Absolute Iron Research Articles

Absolute versus functional iron deficiency.

Absolute versus functional iron deficiency.

The Global Prevalence of Iron Deficiency in Collegiate Athletes: A Systematic Review and Meta-Analysis.

Athletes are at high risk of iron deficiency even without anemia. In this systematic review and meta-analysis that included 17,519 athletes in 122 references from 23 countries, participating in 62 unique sports over a 41-year timeframe, approximately 53.9% of student-athletes were found to be hypoferritinemic (ferritin concentration below 50mcg/L) with 23.0% percent showing absolute iron deficiency based on current definitions (ferritin concentration below 20mcg/L). These findings strongly suggest that changes in clinical practice guidelines are warranted to enable routine screening for iron deficiency among adolescent and collegiate athletes.

Hepcidin, GDF-15 and their Impact on Iron Metabolism in CKD

Background Anemia is an important complication in chronic kidney disease (CKD). We studied the diagnostic accuracy of hepcidin and growth differentiation factor-15 (GDF-15) as early markers of iron deficiency anemia (IDA) in non-dialysis (ND-CKD) patients. Materials and Methods This was a cross-sectional, case-control study comprising 100 cases of CKD (newly diagnosed and non-dialyzed) and 40 healthy controls. Serum levels of hepcidin and GDF-15 were estimated using ELISA-based assays. Receiver operator characteristics were used to evaluate the diagnostic validity of hepcidin and GDF-15 for absolute and functional iron deficiency anemia. Results About 33% of the cases were females with a mean age of 47.64 (± 13.68) years. The predictive value of hepcidin for diagnosing functional IDA in CKD was found to be 69.1% (95% CI: 52.5% to 82.7%), and that of GDF-15 was found to be 68.8% (95% CI: 52.6% to 82.1%). Hepcidin significantly correlated with hemoglobin (r = 0.278, p = 0.005) and serum iron (r = 0.222; p = 0.025). GDF-15 positively correlated with ferritin (r = 0.346, p < 0.0001) and hsCRP (r = 0.223, p = 0.0088) and negatively correlated with eGFR (r = -0.462, p < 000001), Hb (r = -0.481, p < 0.00001) and TIBC (r = -0.353, p < 0.0001). Conclusion Hepcidin and GDF-15 could predict functional IDA in our patients but not absolute IDA.

Post-transplant renal anemia: a call to action from a national study in routine clinical practice.

Post-transplant anemia is a prevalent yet often overlooked condition that poses significant risks. Current guidelines consider the same treatment recommendations and goals for these patients as for chronic kidney disease patients not on dialysis. Previous reports demonstrated a lack of awareness and suboptimal management, indicating a pressing need for improvement. We therefore wanted to update the information on post-transplant anemia. We aimed to describe the present state of anemia management, goals and adherence to guidelines within a representative sample of the kidney transplant (KTx) population. We designed a retrospective nationwide multicenter study including outpatients from eight KTx hospitals. Nephrologists gathered data from electronic medical records encompassing demographics, comorbidities, KTx characteristics and immunosuppressive therapy, and information pertaining to anemia management (laboratory values, previously prescribed treatments and subsequent adjustments). The European statement on the Kidney Disease: Improving Global Outcomes (KDIGO) guidelines was the reference for definitions, drug prescriptions and targets. Anemia occurring within the initial 6 months post-transplantation was classified as early onset. We included 297 patients with post-transplant anemia aged 62.8 years (standard deviation 13.6), 60% of whom were male. They had received a graft from cardiac death or brain death donors (61.6% and 31.1%, respectively) a median of 2.5 years (0.5-8.7) before. Among them 77% (n=228) were classified as having late post-transplant anemia, characterized by a higher prevalence of microcytic and iron deficiency anemia. A total of 158 patients were on erythropoietic-stimulating agents (ESAs) treatment, yet surprisingly 110 of them lacked iron supplementation. Notably, 44 patients had an indication for iron supplementation and among them, 30 exhibited absolute iron deficiency. Out of the 158 patients receiving ESAs, only 39 surpassed the limit for the ESA resistance index, indicating poor response. This resistance was more frequent among patients with early post-transplant anemia (26.1% vs 9.2%). We have identified iron profile, early post-transplant anemia and estimated glomerular filtration rate as factors associated with the highest risk of resistance. We found that hemoglobin targets are individualized upwards in post-transplant anemia. In this setting, iron therapy continues to be underutilized, especially intravenous, and iron deficiency and prior events (blood transfusion or hospital admission) explain most of the hyporesponsiveness to ESA. This highlights missed opportunities for precise prescription targeting and adherence to established guidelines, suggesting a need for improved management strategies in post-transplant anemia patients.

Assessment of iron metabolism and iron deficiency in incident patients on incident continuous ambulatory peritoneal dialysis.

The aim of this study was to investigate iron status and iron deficiency in incident continuous ambulatory peritoneal dialysis (CAPD) patients and identify influencing factors. Patients with end-stage renal disease were enrolled. Clinical data of iron metabolism and biochemical and dialysis parameters during the first peritoneal dialysis evaluation were collected. Serum ferritin (SF) and transferrin saturation (TSAT) levels were evaluated, and independent influencing factors were identified by correlation and regression analyses. Of 1,128 adult CAPD patients, 41.2% had iron deficiency (ID), 15.7% had absolute iron deficiency, and 8.2% had functional iron deficiency. The average SF level was (276.8 ± 277.9) μg/L, and iron saturation was (29.8 ± 12.7)%. Additionally, 50.2 and 69.3% of patients reached targets in SF level and iron saturation recommended by the Chinese Society of Nephrology. SF level and TSAT were not correlated with estimated glomerular filtration rate, whereas negatively correlated with platelet count and inflammatory factors. Low platelet count, presence of diabetes mellitus and high interleukin 6 levels were independent factors of lower TSAT. ID is common in patients with CAPD. Women and those with thrombocytopenia, diabetes, and inflammation are at higher risk for iron storage or reduced iron utilization. In the initial CAPD stage, a reasonable iron supplement strategy may be established for CAPD patients with high-risk factors.

Absolute and Functional Iron Deficiency in the US, 2017-2020

The prevalence of absolute and functional iron deficiency among adults in the US is unknown. To estimate the prevalence of absolute and iron deficiency and iron supplement use in the US across age, sex, and comorbidity categories. This cross-sectional study analyzed data from the National Health and Nutritional Examination Survey (NHANES) 2017 to 2020 prepandemic cycle. Participants included noninstitutionalized, civilian women and men aged 18 years or older who had available serum ferritin, iron, and unsaturated iron binding capacity measurements. Data analysis was performed from March 21, 2023, to July 5, 2024. Absolute iron deficiency and functional iron deficiency. Absolute iron deficiency was defined as serum ferritin less than 30 ng/mL regardless of transferrin saturation. Functional iron deficiency was defined as serum ferritin greater than or equal to 30 ng/mL with transferrin saturation less than 20%. The prevalence of absolute and functional iron deficiency was estimated among all adults in the US and separately among women and men according to age category (>18 years to <50 years, 50-65 years, and ≥65 years) using recommended sample weights and sampling design factors to provide estimates representative of the national, noninstitutionalized civilian population. The 95% CIs were calculated using the Korn-Graubard method. A total of 8021 US adults (mean age, 48 years; 95% CI, 47-49 years; 52% [95% CI, 50%-53%] female) were included in this analysis. An estimated 14% (95% CI, 13%-15%) of adults in the US met the criteria for absolute iron deficiency, and an estimated 15% (95% CI, 14%-17%) met the criteria for functional iron deficiency. Among US adults without anemia, heart failure, chronic kidney disease, or current pregnancy, the estimated prevalence of absolute iron deficiency was 11% (95% CI, 10%-11%), and that of functional iron deficiency was 15% (95% CI, 14%-17%). The prevalence of functional iron deficiency exceeded that of absolute iron deficiency in all US adults except women younger than 50 years. Iron supplement use ranged from 22% (95% CI, 12%-37%) to 35% (95% CI, 29%-42%) of women with iron deficiency and 12% (95% CI, 5%-21%) to 18% (95% CI, 8%-32%) of men with iron deficiency depending on age. These findings suggest that absolute and functional iron deficiency affect a large proportion of American adults even in the absence of anemia, heart failure, or chronic kidney disease. Further research on the role of functional iron deficiency in adverse health outcomes and on iron deficiency screening strategies is needed.

Anemia and Iron Profile in Hemodialysis and Nonhemodialysis Patients with Chronic Kidney Disease

Abstract BACKGROUND: Chronic kidney disease (CKD) is a global health concern, with anemia being a significant complication. Anemia in CKD patients is multifactorial and often leads to poorer outcomes. Assessing the iron profile, including serum ferritin, iron, and transferrin saturation, is crucial for identifying absolute or functional iron deficiency anemia (IDA). An objective evaluation of the iron profile is essential for effective and comprehensive management of anemia. MATERIALS AND METHODS: The study involved 100 adult patients with CKD and anemia, who were divided into two groups based on age and sex. The patients were divided into two groups: one received regular hemodialysis (HD) 2–3 times per week, whereas the other received no dialysis or dialysis infrequently. Exclusion criteria included infections, inflammation, renal injury, neoplasms, acute hemolysis, and thalassemia. RESULTS: Anemia is a common complication in patients with CKD, both those on HD and non-HD. Among the types of anemia observed, 50% of HD patients and 72% of non-HD CKD patients have normochromic anemia. In addition, 46% of HD patients and 24% of non-HD patients have IDA. Specifically, 24% of HD patients have absolute IDA and 22% have functional IDA, compared to 12% of both absolute and functional IDA in non-HD CKD patients, with a significant statistical difference between the two groups. Furthermore, serum iron and transferrin saturation levels show significant differences between HD and non-HD CKD patients. CONCLUSION: Anemia, especially IDA in CKD patients undergoing HD, requires accurate diagnosis through transferrin saturation and serum iron levels, and customized treatment based on dialysis status and anemia type is crucial.

Impact of vitamin D deficiency on iron status in children with type I diabetes

Vitamin D deficiency (VDD) and anemia are both public health nutrition concerns. An association between VDD and anemia has been suggested in various healthy and diseased populations. The current study aimed to elucidate the effect of VDD on iron status in children with type I diabetes mellitus (T1DM). The study recruited two groups of children with T1DM: control group comprised of 38 T1DM children with sufficient vitamin D (> 30 ng/ml) and a case group, consisted of 52 T1DM children with VDD (< 20 ng/ml). Both groups had comparable gender, age, BMI, and disease duration. The laboratory measurements included analysis of blood indices, markers of iron metabolism, hepcidin and inflammatory markers included interleukin 6 (IL-6) and C-reactive protein (CRP). Compared to control group, T1DM children with VDD differs specifically in terms of some markers of blood indices, such as decreased hemoglobin and increased red blood cell distribution width. Moreover, decreased serum iron, ferritin, total iron-binding capacity and transferrin along with elevated inflammatory markers were observed in case group. Results of the study indicated that VDD had increased the risk of iron deficiency anemia in children with T1DM as well as inflammatory related anemia. Furthermore, in T1DM children, VDD had raised the incidence of both absolute and functional iron deficiency, with greater incidence of the former. This study may indicate that VDD may be a risk factor that may worsen iron deficiency anemia in T1DM.

Prevalence of iron deficiency and anemia in pediatric heart transplant recipients.

The prevalence of iron deficiency and anemia in the setting of modern-day maintenance immunosuppression in pediatric heart transplant (HTx) recipients is unclear. The primary aim was to determine the prevalence of iron deficiency (serum ferritin<30ng/mL±transferrin saturation<20%) and anemia per World Health Organization diagnostic criteria and associated risk factors. Single-center, cross-sectional analysis of 200 consecutive pediatric HTx recipients(<21 years old) from 2005 to 2021. Data were collected at 1-year post-HTx at the time of annual protocol biopsy. Median age at transplant was 3 years (IQR.5-12.2). The median ferritin level was 32ng/mL with 46% having ferritin<30ng/mL. Median transferrin saturation (TSAT) was 22% with 47% having TSAT<20%. Median hemoglobin was 11g/dL with 54% having anemia. Multivariable analysis revealed lower absolute lymphocyte count, TSAT<20%, and estimated glomerular filtration rate<75mL/min/1.73m2 were independently associated with anemia. Ferritin<30ng/mL in isolation was not associated with anemia. Ferritin<30ng/mL may aid in detecting absolute iron deficiency while TSAT<20% may be useful in identifying patients with functional iron deficiency±anemia in pediatric HTx recipients. Iron deficiency and anemia are highly prevalent in pediatric HTx recipients. Future studies are needed to assess the impact of iron deficiency, whether with or without anemia, on clinical outcomes in pediatric HTx recipients.

#1275 Post-transplant renal anaemia: a call to action from a national study in routine clinical practice

Abstract Background and Aims Post-transplant anaemia (PTA) is common, frequently unnoticed and carries associated risks. Current guidelines consider the same treatment recommendations and goals for these patients as for chronic kidney disease-non dialysis (CKD-NDD). Previous reports demonstrated low awareness and management that could improve. Aims: To describe current anaemia management, goals, and adherence to guidelines in a representative sample of kidney transplant (KT) recipients. Method Retrospective nationwide multicentre study including patients from 8 KT hospitals. Nephrologists collected demographics, comorbidities, KT data and immunosuppressive therapy and data related to anaemia management (laboratory values, previously prescribed treatments, and subsequent adjustments) from electronic medical records. We classified as early anaemia that within the first 6 months. The European statement on KDIGO guidelines was the reference for definitions, drug prescriptions and targets. Results We included 297 recipients with PTA aged 62.8 y (SD 13.6) and 60% male. They had received a graft from donors after cardiac death or brain death) (61.6%. 31.1% respectively) a median of 2.5 years [0.5-8.7] before. A total of 158 patients were on treatment with erythropoietin stimulating agents (ESAs) and the distribution of haemoglobin (Hb) and iron are summarized in Table 1. Among 110 patients on ESA treatment but without iron prescription, 44 had an indication to receive iron and 30 of them had absolute iron deficiency (ID). Only 39/158 patients exceeded the ESA resistance index (ERI) limit, and this condition was more frequent in early PTA (26.1 vs 9.2%). Absolute or functional ID accounted for the majority of ESA resistance (28.2 vs 17.1; p &amp;lt; 0.001). Conclusion Hemoglobin levels in these patients are within the upper KDIGO. Iron therapy continues to be underused (especially intravenous), while iron deficiency and prior events explain most of ESA hyporesponsiveness. We identify missed opportunities for accurate prescription targeting and adherence to guidelines.

Critical re-evaluation of the identification of iron deficiency states and effective iron repletion strategies in patients with chronic heart failure.

According to current guidelines, iron deficiency is defined by a serum ferritin level <100 ng/ml or a transferrin saturation (TSAT) <20% if the serum ferritin level is 100-299 μg/L. These criteria were developed to encourage the use of intravenous iron as an adjunct to erythropoiesis-stimulating agents in the treatment of renal anaemia. However, in patients with heart failure, these criteria are not supported by any pathophysiological or clinical evidence that they identify an absolute or functional iron deficiency state. A low baseline TSAT-but not serum ferritin level-appears to be a reliable indicator of the effect of intravenous iron to reduce major heart failure events. In randomized controlled trials, intravenous iron decreased the risk of cardiovascular death or total heart failure hospitalization in patients with a TSAT <20% (risk ratio 0.67 [0.49-0.92]) but not in patients with a TSAT ≥20% (risk ratio 0.99 [0.74-1.30]), with the magnitude of the risk reduction being proportional to the severity of hypoferraemia. Patients who were enrolled in clinical trials solely because they had a serum ferritin level <100 μg/L showed no significant benefit on heart failure outcomes, and it is noteworthy that serum ferritin levels of 20-300 μg/L lie entirely within the range of normal values for healthy adults. Current guidelines reflect the eligibility criteria of clinical trials, which inadvertently adopted unvalidated criteria to define iron deficiency. Reliance on these guidelines would lead to the treatment of many patients who are not iron deficient (serum ferritin level <100 μg/L but normal TSAT) and ignores the possibility of iron deficiency in patients with a low TSAT but with serum ferritin level of >300 μg/L. Importantly, analyses of benefit based on trial eligibility-driven guidelines substantially underestimate the magnitude of heart-failure-event risk reduction with intravenous iron in patients who are truly iron deficient. Based on all available data, we recommend a new mechanism-based and trial-tested approach that reflects the totality of evidence more faithfully than the historical process adopted by clinical investigators and by the guidelines. Until additional evidence is forthcoming, an iron deficiency state in patients with heart failure should be defined by a TSAT <20% (as long as the serum ferritin level is <400 μg/L), and furthermore, the use of a serum ferritin level <100 μg/L alone as a diagnostic criterion should be discarded.

Current approach to the management of preoperative iron deficiency anemia in colorectal cancer patients: a review of literature.

&lt;b&gt;Introduction:&lt;/b&gt; The prevalence of preoperative anemia is the highest in the group of colorectal cancer (CRC) patients and may reach over 75%. The prevalence of anemia in CRC patients increases even further following surgery. Approximately 75-80% of anemic CRC patients present with absolute or functional iron deficiency (ID). Preoperative anemia constitutes an independent risk factor for allogeneic blood transfusion (ABT), postoperative complications, prolonged length of hospital stay, and increased mortality. ABT is itself associated with increased morbidity and mortality.&lt;b&gt;Aim:&lt;/b&gt; The aim of this review article was to present the pathophysiology and the current approach to the diagnostics and treatment of preoperative iron deficiency anemia (IDA) in CRC patients.&lt;b&gt;Material and methods:&lt;/b&gt; Extensive search of medical literature databases was performed (Pubmed, Embase). The key words that were used were as follows: CRC, colorectal surgery, ID, IDA, intravenous iron, Patient Blood Management (PBM).&lt;b&gt;Results:&lt;/b&gt; There are several laboratory parameters that can be used for IDA diagnosis, however, the simplest and most cost- -effective is reticulocyte hemoglobin equivalent (RET-He). Pathophysiologic features of IDA in CRC patients favor treatment with intravenous, as opposed to oral, iron formulations. Applying PBM strategies minimizes the exposure to ABT.&lt;b&gt;Conclusions:&lt;/b&gt; Preoperative IDA is highly prevalent among CRC patients. Preoperative anemia is an independent risk factor for ABT, increased morbidity and mortality, as well as prolonged hospital length of stay. The same negative consequences are associated with ABT. Therefore, preoperative IDA in CRC patients needs to be screened for, diagnosed, and treated before surgery. Effective treatment of preoperative IDA in CRC patients is with intravenous iron formulations. ABT should be the treatment of last resort due to the risk of negative clinical consequences, including an increased rate of cancer recurrence.

Reticulocyte hemoglobin is an excellent biomarker for detecting and diagnosing absolute and functional iron deficiency anemia in hemodialysis patients

Reticulocyte hemoglobin is an excellent biomarker for detecting and diagnosing absolute and functional iron deficiency anemia in hemodialysis patients

Compliance With NCCN Guidelines for Evaluation and Treatment of Anemia Among Patients With Solid Tumors.

NCCN Guidelines for Hematopoietic Growth Factors recommend evaluation and treatment of anemia in patients with cancer. However, a paucity of data exists regarding compliance with these recommendations. A retrospective cohort study was performed of patients diagnosed with any solid tumor at Vanderbilt University Medical Center from 2008 to 2017. Tumor registry-confirmed cancer cases were identified by ICD-O codes using the Synthetic Derivative database. Anemia was defined as hemoglobin (Hgb) level ≤11 g/dL and graded according to CTCAE version 5.0. Absolute, functional, and possible functional iron deficiency were defined based on NCCN Guidelines. A total of 25,018 patients met inclusion criteria. Median age was 60 years. The most common malignancies were respiratory tract, prostate, and nonprostate urologic (11% each). Among 8,695 patients with Hgb levels available prior to diagnosis, 1,484 (17%) were noted to be anemic proximal to diagnosis. Of the 25,018 patients, 11,019 (44%) were anemic within 6 months of diagnosis. Of these patients, 4,686 (43%) had grade 2 (moderate) anemia and 9,623 (87%) had normocytic anemia. Patients with retroperitoneal/peritoneal cancers had the highest prevalence of anemia (83/110; 75%). A total of 4,125 (37%) underwent any evaluation of their anemia, of whom 1,742 (16%) had iron studies performed and 1,528 (14%) had vitamin B12 or folate studies performed. Fewer than half of patients with anemia received treatment (n=4,318; 39%), including blood transfusion (n=3,528; 32%), oral iron supplementation (n=1,279; 12%), or intravenous iron supplementation (n=97; 1%). Anemia treatment was significantly more frequent as the grade of anemia increased (any treatment among grade 1/mild: 12%; grade 2/moderate: 31%; grade 3/severe: 77%; χ2 [2, n=11,019]=3,020.6; P<.001). Patients with penile and testicular cancers had the highest prevalence of anemia evaluation (n=57; 79%). Anemia is common in patients with solid tumors; yet, compliance with NCCN Guidelines for evaluation and treatment of anemia remains low. There are opportunities to improve compliance with guidelines across the spectrum of cancer care.

Iron Metabolism and Inflammatory Mediators in Patients with Renal Dysfunction.

Chronic kidney disease (CKD) affects around 850 million people worldwide, posing significant challenges in healthcare due to complications like renal anemia, end-stage kidney disease, and cardiovascular diseases. This review focuses on the intricate interplay between iron metabolism, inflammation, and renal dysfunction in CKD. Renal anemia, prevalent in CKD, arises primarily from diminished erythropoietin (EPO) production and iron dysregulation, which worsens with disease progression. Functional and absolute iron deficiencies due to impaired absorption and chronic inflammation are key factors exacerbating erythropoiesis. A notable aspect of CKD is the accumulation of uremic toxins, such as indoxyl sulfate (IS), which hinder iron metabolism and worsen anemia. These toxins directly affect renal EPO synthesis and contribute to renal hypoxia, thus playing a critical role in the pathophysiology of renal anemia. Inflammatory cytokines, especially TNF-α and IL-6, further exacerbate CKD progression and disrupt iron homeostasis, thereby influencing anemia severity. Treatment approaches have evolved to address both iron and EPO deficiencies, with emerging therapies targeting hepcidin and employing hypoxia-inducible factor (HIF) stabilizers showing potential. This review underscores the importance of integrated treatment strategies in CKD, focusing on the complex relationship between iron metabolism, inflammation, and renal dysfunction to improve patient outcomes.

Absolute iron deficiency, coronary artery calcification and cardiovascular mortality in maintenance haemodialysis patients.

The effects of iron on vascular calcification in rats and vascular smooth muscle cells were recently reported, but clinical studies on iron and vascular calcification are scant. We studied the associations of absolute iron deficiency, coronary artery calcification and mortality in patients with maintenance haemodialysis (MHD). Transferrin saturation (TSAT), ferritin, mean corpuscular haemoglobin (MCH) and Agatston coronary artery calcium score (CACS) were studied at baseline in MHD patients and followed up for 3 years. Cox proportional hazard analyses for mortality and linear regression analyses for CACS were performed. In 306 patients, the median age was 67 (56-81) years, dialysis duration was 76 (38-142) months, and diabetes prevalence was 42.5%. Fifty-two patients had died by 3 years. Patients with absolute iron deficiency (TSAT <20% and ferritin <100 ng/mL) (n = 102) showed significantly higher CACS (p = .0266) and C-reactive protein (p = .0011), but a lower frequency of iron formulation administration compared with patients without absolute iron deficiency at baseline (n = 204). Absolute iron deficiency was a significant predictor for 3-year cardiovascular (CV) mortality (hazard ratio: 2.08; p = .0466), but not for 3-year all-cause mortality. CACS was significant predictor for both 3-year CV and all-cause mortality (p <.05). Absolute iron deficiency and MCH were significant determinants of CACS (p < .05). MHD patients with absolute iron deficiency showed significantly higher CACS than others, and absolute iron deficiency was a significant risk factor for coronary artery calcification and 3-year CV mortality in MHD patients, but was not a significant predictor for 3-year all-cause mortality.

Iron Deficiency: A Silent Threat in Patients With Heart Failure With Reduced Ejection Fraction.

Background Iron deficiency is a prevalent and clinically significant comorbidity in patients with heart failure with reduced ejection fraction (HFrEF). Despite its high prevalence, its impact on clinical outcomes, mortality, and various physiological parameters remains a subject of ongoing investigation. The findings of this study are anticipated to contribute valuable insights into the management and prognosis of patients with HFrEF, potentially informing future interventions and improving patient outcomes. This study aimed to assess the clinical profile of iron deficiency and its implications on morbidity and mortality in patients with HFrEF. Methodology A prospective cohort study was conducted at King Edward Memorial Hospital, India, involving 371 patients with HFrEF. Participants underwent comprehensive clinical and laboratory assessments, evaluating iron deficiency with signs, symptoms, comorbidities, dyspnea, elevated jugular venous pressure (JVP), past medical history, and various hematological and biochemical parameters. Results Overall, 50% of HFrEF participants were iron deficient (n = 185), of whom 80% (n = 148) had anemia against 43% (n = 81) anemics in iron repletes (n = 186). Of the 185 iron-deficient patients, 44 (11.86%) had absolute iron deficiency and 141 (38%)had functional iron deficiency. Iron deficiency significantly correlated with increased mortality in HFrEF patients (χ2 (1, N = 371) = 3.88, p = 0.048). A large positive correlation was observed between absolute iron deficiency and dyspnea severity (r2 = 0.949, p = 0.026).Statistically significant differences were found in hemoglobin (anemia), serum iron, serum ferritin, total iron-binding capacity, and transferrin saturation between iron-deficient and iron-replete patients (p < 0.05). However, no statistically significant difference in left ventricular ejection fraction between iron-deficient and replete patients was noted. Conclusions Iron deficiency emerges as more than a mere comorbidity in heart failure, becoming a prognostic factor with multifaceted outcomes. Its impact extends beyond cardiovascular consequences, encompassing adverse manifestations such as anemia, ascites, edema, dyspnea, elevated JVP, and a heightened risk of mortality. This intricate interplay positions iron deficiency as a critical determinant, significantly influencing the clinical trajectory and outcomes for patients with HFrEF.

Functional iron deficiency anemia was associated with higher mortality in chronic kidney disease patients: the NHANES III follow-up study

Anemia, a common complication of chronic kidney disease (CKD), is associated with poor prognosis. However, it is not completely clear whether this association is caused by anemia per se or other comorbidities. Whether different types of iron deficiency anemia can predict the outcomes of CKD remains unclear. The dataset from NHANES III was analyzed and Cox multivariate regression models and propensity score matching (PSM) method were used to evaluate the effect of anemia on mortality. Of 4103 patients with CKD, 14.6% had anemia. Among those with anemia, 38.8% had absolute iron deficiency (AID), and 19.8% had functional iron deficiency (FID). During the median follow-up time of 13.8 years, 2964 deaths and 804 cardiovascular deaths were observed. Anemia was robustly associated with a high risk of all-cause mortality in CKD patients after adjusting covariates by two multivariate regression models (Model 1: HR = 1.485, 95%CI:1.340–1.647, p < 0.001; Model 2: HR = 1.391, 95%CI:1.250–1.546, p < 0.001). In the PSM cohort, anemia was still an independent risk factor for all-cause mortality (Model 1: HR = 1.443, 95%CI: 1.256–1.656, p < 0.001; Model 2: HR = 1.357, 95%CI:1.177–1.564, p < 0.001). In the CKD population, anemia patients with FID had the highest risk of mortality than the other anemia groups (p < 0.05), while AID had a mortality rate similar to those without anemia (p > 0.05). In conclusion, anemia was associated with a worse prognosis in patients with CKD, which may be attributed to the higher mortality risk of FID rather than AID. AID wasn’t associated with a higher mortality rate compared with CKD patients without anemia.

Effect of roxadustat on iron metabolism in patients with peritoneal dialysis: a real-world 24-week study

BackgroundRoxadustat is an oral hypoxia inducing factor-prolyl hydroxylase inhibitor (HIF-PHI) that regulates iron metabolism in patients with chronic kidney disease (CKD) primarily by reducing hepcidin levels and mobilizing internal iron stores. More data are needed to demonstrate the efficacy of roxadustat in regulating iron metabolism in patients with peritoneal dialysis (PD) compared with erythropoiesis stimulating agents (ESAs).MethodsThis prospective cohort study enrolled PD patients with a mean hemoglobin level of 60–100 g/L. All subjects were randomized into two groups at a ratio of 2:1 the roxadustat group (106 cases), and the ESA group (53 cases). The primary endpoint was the change in the iron biomarker levels and the proportion of patients with absolute iron deficiency and functional iron deficiency.ResultsCompared with ESAs, roxadustat significantly decreased hepcidin level (difference, − 20.09 ng/mL; 95% CI, − 30.26 to − 9.92), attenuated the increase in serum soluble transferrin receptor (sTFR) level (difference, − 7.87 nmol/L; 95% CI, − 12.11 to − 3.64), and reduced the proportion of patients with functional iron deficiency (roxadustat, 11.43%; ESA, 33.33%). There was no significant difference in safety of the two groups over the duration of the study.ConclusionsCompared with ESA group, roxadustat group showed significant differences in all iron biomarker levels except serum ferritin (sFt) and transferrin saturation (TSAT). These results suggest that roxadustat was superior to ESAs as a therapy for iron metabolism in PD patients.Trial registration: This study completed Chinese Clinical Trial Registration on March 4, 2022 (registration number: ChiCTR2200057231).Graphical abstract

Absolute Iron Deficiency, Coronary Artery Calcification, and Mortality in Dialysis Patients

Absolute Iron Deficiency, Coronary Artery Calcification, and Mortality in Dialysis Patients