Expert Panel Consensus on Management of Iron Deficiency Anemia and Use of Ferric Carboxymaltose in Hemodialysis-Dependent Chronic Kidney Disease Patients

Introduction

Iron deficiency affects more than 50% of dialysis patients and is a significant contributor to anemia in CKD.¹ Anemia is associated with many adverse clinical outcomes, such as accelerated cognitive decline, disrupted sleep patterns, faster CKD progression, heightened risk of cardiovascular and cerebrovascular events, increased rates of hospitalization, elevated all-cause mortality, and reduced quality of life.² KDIGO Anemia Work Group 2024 guidelines define anemia in CKD as hemoglobin (Hb) levels <13.0 and <12.0 g/dL in men and women, respectively.³ The prevalence of anemia increases with the progression of CKD stages.⁴

Data from the United States National Health and Nutrition Examination Survey (NHANES) showed that ∼4.8 million individuals (∼15.4%) were affected by CKD-related anemia, with 17.4%, 50.3%, and 53.4% of patients with stages III, IV, and V CKD, respectively.⁵ Additional pooled estimates indicate that anemia affects <10% of patients in CKD stages I–II, 20–40% in stage III, 50-60% in stage IV, and >70% in stage V, with nearly 90% of patients on dialysis being anemic.⁶ Country-specific reports show substantial variation: the prevalence of anemia in CKD is reported as 39.3% in India, 14% in the United States, and 51.5% in China. A stage-wise breakdown indicates anemia prevalence of 22.4%, 41.3%, and 53.9% in CKD stages III, IV, and V, respectively.⁷

The burden of anemia in CKD is particularly high in India, with a reported prevalence ranging from 39.0% to 82.4%. Notably, 8.1% of patients were classified as severely anemic.^7,8 Similarly, a cross-sectional study conducted at a tertiary care center in Karnataka found anemia in 90% of patients with CKD, with 50% experiencing moderate and 25% experiencing severe anemia. Normocytic normochromic morphology was the predominant pattern, observed in 75% of cases.⁹

Iron deficiency, either absolute or functional, is a major contributor to anemia in CKD. In a large U.S. Veterans study (N=933,463), 30% of anemic CKD patients had absolute IDA and 19% had functional IDA. Functional IDA was linked to higher mortality and cardiovascular hospitalizations, while absolute IDA was associated only with increased hospitalization risk.¹⁰ Data from Indian studies point to a critical gap in iron deficiency screening among anemic CKD patients. A cross-sectional study from the Kaveri delta region of Tamil Nadu, involving 221 CKD patients, reported a 39% prevalence of iron deficiency anemia, with markedly lower serum ferritin levels, especially among women aged 31–40 years.¹¹

Absolute iron deficiency occurs when iron stores in the liver, spleen, and bone marrow are severely depleted, often due to dialysis-related blood loss, gastrointestinal bleeding, or inadequate oral intake.¹² Functional iron deficiency occurs despite adequate iron stores, typically assessed by bone marrow iron staining or blood tests. It results from an imbalance between iron supply and demand. Inflammation-induced hepcidin elevation limits iron availability.¹³

Erythropoiesis-stimulating agents (ESAs), the mainstay of the therapy of anemia in CKD, accelerate red blood cell production, often exceeding iron mobilization capacity. Additionally, the response to ESA is influenced by several factors.¹¹ The use of ESAs, especially in an HD population, may necessitate the need for iron supplementation. Intravenous (IV) iron supplements, rather than oral iron, provide an adequate supply for red blood cell production, resulting in better outcomes.^14,15 Several IV iron formulations are available, including iron sucrose, ferric gluconate, ferric derisomaltose, and ferric carboxymaltose (FCM), each differing in its dosing regimen, stability, and safety profile.¹⁶ In recent years, FCM has emerged as the preferred choice for intravenous use due to its advantages of high-dose administration with fewer infusions, along with a favorable safety profile.¹⁷

FCM is a non-dextran iron formulation known for its stability, facilitating iron uptake via the reticuloendothelial system, while minimizing free iron release.¹⁸ In 2007 and 2011, FCM was approved in Europe and India, respectively, for the treatment of iron-deficiency anemia. IV FCM’s safety and effectiveness has been documented in patients with HD-CKD, making it one of the preferred agents for the treatment of anemia of CKD.^19,20 This consensus document aims to provide recommendations on FCM use tailored to the Indian healthcare context so as to optimize the treatment of IDA in HD-CKD and improve patient outcomes.

Methodology

A Delphi study was conducted in two phases: an online survey and an in-person meeting [Figure 1]. We have selected only qualified Nephrologists from different regions of India. A literature review was performed to identify unmet clinical needs and to develop IDA management, including FCM’s role in hemodialysis-dependent CKD (HD-CKD) patients. A systematic search was performed using the electronic databases MEDLINE (via PubMed) and Scopus to identify relevant studies. The search strategy incorporated a combination of Medical Subject Headings (MeSH) terms and free-text keywords, including “iron deficiency anemia,” “ferric carboxymaltose,” “hemodialysis-dependent chronic kidney disease,” “intravenous iron,” “chronic kidney disease,” and “iron therapy.” Boolean operators (AND, OR, NOT) were used to refine and optimize the search results. Studies were included if they were published in English, focused on HD-CKD patients, and specifically evaluated the use of FCM for the management of IDA. Eligible study types included meta-analyses, systematic reviews, clinical guidelines, and original research articles. Non-English publications, case reports, and conference abstracts were excluded.

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Figure 1:

Consensus development methodology for the management of IDA in HD-CKD patients using FCM. IDA: Iron deficiency anemia, HD-CKD: Hemodialysis-Chronic kidney disease, FCM: Ferric carboxymaltose.

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A steering committee comprising three experienced nephrologists was formed to guide the process, supported by a number of other nephrologists.

In Phase 1, consensus statements were distributed to 70 experts via an online form for responses using a 5-point Likert scale (1-Strongly Disagree, 2-Disagree, 3-Neutral, 4-Agree, 5-Strongly Agree). In Phase 2, an in-person meeting of 20 was convened with live polling. Consensus was achieved (≥70%) on 10 statements. Statements with <70% consensus were revised, and the final consensus statements were finalised.

Expert opinion

Consensus #1: IDA is more prevalent in HD-CKD patients as compared to non-dialysis CKD patients.

Rationale: As kidney disease progresses, anemia increases in prevalence, affecting up to 90% of the dialysis population.⁶ The primary cause of anemia in CKD patients is erythropoietin insufficiency. A large number of observational studies and clinical trials have established the key role of iron deficiency in anemia of CKD.^21–23 A complex interplay involving elevated hepcidin levels, driven by chronic inflammation, particularly interleukin activity, and reduced glomerular filtration rate inhibits iron absorption and release, limiting its availability for effective erythropoiesis, thereby contributing to the development and persistence of anemia.²⁴ IDA occurs is more common in HD-dependent CKD patients due to blood loss from frequent sampling and blood retained in the dialysis machine, as well as inflammation-driven iron sequestration, poor iron absorption, and increased iron demand from ESA use.^25–27

Consensus #2: IDA diagnosis in HD-CKD patients involves the determination of Hb, Serum Ferritin, TSAT, and TIBC.

Rationale: IDA diagnosis relies on the estimation of Hb, serum ferritin, transferrin saturation (TSAT), and total iron-binding capacity (TIBC). These tests are widely available in clinical laboratories. Although the percentage of hypochromic RBCs and reticulocyte hemoglobin content are considered better indicators, they are largely limited to research settings.

TSAT is recommended in several guidelines and studies due to its excellent sensitivity and specificity.²⁸ A simplified diagnostic approach for patients with CKD suggests diagnosing iron deficiency using the following criteria: serum ferritin levels <100 μg/L or TSAT <20%. A TSAT test is necessary to confirm iron deficiency if serum ferritin levels fall between 100 and 300 μg/L.²⁹ The Japanese Society for Dialysis Therapy (JSDT) Guidelines for Renal Anemia in CKD recommend evaluating serum ferritin levels and TSAT to assess iron deficiency in HD patients and determine the need for IV iron supplementation.³⁰ The 2012 KDIGO guideline did not clearly define iron supplementation thresholds for HD-CKD patients. In contrast, the 2024 KDIGO draft guidelines for anemia management recommend initiating iron therapy when TSAT is below 30% and serum ferritin levels are below 500 ng/mL.^3,31

The findings of the PIVOTAL trial, a large randomized controlled trial, demonstrated that proactive IV iron therapy to maintain ferritin levels above 700 ng/mL and TSAT at around 40% was effective and safe. However, it leaves open the question of whether moderate iron targets might be equally effective.^1,2 Additionally, the DRIVE trial, a large randomized controlled trial, found that even with ferritin >800 ng/mL, IV iron improved haemoglobin levels and reduced ESA requirements in CKD G5HD patients.^3,32

Consensus #3: To diagnose IDA in HD-CKD patients, serum ferritin should be < 200 ng/mL.

Rationale: The panel agreed that a serum ferritin level <200 ng/mL is crucial for diagnosing absolute IDA in HD-CKD. European Renal Best Practice (ERBP) guidelines recommend that in CKD, absolute iron deficiency is likely when TSAT is ≤20% and serum ferritin is ≤200 ng/mL in those undergoing HD.³³ The KDIGO 2012 guideline recommended iron therapy initiation when TSAT <30% and ferritin <500 ng/mL, but acknowledged lower ferritin levels as more indicative of absolute deficiency.³¹ The KDIGO 2024 guideline reinforces the use of TSAT ≤20% and ferritin ≤200 ng/mL for diagnosing absolute IDA, emphasizing the need for individualized assessment and the integration of inflammation markers.³ In addition, a review article,³⁴ proposed that serum ferritin <30 μg/L indicates absolute iron deficiency in individuals without inflammation, while levels <100 μg/L or TSAT <20% suggest deficiency in the presence of inflammation. For ferritin values between 100-300 μg/L, a TSAT assessment is recommended to confirm the diagnosis.³⁴

Consensus #4: To diagnose IDA in HD-CKD patients, TSAT should be <30%.

Rationale: There has been a shift in opinion over the past 3–4 years. Earlier, for the diagnosis of IDA in HD-CKD patients, TSAT levels of <20% and serum ferritin levels of <200 ng/mL were accepted parameters.³⁵ Currently, experts suggest that TSAT and serum ferritin thresholds can be safely increased to 30% and 800 ng/mL, respectively, setting new upper limits for iron administration. These revised thresholds are being considered for iron therapy for patients with CKD.

The KDIGO 2024 guideline suggests using TSAT <30% and ferritin ≤500 ng/mL as thresholds for identifying iron deficiency in HD-CKD patients, which also guides the initiation of IV iron therapy.³ This alignment highlights the diagnostic and therapeutic value of these markers. Supporting evidence comes from several key trials. The PIVOTAL trial enrolled patients with TSAT <30% and ferritin <400 ng/mL.³⁶ The DRIVE I and II trials included patients with TSAT ≤25% and ferritin between 500-1200 ng/mL; IV iron led to improved Hb levels and reduced ESA use despite elevated ferritin, underscoring TSAT’s reliability in identifying functional iron deficiency in inflammatory states.³⁷ Both trials consistently support TSAT <30% as a diagnostic threshold for guiding iron therapy.

Refer to Table 1 for guidelines and recommendations for the threshold TSAT value to diagnose IDA in HD-CKD patients.

Consensus #5: TSAT should be used as the primary parameter for diagnosing IDA in HD-CKD patients.

Rationale: Assessing serum ferritin levels and TSAT helps guide anemia treatment in HD-CKD patients.³⁸ TSAT is less influenced by inflammation. Reduced iron availability leads to a low TSAT level.³⁴ Inflammation appears to have minimal impact on TSAT, as this parameter fluctuates less than serum ferritin in inflammatory conditions. Thus, TSAT is a more reliable marker for iron deficiency in chronic diseases.³⁹ Studies have supported TSAT as an indicator of iron metabolism by examining its influence on the hemoglobin response in dialysis patients.⁴⁰ A study involving 10 ferritin assays and five TSAT assays found a 63% variation in reported serum ferritin levels, but only a 10% variation for TSAT.³⁴ According to KDIGO 2012, initial anemia workup in CKD should include CBC, reticulocyte count, serum ferritin, TSAT, and vitamin B12 and folate levels.³¹ The KDIGO 2024 continues to recommend both ferritin and TSAT for assessing iron status and guiding IV iron therapy.³

Consensus #6: IV iron therapy should be initiated in IDA in HD-CKD patients when TSAT is ≤30% and Serum Ferritin ≤500 ng/mL.

Rationale: IV iron therapy has been recommended for the treatment of IDA by the KDIGO 2012 & 2024 guidelines in HD-CKD patients when TSAT is ≤30% and serum ferritin is ≤500 ng/mL.^3,31 The panel agrees that these thresholds are effective indicators for initiating IV iron therapy to manage iron deficiency in this patient population. Refer to Table 2 for guidelines for initiating IV iron therapy for IDA in HD-CKD patients.

Consensus #7: FCM is the preferred IV iron in managing IDA in HD-CKD patients.

Rationale: A majority of the panel members agreed that FCM is the IV iron of choice for patients with IDA in HD-CKD. The panel identified that the cost of FCM is a barrier to its wider adoption.

FCM is a non-dextran iron complex for rapid IV administration in large doses.¹⁸ In a real-world study involving HD patients by Hofman et al., all groups saw an increase in Hb (anemic [1.4 g/dL, p < 0.001] and iron deficient patients [0.6 g/dL, p < 0.001]); however, patients who got FCM needed a lower weekly iron dose than those who received IS (48 vs. 55 mg/week, p = 0.04). Therefore, transitioning from iron sucrose (IS) to FCM led to improved iron status despite a lower weekly dose. Additionally, the switch was associated with a reduction in ESA dosage, while Hb levels increased.⁴¹ A smaller percentage of those receiving FCM experienced at least one drug-related adverse event compared to those treated with IS.¹⁸ A systematic review and meta-analysis by Bharadwaj et al. compared intravenous FCM with iron sucrose (IS) for the treatment of IDA. The FCM group showed a significantly greater increase in hemoglobin levels [standardized mean difference: 0.59 g/dL; 95% CI: 0.26-0.93; p = 0.001] and ferritin levels [normalized mean difference: 54.85 µg/L; 95% CI: 36.33-74.37; p = 0.001], along with a 26% lower incidence of adverse effects compared to the IS group (p = 0.001).⁴²

Refer to Table 3 for studies on FCM use in IDA patients undergoing HD.

Consensus #8: The FCM should be administered in patients with IDA HD-CKD, in a dose of 15 mg/kg body weight.

Rationale: The panel highlighted that the traditional calculation of iron deficiency using the Ganzoni equation has become redundant with the advent of newer IV iron therapies that enable more efficient and rapid correction of iron levels, thereby reducing the need for precise deficiency calculations. FCM lacks dextran and thus has a low potential for immunogenicity and risk of triggering anaphylactic reactions. As a result, higher doses (15 mg/kg, up to a maximum of 1000 mg per infusion) can be administered in a single, rapid session (15-minute infusion) without a preliminary test dose.⁴³

Bailie et al. conducted a randomized, double-blind, placebo-controlled, crossover trial involving 559 patients with iron deficiency anemia to evaluate the safety of intravenous ferric carboxymaltose (FCM; 15 mg/kg, maximum 1000 mg over 15 minutes). Treatment-emergent adverse events were reported in 29.3% of patients following FCM administration and 19.7% after placebo, the majority being Grade 1 or 2. Drug-related adverse events (9.3% with FCM vs. 4.8% with placebo) were infrequent. Overall, FCM was well tolerated with a low incidence of serious adverse reactions.⁴⁴ A review article by Cancado and Friedrisch reported that, in most trials, patients received either FCM at 1000 mg (or 15 mg/kg for those weighing less than 66 kg) administered over 15 minutes or oral ferrous sulfate. FCM was at least as effective as ferrous sulfate in improving Hb levels and achieving a hematologic response at various time points. FCM led to more rapid improvements in Hb levels and iron stores compared to ferrous sulfate.⁴⁵

Consensus #9: Initiation of iron therapy should be done either with a high dose or with 200 mg per dialysis session until the total initiation dose is achieved.

Rationale: The current clinical practice for IDA management in patients with HD-CKD frequently involves high-dose FCM, given either as two 500 mg doses one week apart or as a single 1000 mg dose (a high-dose, low-frequency approach). Experts attribute this to the minimal free iron FCM release. It also has implications for the provision of iron supplements. Further data from real-world studies are needed to validate this approach and guide optimal dosing.

In a study by Covic et al., administering IV iron (FCM) at 100-200 mg/day, two to three times weekly, for ≤6 weeks, proved both good tolerance and an increase in Hb and iron stores. Most patients (61.7%) responding to the treatment showed a clinically significant increase in Hb levels (≥1.0 g/dL).¹⁹ In a randomized, active-controlled, multicenter trial, single doses of 200 mg in patients with HD-CKD and up to 1000 mg in those with NDD-CKD were well tolerated and demonstrated efficacy comparable to that of standard medical care.²⁰ Refer to Table 4 for guidelines recommendations from the NICE 2021 guidelines.

Consensus #10: The maintenance dose of FCM (post-correction of initial Iron deficit) in IDA HD-CKD patients is 100-200 mg every 2-4 weeks.

Rationale: Maintenance doses are generally given every 2-4 weeks, starting with an initial loading dose, followed by 100 mg each month. Concerns were raised about the potential for overuse of iron if serum ferritin levels are not regularly monitored, leading to excessively high serum ferritin levels (e.g., 2000, 3000, or 4000 ng/mL). The cost of serum iron testing and other iron parameters can exceed the cost of iron supplements.

Diebold et al. conducted an observational study in hemodialysis patients receiving a stable maintenance regimen of ferric carboxymaltose (FCM) at doses of 100 mg or 200 mg every four weeks. Serum ferritin and transferrin saturation (TSAT) levels were monitored over a four-week period following FCM administration. A 100 mg dose resulted in a mean increase in serum ferritin of 113 ± 72.2 μg/L (p < 0.001), which remained significantly elevated for two weeks. In contrast, the 200 mg dose produced a greater rise of 188.5 ± 67.56 μg/L (p < 0.001), sustained through the third week. TSAT increased by 12.0 ± 9.7% (p < 0.001) with 100 mg FCM and by 23.1 ± 20.4% (p = 0.002) with 200 mg FCM; however, TSAT levels returned to baseline within four days in both groups.⁴⁶ A narrative review by Pandey et al. suggested that to maintain stable iron stores in patients on HD, monthly IV iron doses commonly range from 100 to 400 mg, compensating for ongoing iron losses due to blood sampling, losses in the HD circuit, and occult gastrointestinal bleeding.⁴⁷

Consensus #11: IV iron should be used in IDA HD-CKD patients for maintaining TSAT >30% and serum ferritin between 500-800 ng/mL.

Rationale: The panel agreed that patients on HD receiving IV iron therapy should be guided by maintaining a TSAT >30% and serum ferritin levels between 500-800 ng/mL. This strategy optimizes iron status and supports erythropoiesis, ensuring effective anemia management in this population. Iron therapy should be based on iron status test results and the patient’s clinical condition.⁴⁸

The National Institute for Health and Care Excellence (2015)⁴⁹ and the Renal Association (2017)⁵⁰ Guidelines recommend a serum ferritin threshold of 800 ng/mL for withholding IV iron in dialysis patients.⁵¹ The KDIGO 2012 guidelines recommended initiating IV iron therapy if the TSAT is ≤30% and the serum ferritin level is ≤500 ng/mL, and suggested withholding iron when the ferritin level exceeds 800 ng/mL.³¹ The KDIGO 2024 reaffirms these thresholds, recommending the initiation of IV iron in HD patients with a TSAT ≤30% and ferritin ≤500 ng/mL, and supports a proactive approach to maintaining stable iron status.³

The DRIVE study demonstrated that IV ferric gluconate significantly improved haemoglobin levels in anemic HD patients with ferritin 500–1200 ng/mL and TSAT <25%, compared to no iron. The response was independent of baseline ferritin, with greater TSAT improvement and no increase in adverse events. These findings support IV iron use even at higher ferritin levels when TSAT is low.³²

Consensus #12: Hemoglobin levels should be tested monthly in HD-CKD patients receiving FCM.

Rationale: The panel agrees that Hb levels should be monitored monthly in HD-CKD patients receiving FCM. Regular monitoring ensures effective anemia management, helps assess the response to therapy, and prevents complications. The Renal Association’s clinical practice guidelines on anemia in CKD recommend regularly monitoring iron levels every 1 to 3 months in patients receiving IV iron to prevent toxicity (Strength of recommendation: 2, Level of evidence: B).⁵⁰ The KDIGO 2012 guidelines recommend that the frequency of Hb monitoring, regardless of CKD stage, should be guided by the Hb level, patients with more severe anemia or a faster Hb decline may require more frequent monitoring. For adults with CKD stage V on HD (CKD 5HD) not receiving ESA treatment, monthly monitoring is recommended at a minimum. In CKD 5HD patients, Hb levels are checked before a mid-week HD session.³¹ The KDIGO 2024 guideline reinforces this practice, stating that in CKD G5HD patients treated with iron, monthly testing of hemoglobin, serum ferritin, and TSAT is reasonable to guide therapy decisions and maintain safe, effective anemia control.³

Consensus #13: Iron profiles (Serum Ferritin, TSAT, and TIBC) should be monitored every 3 months to ensure effective FCM therapy in patients with HD-CKD.

Rationale: The experts entirely agreed that iron profiles, including serum ferritin, TSAT, and TIBC, should be monitored every three months to ensure the appropriate dosing of the Iron (FCM) therapy in patients with HD-CKD. Regular monitoring is essential to prevent iron overload or deficiency.

This recommendation aligns with current international guidelines. The 2021 NICE guidelines recommend testing for iron deficiency and assessing potential responsiveness to iron therapy and long-term iron needs every three months. Iron testing should be done every 1 to 3 months for individuals undergoing HD.⁵² The KDIGO 2012 guidelines recommend that for stage V HD patients, monitoring should occur at least monthly (4 weeks).³¹ KDIGO 2024 further supports testing hemoglobin, ferritin, and TSAT every 3 months in non-dialysis or CKD G5PD patients, and monthly in CKD G5HD patients.³ Similarly, JSDT guidelines recommend measuring the serum ferritin and TSAT at least every three months. The guidelines further recommend monthly serum ferritin measurement while HD patients are on iron supplementation.³⁰

The importance of appropriate timing in iron assessment is supported by a prospective observational study evaluating intravenous FCM in hemodialysis patients. Administration of 100 mg or 200 mg FCM led to transient, dose-dependent elevations in ferritin and TSAT. Ferritin remained elevated for up to 2-3 weeks, while TSAT returned to baseline within 4 days. These findings underscore the need to align iron profile testing with dosing schedules to avoid misinterpretation of true iron status.⁴⁶

Consensus #14: FCM has a balanced risk-benefit profile in IDA patients with HD-CKD.

Rationale: The panel unanimously agrees that FCM has a good safety profile for treating IDA in patients with HD-CKD. Studies suggest that an iron complex’s toxic effects can be predicted based on its physicochemical properties, such as molecular mass, and kinetic and thermodynamic stability. FCM is a strong, stable iron complex that exhibits the characteristics of an ideal iron compound. Due to its high structural uniformity and slow degradation kinetics, IV FCM administration leads to low toxicity and efficient iron delivery to the reticuloendothelial system, with distribution to the bone marrow, liver, and spleen.^53,54

A randomized study showed a temporary and asymptomatic drop in serum phosphate levels following FCM administration in HD patients, which may last up to three months.¹⁹

This decline in phosphate levels is mediated through fibroblast growth factor 23 (FGF23)-dependent pathways. However, in patients with stage V CKD, who frequently present with persistent hyperphosphatemia, the phosphate-lowering effect of FCM is typically mild, well tolerated. It may offer a potential therapeutic benefit rather than pose a clinical risk. Thus, the overall safety and pharmacological profile of FCM supports its use as a preferred IV iron therapy in this population.⁵⁵

Consensus #15: FCM improves cardiovascular outcomes in IDA HD-CKD patients.

Rationale: A majority of the panel agreed that FCM enhances cardiovascular outcomes in patients with IDA undergoing HD-CKD, particularly in reducing hospitalization rates and improving overall cardiovascular health. Dalal et al. conducted a meta-analysis of two randomized controlled trials involving 760 patients with chronic heart failure (CHF), comparing ferric carboxymaltose (FCM; n = 455) to placebo (n = 305). FCM significantly reduced hospitalizations for worsening heart failure (Risk Ratio [RR] 0.34; 95% CI: 0.19–0.59; p = 0.0001) and for any cardiovascular cause (RR 0.49; 95% CI: 0.35–0.70; p < 0.0001), with no heterogeneity (I² = 0%). No significant difference was found for mortality due to worsening HF (RR 0.41; 95% CI: 0.02–7.36; p = 0.55) or cardiovascular death (RR 0.80; 95% CI: 0.40–1.57; p = 0.51). The findings support FCM’s role in reducing hospital burden, though its impact on mortality remains inconclusive.⁵⁶ Although these results are promising, more research is needed to confirm the long-term benefits of FCM on heart health in this group.

Discussion

In this consensus, we introduce the I2 M2 framework—Investigate, Initiate, Monitor, and Maintain—as a systematic approach to anemia management in patients with HD-CKD [Figure 2]. The “Investigate” step involves conducting appropriate diagnostic tests, such as Hb, serum ferritin, TSAT, and TIBC to confirm IDA and assess the overall iron status. In the “Initiate” phase, treatment is started using the initial/loading total FCM dose, with the total iron requirement calculated based on the individual patient’s weight and other relevant parameters. The “Monitor” phase evaluates the patient’s Hb levels with a minimum 4-week interval between assessments to ensure response to iron replacement. Finally, the “Maintain” phase involves re-evaluating the iron profile every 3 months to assess the necessity of a maintenance FCM dose, thereby ensuring long-term IDA management. This structured approach provides a comprehensive strategy for optimizing anemia management in patients with HD-CKD.

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Figure 2:

I²M² approach for anemia management in HD-CKD patients. FCM: Ferric carboxymaltose, Hb: Hemoglobin, IDA: Iron deficiency anemia, TIBC: Total iron binding capacity, TSAT: Transferrin saturation, HD-CKD: Hemodialysis-chronic kidney disease.

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Algorithm

Figure 3 outlines a stepwise approach to the diagnosis and management of iron deficiency in HD-CKD patients. Expert recommendations [Table 5] aim to fill critical gaps in data and clinical practice guidelines in the Indian context, offering practical guidance for optimizing IDA management and improving patient outcomes in this population.

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Figure 3:

Proposed algorithm for diagnosis and management of IDA in patients with HD-CKD. ID: Iron deficiency, IV: Intravenous, TSAT: Transferrin saturation, TIBC: Total iron binding capacity, IDA: Iron deficiency anemia, HD-CKD: Hemodialysis-chronic kidney disease.

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This consensus provides a structured framework, the I2 M2 approach, for managing IDA in patients with HD-CKD. It emphasizes FCM as the preferred IV iron formulation due to its efficacy and safety profile, especially when TSAT is ≤30% and serum ferritin is ≤500 ng/mL. Expert consensus aims to fill critical gaps in data and clinical practice guidelines in the Indian context, offering practical guidance for optimizing IDA management and improving patient outcomes in this population.