 weeks. The overall median rHuEPO dose at target Hb was 150 U/kg per week. Hemodialysis patients tended to require more rHuEPO to maintain a normal Hb (median 250 U/kg per week). Transfusion requirements and panel-reactive antibody levels decreased during the 12 weeks. Iron deficiency and/or hypertension occurred in 30% of children. In conclusion, rHuEPO at 150 U/kg per week is safe and effective in treating anemia in children with chronic renal disease.
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PMID:Safety and efficacy of erythropoietin in children with chronic renal failure. 1065 38


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