Anemia: Targets, ESAs, and Hyporesponsiveness

Bottom Line

The hemoglobin lesson is the most expensive lesson in nephrology. It took two decades of trials to learn that a normal number is not a healthy patient.

• KDIGO rewrote the anemia guideline in January 2026 — its first full update since 2012, summarized for internists in Annals in September 2026 ^1,2,3. For dialysis it keeps ESA initiation at a hemoglobin (Hb) of 9.0–10.0 g/dL or below (2D), makes the ceiling a recommendation — target below 11.5 g/dL (1D) — and prefers an ESA over a HIF-PH inhibitor as first-line therapy (2D) ¹.
• The US label is stricter than the guideline. Epoetin labeling says to reduce or interrupt the dose when Hb approaches or exceeds 11 g/dL in dialysis patients ⁴. A unit protocol has to pick one number and say so.
• The hemodialysis target trials are the Normal Hematocrit Trial and Parfrey 2005 ^5,6. CHOIR, CREATE, and TREAT — the trials most often quoted — enrolled non-dialysis CKD ^7,8,9. The direction of harm is the same; the population is not.
• ESA hyporesponsiveness is a prognosis, not a dosing problem. Poor responders die more, whichever drug they receive ^10,11,12. Find the cause — iron, inflammation, access infection, underdialysis, hyperparathyroidism, blood loss — and avoid escalating beyond double the stable dose ¹.
• KDIGO 2026 allows a 3–4-month HIF-PHI trial for persistent hyporesponsiveness when there is a reason to raise Hb (practice points 3.7.2–3.7.4). The caveat: the truly hyporesponsive and inflamed patients were excluded from the HIF-PHI trials ^1,13.

What Changed: KDIGO 2012 to KDIGO 2026

The 2026 guideline supersedes the 2012 document. For hemodialysis, the changes that matter most are below; the 2012 column also reflects the KDOQI US commentary on that guideline ^1,13,14,15.

Rec = graded recommendation; PP = practice point (ungraded). In KDIGO notation, 1 is a recommendation and 2 a suggestion; the letter grades the certainty of evidence, from A (high) to D (very low). Both headline hemoglobin numbers on this page rest on D-grade evidence.

1. Why Hemodialysis Patients Are Anemic

Five mechanisms stack. Only one of them is erythropoietin.

Relative erythropoietin deficiency. The anemia of CKD is typically normocytic and normochromic and is driven primarily by a relative reduction in renal erythropoietin (EPO) synthesis, reflecting both lost kidney mass and a disrupted renal oxygen-sensing mechanism ¹³. “Relative” is the key word: the EPO level is inappropriately low for the degree of anemia, not necessarily low in absolute terms.

Hepcidin and inflammation. Inflammation drives hepatic hepcidin, which downregulates the iron exporter ferroportin on enterocytes and macrophages. Dietary iron is not absorbed and stored iron is not released ^13,16. The result is iron-restricted erythropoiesis: a normal or high ferritin with a low transferrin saturation (TSAT) ^13,17. This is why oral iron works poorly in hemodialysis, why ferritin misleads, and why every infection, catheter, and failed graft shows up in the ESA dose.

Blood loss on dialysis. Every treatment costs blood — sampling, dialyzer and circuit residual, clotting, and post-needle bleeding. Sargent’s measured-loss studies, done with 1990s-era circuits, projected 2,516 to 5,126 mL of blood lost per year on conventional thrice-weekly hemodialysis ¹⁸. As derived arithmetic (not from the source): at Hb 11 g/dL a milliliter of blood carries roughly 0.38 mg of iron, so those losses equal roughly 0.9 to 1.9 g of iron per year. That is why nearly every hemodialysis patient on an ESA needs ongoing IV iron.

Shortened red-cell survival. In a small chromium-51 study of 22 patients, red-cell half-life was 14.5 days in thrice-weekly hemodialysis patients versus 23.5 days in healthy controls — unchanged from measurements made half a century earlier and not improved by nocturnal or short-daily hemodialysis ¹⁹.

Contributors that can be fixed. Underdialysis blunts the EPO response: raising the urea reduction ratio (URR) from 60.7% to 72% for six weeks raised hematocrit from 28.4% to 32.3% in an uncontrolled comparison ²⁰. Severe secondary hyperparathyroidism with marrow fibrosis tripled the EPO dose needed (174 versus 56 U/kg three times weekly) ²¹. KDIGO 2026 lists the rest: nonadherence, hypothyroidism, infection or inflammation, dialysis-related and gastrointestinal blood loss, malnutrition, iron or B12/folate deficiency, marrow disorders including pure red-cell aplasia (PRCA), hemolysis, and malignancy ¹.

2. Evaluation and Monitoring

Definition and the initial panel

KDIGO 2026 keeps the WHO definition of anemia — Hb below 13 g/dL in men and below 12 g/dL in women — and replaces the old initial panel with a CBC, reticulocyte count, ferritin, and TSAT (PP 1.2.1) ¹. B12 and folate are no longer routine at diagnosis; they move to an expanded panel ¹. The European Renal Best Practice (ERBP) commentary pushes back: test them in macrocytosis, cognitive impairment, malnutrition, diabetes, advanced age, and frailty — which describes much of a dialysis unit ¹³.

Hemoglobin beats hematocrit in dialysis because hematocrit swings more with plasma volume ¹³. Draw it pre-dialysis, on a consistent day of the week, so that the monthly number reflects biology rather than ultrafiltration.

How often

Source for the KDIGO column: ¹. KDIGO 2026’s “every 3 months” is a minimum, and it is looser than KDIGO 2012, which asked for Hb at least monthly during maintenance ESA therapy in dialysis ¹⁴. Nothing in the 2026 guideline argues against monthly testing, and the label asks for it.

Ferritin and TSAT: what they can and cannot tell you

• Ferritin is an acute-phase reactant. A ferritin above 800 ng/mL with a TSAT below 20% has become a common pattern in dialysis, and it usually means inflammation-locked iron rather than overload ¹⁷.
• TSAT reflects iron available to the marrow right now. It is sensitive to timing: it jumps after an IV iron dose, and most observational studies never report when TSAT was drawn relative to iron ¹³. Draw iron studies at the scheduled draw, before that session’s iron dose, and record the date of the last IV iron.
• A high ferritin does not mean no response to iron. DRIVE (RCT) randomized 134 anemic hemodialysis patients with ferritin 500–1,200 ng/mL and TSAT ≤25% on high-dose epoetin to ferric gluconate 125 mg for eight sessions or no iron. Hb rose 1.6 versus 1.1 g/dL at six weeks (P=0.028), and the benefit was the same above and below a ferritin of 800 ²³. Six weeks is short, and DRIVE says nothing about long-term safety at those ferritins.

Reticulocyte hemoglobin (CHr or Ret-He)

Reticulocyte hemoglobin measures iron delivered to red cells made in the last few days. In 164 hemodialysis patients, a CHr below 26 pg predicted a reticulocyte response to IV iron with sensitivity 100% and specificity 80%, outperforming ferritin and TSAT — in a 32-patient challenge subset (diagnostic cohort) ²⁴. KDIGO 2026 did not adopt CHr; ERBP notes that other guidelines do ¹³. Where the laboratory reports it, reticulocyte hemoglobin is a reasonable tiebreaker when ferritin and TSAT disagree. Several cutoffs circulate, and none is guideline-endorsed in 2026.

When to look further

If iron indices do not explain the anemia, KDIGO’s expanded panel (PP 1.2.2) is a peripheral smear, haptoglobin, LDH, CRP, B12, folate, liver tests, serum protein electrophoresis with immunofixation and free light chains, urine Bence-Jones protein, TSH, PTH, and fecal occult blood ¹. Add reticulocytes to separate a hypoproliferative marrow from hemolysis or bleeding ¹³.

3. Hemoglobin Targets and ESA Safety

The trials

Meta-analyses of RCTs. Across nine target trials (n=5,143), higher targets increased all-cause mortality (RR 1.17, 1.01–1.35) and access thrombosis (RR 1.34, 1.16–1.54) ²⁶. Across 27 trials (n=10,452), higher targets increased stroke (RR 1.51), hypertension (RR 1.67), and access thrombosis (RR 1.33); mortality was not significantly higher (RR 1.09, 0.99–1.20) ²⁷. The 2023 Cochrane network meta-analysis (117 trials, 25,237 participants) found that ESAs prevent transfusion versus placebo with low-to-moderate certainty and have uncertain effects on death ²⁸.

Reading these trials critically

• Population. Three of the five famous trials enrolled non-dialysis CKD. The hemodialysis evidence is the Normal Hematocrit Trial (a harm signal in patients with heart disease) and Parfrey (no structural benefit, more cerebrovascular events). The direction agrees; the applicability is borrowed.
• The published Normal Hematocrit Trial understated the harm. Coyne compared the 1996 FDA-filed report with the 1998 NEJM paper: randomization to the higher target increased the primary endpoint and death with conventional 95% confidence intervals that excluded 1, and the reported physical-function benefit was a secondary association with achieved Hb, not a randomized effect ²⁵. The normal-hematocrit arm also received more IV iron dextran and had lower dialysis adequacy ⁵.
• Target or dose? In CHOIR, the harm tracked a high epoetin dose and failure to reach target, not the achieved Hb itself ²⁹. In TREAT, the lowest-quartile initial responders received higher doses and had more cardiovascular events (aHR 1.31) and deaths (aHR 1.41) ¹⁰. In the Normal Hematocrit Trial’s high arm, the least responsive quartile had 34% one-year mortality versus 14% in the most responsive ¹¹. These are secondary analyses, confounded by the sickness that causes hyporesponse, but they are why “don’t escalate into resistance” became doctrine.
• Surrogate endpoints cut both ways. Hb is a surrogate. The trials that moved it furthest moved outcomes the wrong way.

The FDA position

The ESA boxed warning (epoetin alfa label, revised April 2024) states that ESAs increase the risk of death, myocardial infarction, stroke, venous thromboembolism, thrombosis of vascular access, and tumor progression; that targeting Hb above 11 g/dL increased serious cardiovascular risk; that no trial has identified a hemoglobin target, ESA dose, or dosing strategy that does not increase these risks; and that the lowest dose sufficient to reduce transfusion should be used ⁴. For adults on dialysis the label says: initiate when Hb is below 10 g/dL; reduce or interrupt when Hb approaches or exceeds 11 g/dL ⁴.

The guideline position

• Start: Hb 9.0–10.0 g/dL or below in dialysis (Rec 3.2.1, 2D) ¹.
• Ceiling: target below 11.5 g/dL (Rec 3.3.1, 1D) — now a “we recommend” ¹. The 2012 “never intentionally above 13 (1A)” statement no longer appears as a separate recommendation.
• Individualize within that range for symptoms, transfusion risk, and cardiovascular or cancer risk (PP 3.1.1, 3.3.1) ¹.
• ERBP dissents at the floor. It would not let Hb routinely fall below 10 g/dL and endorses a 10–12 g/dL maintenance band ¹³. The KDOQI commentary on the 2012 guideline made a related point: there was little evidence that 11–11.5 is unsafe, and a lower bound of 9 may increase transfusion ¹⁵.

What happened when the US lowered its targets

After the 2011 bundled payment and FDA label change, the share of US hemodialysis patients with Hb above 11 g/dL fell from 68% (2006) to 28% (2016), and the share below 9 g/dL rose from 5% to 9%. Adjusted MACE (aHR 0.95), stroke (0.83), and mortality (0.87) were lower after the policy change; MI was slightly higher (1.04) ³⁰. Transfusions rose, but modestly — approximately a 7% relative increase in the monthly probability of transfusion ³¹. These are observational, interrupted-time-series data layered on secular improvements in dialysis care. They are consistent with the trials. They do not prove them.

4. Erythropoiesis-Stimulating Agents

The agents

Starting doses and adjustments are from KDIGO 2026 Table 7 ¹. No ESA has shown an outcome advantage over another; the Cochrane network meta-analysis found comparative effects uncertain ²⁸.

Route: IV or subcutaneous

In a VA trial (RCT) of 208 hemodialysis patients, subcutaneous epoetin maintained hematocrit with a 32% lower dose than IV ³⁵. That saving applies to short-acting epoetin, not to darbepoetin or methoxy PEG-epoetin beta ¹³. KDIGO 2026 leaves the route to patient preference, local practice, and cost (PP 3.4.2.1) ¹; the epoetin label recommends IV for hemodialysis ⁴. The historical cautionary tale is anti-EPO antibody pure red-cell aplasia, linked mainly to subcutaneous exposure — 13 patients with neutralizing antibodies in Casadevall’s original series ^13,36. Giving the ESA IV into the circuit, as US units do, is reasonable.

Dose-adjustment rules: convergent across label and guideline

• Do not increase more often than every 4 weeks. Decreases may be more frequent ^1,4.
• Rapid rise: Hb up more than 1 g/dL in any 2-week period → reduce by 25% or more (label) ⁴. KDIGO: a rise of more than 1.0 g/dL in 2–4 weeks after initiation → reduce by 25–50% (PP 3.4.1.2) ¹.
• Slow rise: Hb up less than 1 g/dL after 4 weeks → increase by 25% ⁴.
• Falling Hb: “to avoid a rapid decline in Hb, consider reducing the ESA dose rather than holding ESA therapy, as long as the Hb does not exceed 11.5 g/dL” (PP 3.4.3.2) ¹.
• Twelve weeks without response: further escalation is unlikely to help and may increase risk; evaluate other causes ⁴.

ESA hyporesponsiveness

Definition. KDIGO 2026 keeps its 2012 relative definitions (Table 10) ¹:

• Initial: no Hb increase after the first month on appropriate weight-based dosing.
• Acquired: two dose increases of up to 50% beyond a previously stable dose are needed to hold Hb steady.
• Stop point: avoid repeated escalation beyond double the initial or previously stable dose.

Absolute-dose definitions also circulate — for example, KDOQI’s more than 450 IU/kg/week of IV epoetin or more than 300 IU/kg/week subcutaneously ^1,13. Prevalence depends almost entirely on which definition is used ¹³.

Prognosis. In a secondary analysis of ASCEND-D (observational within a trial), baseline hyporesponsiveness — 12–20% of patients by three definitions — predicted MACE with an aHR of 1.32–1.36, with no interaction by randomized drug ¹². The patient is the risk; the drug is not the rescue.

Causes and first moves.

A stepwise workup. The sequence below condenses the causes above into an order of operations ^1,13:

1. Iron first. TSAT below 20% or a low CHr → IV iron. A ferritin below 45 or MCV below 80 → blood-loss evaluation.
2. Then inflammation. A rising CRP or a plausible source → treat the catheter, wound, failed graft, or occult infection.
3. Then the rest of the list. Check Kt/V, PTH, B12 and folate, TSH, LDH and haptoglobin, the smear, and protein electrophoresis with free light chains.
4. Cause found → treat it and reassess in 4–8 weeks.
5. No cause, no symptoms, low transfusion risk → accept a lower Hb and do not escalate beyond twice the stable dose.
6. No cause, but symptomatic or at transfusion risk → a 3–4-month HIF-PHI trial or transfusion; stop the HIF-PHI if there is no response.
7. Sudden severe anemia with reticulocytes near zero → suspect PRCA: stop the ESA and involve hematology.

Practice points 3.7.2–3.7.4 allow the 3–4-month HIF-PHI trial for persistent hyporesponsiveness when there is a reason to raise Hb, at the lowest effective dose, discontinued if it fails ¹. ERBP supports the trial but notes that the truly hyporesponsive and inflamed patients were excluded from the HIF-PHI trials ¹³ — so the trial is a reasonable experiment, not an evidence-based rescue. For suspected ESA-related PRCA: stop the ESA, transfuse as needed, involve hematology, and consider a HIF-PHI (PP 3.7.6) ¹. US availability and the HIF-PHI trial evidence are covered in the companion page.

ESA adverse effects that matter at the chair

• Hypertension. About 25% of dialysis patients needed new or increased antihypertensives after epoetin initiation; uncontrolled hypertension is a contraindication, and the label says to reduce or withhold the ESA if blood pressure becomes difficult to control ⁴. The pressor effect is partly independent of the rise in red-cell mass ³⁸.
• Access thrombosis. Higher targets raise access thrombosis by approximately a third ^26,27, and the label lists thrombosis of vascular access in the boxed warning ⁴.
• Stroke. TREAT: HR 1.92 ⁹.
• Seizures, especially in the first months of therapy — monitor for premonitory symptoms ⁴.
• Cancer. The boxed warning covers tumor progression; KDIGO asks for shared decision-making about ESA use in active or prior cancer, especially when treatment aims at cure (PP 3.4.3.5) ^1,4.
• Circuit clotting. Patients on an ESA may need more heparin during hemodialysis ⁴.

Evidence Gaps

1. No modern hemodialysis trial of Hb targets within the 9.5–11.5 range. The 11.5 ceiling is a 1D recommendation built on older, mostly non-dialysis trials ¹.
2. Target versus dose. Is the harm from a high Hb, from high ESA exposure, or from the illness that causes hyporesponse? Only secondary analyses speak to it ^10,11,29.
3. Treating hyporesponsiveness. No RCT shows that any intervention in hyporesponders improves outcomes; anti-inflammatory approaches such as IL-6 blockade remain investigational ¹³.
4. Sex differences. Women on dialysis need higher ESA doses; whether the same targets apply is unknown ¹³.
5. Patient-reported outcomes. The fatigue and quality-of-life benefits of ESAs remain modest or uncertain ^7,9.

At the Chair

References

Numbered for this page. Each reference was checked against its PubMed record or the primary document (guideline, FDA label, agency page) in September 2026.

1. Kidney Disease: Improving Global Outcomes (KDIGO) Anemia Work Group. KDIGO 2026 Clinical Practice Guideline for the Management of Anemia in Chronic Kidney Disease (CKD). Kidney Int. 2026;109(1S):S1-S99. PMID: 41485812
2. Babitt JL, Berns JS, Bozkurt B, et al. Executive Summary of the KDIGO 2026 Clinical Practice Guideline for the Management of Anemia in Chronic Kidney Disease (CKD). Kidney Int. 2026;109(1):44-56. PMID: 41485807
3. Hedayati SS, Babitt JL, Berns JS, et al. Evaluation and Management of Anemia in Chronic Kidney Disease: Synopsis of the Kidney Disease: Improving Global Outcomes 2026 Clinical Practice Guideline. Ann Intern Med. 2026 Sep 15 (online ahead of print). PMID: 42735412
4. Amgen Inc. EPOGEN (epoetin alfa) injection, prescribing information. Revised April 2024 (FDA Reference ID 5373326).
5. Besarab A, Bolton WK, Browne JK, et al. The effects of normal as compared with low hematocrit values in patients with cardiac disease who are receiving hemodialysis and epoetin. N Engl J Med. 1998;339(9):584-590. PMID: 9718377
6. Parfrey PS, Foley RN, Wittreich BH, et al. Double-blind comparison of full and partial anemia correction in incident hemodialysis patients without symptomatic heart disease. J Am Soc Nephrol. 2005;16(7):2180-2189. PMID: 15901766
7. Singh AK, Szczech L, Tang KL, et al. Correction of anemia with epoetin alfa in chronic kidney disease (CHOIR). N Engl J Med. 2006;355(20):2085-2098. PMID: 17108343
8. Drüeke TB, Locatelli F, Clyne N, et al. Normalization of hemoglobin level in patients with chronic kidney disease and anemia (CREATE). N Engl J Med. 2006;355(20):2071-2084. PMID: 17108342
9. Pfeffer MA, Burdmann EA, Chen CY, et al. A trial of darbepoetin alfa in type 2 diabetes and chronic kidney disease (TREAT). N Engl J Med. 2009;361(21):2019-2032. PMID: 19880844
10. Solomon SD, Uno H, Lewis EF, et al. Erythropoietic response and outcomes in kidney disease and type 2 diabetes. N Engl J Med. 2010;363(12):1146-1155. PMID: 20843249
11. Kilpatrick RD, Critchlow CW, Fishbane S, et al. Greater epoetin alfa responsiveness is associated with improved survival in hemodialysis patients. Clin J Am Soc Nephrol. 2008;3(4):1077-1083. PMID: 18417744
12. McCausland FR, et al. Association of different definitions of erythropoiesis-stimulating agent hyporesponsiveness with major adverse cardiovascular events: insights from ASCEND-D. Kidney360. 2025;6(9):1541-1548. PMID: 40333020
13. Del Vecchio L, Cases A, Eisenga MF, et al. KDIGO 2026 Clinical Practice Guideline for Anemia in Chronic Kidney Disease (CKD): a commentary from the European Renal Best Practice (ERBP). Nephrol Dial Transplant. 2026;41(8):1554-1572. PMID: 41604211
14. Kidney Disease: Improving Global Outcomes (KDIGO) Anemia Work Group. KDIGO Clinical Practice Guideline for Anemia in Chronic Kidney Disease. Kidney Int Suppl. 2012;2(4):279-335. (Not indexed in PubMed; recommendation statements verified against the KDIGO-hosted full text.)
15. Kliger AS, Foley RN, Goldfarb DS, et al. KDOQI US commentary on the 2012 KDIGO Clinical Practice Guideline for Anemia in CKD. Am J Kidney Dis. 2013;62(5):849-859. PMID: 23891356
16. Babitt JL, Lin HY. Molecular mechanisms of hepcidin regulation: implications for the anemia of CKD. Am J Kidney Dis. 2010;55(4):726-741. PMID: 20189278
17. Wish JB. Assessing iron status: beyond serum ferritin and transferrin saturation. Clin J Am Soc Nephrol. 2006;1(Suppl 1):S4-S8. PMID: 17699374
18. Sargent JA, Acchiardo SR. Iron requirements in hemodialysis. Blood Purif. 2004;22(1):112-123. PMID: 14732819
19. Ly J, Marticorena R, Donnelly S. Red blood cell survival in chronic renal failure. Am J Kidney Dis. 2004;44(4):715-719. PMID: 15384023
20. Ifudu O, Feldman J, Friedman EA. The intensity of hemodialysis and the response to erythropoietin in patients with end-stage renal disease. N Engl J Med. 1996;334(7):420-425. PMID: 8552143
21. Rao DS, Shih MS, Mohini R. Effect of serum parathyroid hormone and bone marrow fibrosis on the response to erythropoietin in uremia. N Engl J Med. 1993;328(3):171-175. PMID: 8417383
22. Akebia Therapeutics. VAFSEO (vadadustat) tablets, prescribing information with boxed warning, revised March 2024 (FDA Reference ID 5354686).
23. Coyne DW, Kapoian T, Suki W, et al. Ferric gluconate is highly efficacious in anemic hemodialysis patients with high serum ferritin and low transferrin saturation: results of the Dialysis Patients' Response to IV Iron with Elevated Ferritin (DRIVE) Study. J Am Soc Nephrol. 2007;18(3):975-984. PMID: 17267740
24. Fishbane S, Galgano C, Langley RC Jr, et al. Reticulocyte hemoglobin content in the evaluation of iron status of hemodialysis patients. Kidney Int. 1997;52(1):217-222. PMID: 9211366
25. Coyne DW. The health-related quality of life was not improved by targeting higher hemoglobin in the Normal Hematocrit Trial. Kidney Int. 2012;82(2):235-241. PMID: 22437411
26. Phrommintikul A, Haas SJ, Elsik M, Krum H. Mortality and target haemoglobin concentrations in anaemic patients with chronic kidney disease treated with erythropoietin: a meta-analysis. Lancet. 2007;369(9559):381-388. PMID: 17276778
27. Palmer SC, Navaneethan SD, Craig JC, et al. Meta-analysis: erythropoiesis-stimulating agents in patients with chronic kidney disease. Ann Intern Med. 2010;153(1):23-33. PMID: 20439566
28. Chung EY, Palmer SC, Saglimbene VM, et al. Erythropoiesis-stimulating agents for anaemia in adults with chronic kidney disease: a network meta-analysis. Cochrane Database Syst Rev. 2023;2:CD010590. PMID: 36791280
29. Szczech LA, Barnhart HX, Inrig JK, et al. Secondary analysis of the CHOIR trial epoetin-alpha dose and achieved hemoglobin outcomes. Kidney Int. 2008;74(6):791-798. PMID: 18596733
30. Park H, Desai R, Liu X, et al. Medicare bundled payment policy on anemia care, major adverse cardiovascular events, and mortality among adults undergoing hemodialysis. Clin J Am Soc Nephrol. 2022;17(6):851-860. PMID: 35589388
31. Hirth RA, Turenne MN, Wilk AS, et al. Blood transfusion practices in dialysis patients in a dynamic regulatory environment. Am J Kidney Dis. 2014;64(4):616-621. PMID: 24560166
32. Fishbane S, Singh B, Kumbhat S, et al. Intravenous epoetin alfa-epbx versus epoetin alfa for treatment of anemia in end-stage kidney disease. Clin J Am Soc Nephrol. 2018;13(8):1204-1214. PMID: 29921734
33. Levin NW, Fishbane S, Cañedo FV, et al. Intravenous methoxy polyethylene glycol-epoetin beta for haemoglobin control in patients with chronic kidney disease who are on dialysis: a randomised non-inferiority trial (MAXIMA). Lancet. 2007;370(9596):1415-1421. PMID: 17950856
34. Locatelli F, Hannedouche T, Fishbane S, et al. Cardiovascular safety and all-cause mortality of methoxy polyethylene glycol-epoetin beta and other erythropoiesis-stimulating agents in anemia of CKD: a randomized noninferiority trial. Clin J Am Soc Nephrol. 2019;14(12):1701-1710. PMID: 31420350
35. Kaufman JS, Reda DJ, Fye CL, et al. Subcutaneous compared with intravenous epoetin in patients receiving hemodialysis. N Engl J Med. 1998;339(9):578-583. PMID: 9718376
36. Casadevall N, Nataf J, Viron B, et al. Pure red-cell aplasia and antierythropoietin antibodies in patients treated with recombinant erythropoietin. N Engl J Med. 2002;346(7):469-475. PMID: 11844847
37. Fishbane S, Berns JS. Hemoglobin cycling in hemodialysis patients treated with recombinant human erythropoietin. Kidney Int. 2005;68(3):1337-1343. PMID: 16105069
38. Krapf R, Hulter HN. Arterial hypertension induced by erythropoietin and erythropoiesis-stimulating agents (ESA). Clin J Am Soc Nephrol. 2009;4(2):470-480. PMID: 19218474

Also in the Maintenance Hemodialysis module

Part of the Maintenance Hemodialysis mastery module. Module index.

• M17b: Anemia: iron, HIF-PH inhibitors, and transfusion
• M18: Examining and cannulating the AVF/AVG
• M19: Catheter care, lock solutions, and bloodstream infection
• Module: Treating hypertension on dialysis
• Module: CKD-MBD monitoring on HD
• Module: Adequacy, nutrition, depression/cognition — and what quality metrics miss
• Clinical Mastery: Vascular access selection in older patients starting hemodialysis (ACCESS HD)
• Clinical Mastery: Enterococcal endocarditis in hemodialysis patients
• Complete white paper: Screening and health maintenance in maintenance hemodialysis — §8.1 anemia monitoring, updated to KDIGO 2026