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Anaemia of chronic kidney disease

TL;DR — Anaemia in CKD reflects reduced erythropoietin signalling, iron restriction, inflammation, blood loss and shortened red-cell survival; diagnosis requires looking beyond eGFR. Trials of high haemoglobin targets changed practice: CHOIR found greater cardiovascular risk with the higher target, CREATE did not show cardiovascular benefit, and TREAT found no reduction in its primary composites but nearly doubled stroke risk (Singh 2006, PMID 17108343) (Drüeke 2006, PMID 17108342) (Pfeffer 2009, PMID 19880844). HIF-prolyl-hydroxylase inhibitors raise haemoglobin; cardiovascular noninferiority and long-term class safety must be interpreted by molecule and dialysis setting (Singh 2021, PMID 34739194). KDIGO issued an updated anaemia guideline in 2026 (Babitt 2026, PMID 41485807).

Mechanistic components

Falling endogenous erythropoietin is only one component. Absolute or functional iron deficiency, inflammation, occult bleeding, B12/folate deficiency and marrow disease can coexist.

Target haemoglobin controversy

CHOIR randomized 1,432 patients to epoetin targeting haemoglobin 13.5 versus 11.3 g/dL; over a median 16 months the composite of death, myocardial infarction, heart-failure hospitalization and stroke occurred in 125 versus 97 patients (HR 1.34, 95% CI 1.03–1.74, P=0.03) with no quality-of-life gain (Singh 2006, PMID 17108343). CREATE randomized 603 patients with eGFR 15.0–35.0 to a normal (13.0–15.0 g/dL) versus subnormal (10.5–11.5) target and found no reduction in first cardiovascular events (58 vs 47 events; HR 0.78, 95% CI 0.53–1.14, P=0.20), though more patients in the normalization arm required dialysis (127 vs 111, P=0.03) and general health and physical function scores improved (Drüeke 2006, PMID 17108342).

TREAT

Darbepoetin targeting about 13 g/dL did not improve the primary cardiovascular or renal composites and increased stroke (HR 1.92, 95% CI 1.38–2.68) (Pfeffer 2009, PMID 19880844).

Iron before and with ESA

Iron status, route, infection context and dialysis blood loss shape ESA dose and response. Ferritin and transferrin saturation are imperfect inflammation-sensitive markers.

HIF-PHI

In ASCEND-D (2,964 dialysis patients, median 2.5 years) daprodustat met noninferiority against conventional ESA for both co-primary endpoints: haemoglobin change 0.28 versus 0.10 g/dL (difference 0.18, 95% CI 0.12–0.24) and major adverse cardiovascular events 25.2% versus 26.7% (HR 0.93, 95% CI 0.81–1.07) (Singh 2021, PMID 34739194). Noninferiority in one molecule and setting does not erase molecule-specific regulatory differences.

Outcomes that matter

Transfusion avoidance, fatigue, function, thrombosis, stroke and cardiovascular events matter more than achieving a laboratory target. Patient fatigue measurement remains under-developed (Ju 2018, PMID 29551585).

Target-haemoglobin evidence

Trial Comparison Primary clinical reading
CHOIR Epoetin targets 13.5 vs 11.3 g/dL (n=1,432) Composite events 125 vs 97; HR 1.34 (1.03–1.74) (Singh 2006, PMID 17108343)
CREATE Early normalization vs partial correction (n=603) First CV event HR 0.78 (0.53–1.14); more dialysis starts (127 vs 111) (Drüeke 2006, PMID 17108342)
TREAT Darbepoetin target ≈13 g/dL vs placebo/rescue Neutral primary composites; stroke HR 1.92 (1.38–2.68) (Pfeffer 2009, PMID 19880844)
ASCEND-D Daprodustat vs conventional ESA in dialysis (n=2,964) MACE 25.2% vs 26.7%, HR 0.93 (0.81–1.07); haemoglobin difference +0.18 g/dL (0.12–0.24) (Singh 2021, PMID 34739194)

The trial that set the ceiling on haemoglobin targets

TREAT randomized 4,038 patients with type 2 diabetes, CKD and anaemia to darbepoetin alfa targeting haemoglobin near 13 g/dL (n = 2,012) or placebo with rescue darbepoetin below 9.0 g/dL (n = 2,026). Neither primary composite moved: death or cardiovascular event 632 versus 602 (HR 1.05, 95% CI 0.94–1.17; p = 0.41), and death or ESRD 652 versus 618 (HR 1.06, 0.95–1.19; p = 0.29). Fatal or non-fatal stroke almost doubled — 101 versus 53 events (HR 1.92, 95% CI 1.38–2.68; p < 0.001). Transfusions fell (297 versus 496; p < 0.001), and patient-reported fatigue improved only modestly (Pfeffer 2009, PMID 19880844).

The entire modern anaemia target rests on this trade: erythropoiesis-stimulating agents reliably reduce transfusion and marginally improve fatigue, at the cost of a near-doubled stroke risk when pushed toward normal haemoglobin, with no gain in death, cardiovascular events or kidney outcomes. Any recommendation to individualise the haemoglobin target is an attempt to sit inside this trade-off, not to escape it.

Iron: dose, and what high dose does not cost

PIVOTAL randomized 2,141 adults on maintenance haemodialysis to proactive high-dose intravenous iron sucrose (400 mg monthly unless ferritin >700 µg/L or transferrin saturation ≥40%) or reactive low-dose iron (triggered by ferritin <200 µg/L or transferrin saturation <20%). Over median 2.1 years, median monthly iron was 264 mg (IQR 200–336) versus 145 mg (100–190), and median monthly ESA dose was 29,757 versus 38,805 IU (median difference −7,539 IU; 95% CI −9,485 to −5,582). The composite of non-fatal myocardial infarction, non-fatal stroke, heart-failure hospitalisation or death occurred in 320 (29.3%) versus 338 (32.3%) — HR 0.85 (95% CI 0.73–1.00), meeting non-inferiority (p < 0.001) and trending to superiority (Macdougall 2019, PMID 30365356).

The infection question that had constrained iron dosing for two decades was answered in the prespecified secondary analysis: any infection occurred in 46.5% versus 45.5% (63.3 versus 69.4 per 100 patient-years), hospitalisation for infection in 29.6% versus 29.3%, with no effect of iron dose on infection outcomes at all. Catheter access — not iron dose — drove infection risk, and a first cardiovascular event was strongly associated with infection in the preceding 30 days (Macdougall 2020, PMID 32253271).

In non-dialysis CKD the comparison is intravenous versus oral rather than high versus low. FIND-CKD randomized 626 patients with non-dialysis CKD, anaemia and iron deficiency not on ESAs (1:1:2) to intravenous ferric carboxymaltose targeting higher ferritin (400–600 µg/L), lower ferritin (100–200 µg/L), or oral iron. The primary endpoint — initiation of other anaemia management or two consecutive haemoglobin values below 10 g/dL during weeks 8–52 — occurred in 23.5%, 32.2% and 31.8% respectively (high-ferritin FCM versus oral iron HR 0.65, 95% CI 0.44–0.95; p = 0.026), with a greater haemoglobin rise and more patients achieving ≥1 g/dL increase (HR 2.04, 1.52–2.72; p < 0.001), and similar adverse and serious adverse event rates (Macdougall 2014, PMID 24891437). The endpoint is a treatment-escalation composite rather than a patient outcome; the trial establishes that intravenous iron delays ESA use, not that it improves survival or function.

HIF-PHIs: the heart-failure signal

The class-level cardiovascular safety of HIF prolyl hydroxylase inhibitors is discussed on GLP-1 and emerging therapy; the anaemia-specific concern is heart failure. Pooling ASCEND-D (n = 2,964, dialysis) and ASCEND-ND (n = 3,872, non-dialysis), history of heart failure, diabetes and higher systolic blood pressure independently predicted heart-failure hospitalisation regardless of treatment arm. First heart-failure hospitalisations were numerically more frequent with daprodustat than conventional ESA in both non-dialysis (HR 1.22, 95% CI 0.95–1.56; p = 0.12) and dialysis populations (HR 1.10, 0.84–1.45; p = 0.47). In participants with a prior heart-failure history the point estimates were higher — 1.37 (0.89–2.11) in ASCEND-ND and 1.52 (0.97–2.38) in ASCEND-D — against 1.08 (0.79–1.46) and 0.93 (0.66–1.30) in those without, with p-interaction 0.36 and 0.09 (Cunningham 2024, PMID 38383961).

None of these differences is statistically significant, and the p-interaction of 0.09 in the dialysis trial is the kind of signal that is neither dismissible nor actionable. It is a genuinely open safety question, and it points in the same direction as the excess venous thromboembolism seen in placebo-controlled HIF-PHI trials.

Intervention Trial Key result What it does not show
Darbepoetin to Hb ~13 g/dL TREAT, n=4,038 (PMID 19880844) Death/CV HR 1.05 (0.94–1.17); death/ESRD HR 1.06 (0.95–1.19); stroke HR 1.92 (1.38–2.68) That any Hb target improves hard outcomes
High- vs low-dose IV iron PIVOTAL, n=2,141 (PMID 30365356) Composite HR 0.85 (0.73–1.00); ESA dose −7,539 IU/month Superiority was not the design objective
IV iron and infection PIVOTAL secondary (PMID 32253271) Infection 46.5% vs 45.5%; no dose effect Nothing about non-dialysis populations
IV vs oral iron, non-dialysis FIND-CKD, n=626 (PMID 24891437) Escalation endpoint 23.5% vs 31.8%; HR 0.65 (0.44–0.95) Survival, function or symptom benefit
Daprodustat vs ESA ASCEND-D/ND pooled (PMID 38383961) HF hospitalisation HR 1.22 (0.95–1.56) non-dialysis, 1.10 (0.84–1.45) dialysis Whether the prior-HF interaction is real

The 2026 guideline update, read from outside

The KDIGO 2026 anaemia guideline is the first update in more than a decade, and the European Renal Best Practice commentary on it is useful precisely because it records where a second expert body would place the emphasis differently. The commentary notes that the update incorporates recent evidence on intravenous iron and HIF prolyl hydroxylase inhibitors; that it emphasises comprehensive evaluation at diagnosis to identify causes of anaemia beyond erythropoietin insufficiency, with individualised timing and type of treatment; and that it introduces more proactive thresholds for intravenous iron supplementation, especially in haemodialysis patients — consistent with the PIVOTAL result above. It also records that erythropoiesis-stimulating agents remain the recommended first-line therapy, because of persisting cardiovascular safety concerns and methodological limitations of the available HIF-PHI trials (Del Vecchio 2026, PMID 41604211).

The commentary adds three areas the guideline does not address — pregnancy, sex-specific considerations, and interactions with SGLT2 inhibitors or inflammation — and notes regional regulatory divergence between European and US approvals for HIF-PHIs (Del Vecchio 2026, PMID 41604211). That last point is the practical one: the same evidence base has produced different licensed availability on the two continents, so a recommendation that reads as clinical in one setting is regulatory in the other.

The persisting first-line status of ESAs despite the pooled MACE neutrality of HIF-PHIs (PMID 39186635) is a genuine disagreement between evidence and recommendation, and the stated reason — methodological limitations of the HIF-PHI trials rather than an observed harm — is the kind of judgement that belongs in the open record rather than being read as settled.

Decision and interpretation matrix

Dimension Question Guardrail
Diagnostic axis Cause + G category + A category Avoid treating eGFR as the diagnosis
Time axis Chronicity and trajectory Separate acute change from persistent disease
Risk axis Kidney failure + cardiovascular events + death Show competing events
Treatment axis Eligibility, absolute benefit, harm, burden Do not rank drugs by relative effect alone
Measurement axis Assay, equation, repeatability State what was actually measured
Equity axis Testing, referral, access, affordability Audit downstream care, not labels only
Patient axis Symptoms, function, life participation Include outcomes patients prioritize
Evidence axis RCT, cohort, model, guideline Do not collapse designs

Evidence ledger

This ledger makes the page’s evidentiary mix inspectable. It does not imply that every source answers every question.

PMID Record used Role and boundary
17108343 Correction of anemia with epoetin alfa in chronic kidney disease. (Singh 2006, PMID 17108343) Intervention study; eligibility, comparator, endpoint and follow-up bound inference.
17108342 Normalization of hemoglobin level in patients with chronic kidney disease and anemia. (Drüeke 2006, PMID 17108342) Intervention study; eligibility, comparator, endpoint and follow-up bound inference.
19880844 A trial of darbepoetin alfa in type 2 diabetes and chronic kidney disease. (Pfeffer 2009, PMID 19880844) Intervention study; eligibility, comparator, endpoint and follow-up bound inference.
34739194 Daprodustat for the Treatment of Anemia in Patients Undergoing Dialysis. (Singh 2021, PMID 34739194) Intervention study; eligibility, comparator, endpoint and follow-up bound inference.
41485807 Executive Summary of the KDIGO 2026 Clinical Practice Guideline for the Management of Anemia in Chronic Kidney Disease. (Babitt 2026, PMID 41485807) Guideline or commentary; recommendation evidence depends on its review.
29551585 Establishing a Core Outcome Measure for Fatigue in Patients on Hemodialysis. (Ju 2018, PMID 29551585) Consensus or priority-setting exercise; it records participant judgement, not measured outcomes.
38490803 KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease. (KDIGO CKD Work Group 2024, PMID 38490803) Guideline or commentary; recommendation evidence depends on its review.
38519239 Executive summary of the KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease: known knowns and known unknowns. (Levin 2024, PMID 38519239) Guideline or commentary; recommendation evidence depends on its review.
32061315 Global, regional, and national burden of chronic kidney disease, 1990-2017. (GBD CKD Collaboration 2020, PMID 32061315) Modelled projection; the estimate follows from the model inputs and assumptions, not from observed randomized follow-up.
22038337 A population-based approach for the definition of chronic kidney disease: CKD Prognosis Consortium. (Cirillo 2012, PMID 22038337) Synthesis; heterogeneity and included-study definitions constrain transport.
23243116 Cohort profile: the chronic kidney disease prognosis consortium. (Matsushita 2013, PMID 23243116) Observational or conceptual evidence; association is not treatment effect.
37787795 Estimated GFR, Albuminuria, and Adverse Outcomes: individual-participant data meta-analysis. (CKD Prognosis Consortium 2023, PMID 37787795) Synthesis; heterogeneity and included-study definitions constrain transport.
30348535 Relationship of Estimated GFR and Albuminuria to Concurrent Laboratory Abnormalities. (Inker 2019, PMID 30348535) Synthesis; heterogeneity and included-study definitions constrain transport.
34554658 New Creatinine- and Cystatin C-Based Equations to Estimate GFR without Race. (Inker 2021, PMID 34554658) Observational or conceptual evidence; association is not treatment effect.
34563581 A Unifying Approach for GFR Estimation: Recommendations of the NKF-ASN Task Force on Reassessing the Inclusion of Race in Diagnosing Kidney Disease. (Delgado 2022, PMID 34563581) Guideline or commentary; recommendation evidence depends on its review.
26757465 Multinational assessment of equations predicting kidney failure. (Tangri 2016, PMID 26757465) Synthesis; heterogeneity and included-study definitions constrain transport.
23735819 Cardiovascular toxicity of epoetin-alfa in patients with chronic kidney disease. (McCullough 2013, PMID 23735819) Intervention study; eligibility, comparator, endpoint and follow-up bound inference.
19221807 Target hemoglobin trials in chronic kidney disease: design and interpretation issues. (Foley 2009, PMID 19221807) Guideline or commentary; recommendation evidence depends on its review.
20075952 Anemia treatment in chronic kidney disease accompanied by diabetes mellitus or congestive heart failure. (Fishbane 2010, PMID 20075952) Guideline or commentary; recommendation evidence depends on its review.
22537421 Effect of hemoglobin target on progression of kidney disease: a secondary analysis of CHOIR. (Inrig 2012, PMID 22537421) Intervention study; eligibility, comparator, endpoint and follow-up bound inference.
27404556 The Cost-Effectiveness of Anemia Treatment for Persons with Chronic Kidney Disease. (Yarnoff 2016, PMID 27404556) Modelled projection; the estimate follows from the model inputs and assumptions, not from observed randomized follow-up.
39817409 Efficacy and safety of daprodustat in patients on peritoneal dialysis in ASCEND-D. (Dasgupta 2025, PMID 39817409) Intervention study; eligibility, comparator, endpoint and follow-up bound inference.
36565721 Analysis of on-treatment cancer safety events with daprodustat versus conventional erythropoiesis-stimulating agents. (Singh 2023, PMID 36565721) Intervention study; eligibility, comparator, endpoint and follow-up bound inference.
38383961 Daprodustat and Heart Failure in CKD. (Cunningham 2024, PMID 38383961) Intervention study; eligibility, comparator, endpoint and follow-up bound inference.
36791280 Erythropoiesis-stimulating agents for anaemia in adults with chronic kidney disease: a network meta-analysis. (Chung 2023, PMID 36791280) Synthesis; heterogeneity and included-study definitions constrain transport.
24683046 Darbepoetin for the anaemia of chronic kidney disease. (Palmer 2014, PMID 24683046) Synthesis; heterogeneity and included-study definitions constrain transport.

What can and cannot be concluded

  • Risk associations do not by themselves establish that changing the marker changes risk.
  • A relative effect must be paired with baseline risk, follow-up and the exact endpoint.
  • Albuminuria, acute eGFR change, chronic eGFR slope and kidney failure are not interchangeable.
  • Subgroup consistency is not evidence that every subgroup had adequate power.
  • Guideline recommendations combine evidence with values, feasibility, cost and service capacity.
  • Older adults require competing-mortality and treatment-burden framing.
  • Dialysis and transplantation comparisons are vulnerable to eligibility and immortal-time bias.
  • Modelled lifetime benefit is not a randomized observed benefit.
  • A biochemical response without a patient-important outcome remains a surrogate result.
  • This page is research synthesis, not individualized medical advice.

Research-design checklist

  • Define CKD cause, G category, A category and chronicity at baseline.
  • Report the creatinine or cystatin C equation and laboratory calibration.
  • Prespecify acute and chronic eGFR slopes when haemodynamic effects are expected.
  • Keep sustained GFR decline, kidney failure and replacement therapy separable.
  • Report absolute event risks, follow-up and confidence intervals with relative effects.
  • Treat death as a competing event where it can preclude kidney failure.
  • Measure hyperkalaemia, acute kidney injury and treatment discontinuation consistently.
  • Include symptoms, function, life participation and treatment burden.
  • Describe background RAS, SGLT2, MRA and GLP-1 therapy explicitly.
  • Prespecify albuminuria and cause strata without over-reading underpowered interactions.
  • Record screening, prescribing, persistence and monitoring as separate implementation steps.
  • Report representation, access and affordability variables needed for equity analysis.

Open questions

  • What haemoglobin range optimises symptoms and function rather than events? CHOIR, CREATE and TREAT bounded the harms of normalization but did not identify a symptom-optimal target (Singh 2006, PMID 17108343) (Drüeke 2006, PMID 17108342) (Pfeffer 2009, PMID 19880844).
  • Do HIF-PHIs differ from each other, and from ESAs, on long-term thrombosis, malignancy and heart failure? ASCEND-D showed cardiovascular noninferiority for one molecule in dialysis (Singh 2021, PMID 34739194); heart-failure hospitalisations were numerically higher in the non-dialysis setting (Cunningham 2024, PMID 38383961).
  • Which iron marker or strategy best separates absolute from functional deficiency when inflammation distorts ferritin and transferrin saturation?

  • What is the minimum clinically important change in fatigue for CKD anaemia trials, and does it differ by treatment state (Ju 2018, PMID 29551585)? → OQ-18

  • Is there any haemoglobin target at which ESA treatment improves a hard outcome rather than only transfusion need? TREAT found no benefit and a near-doubled stroke risk at a target near 13 g/dL (Pfeffer 2009, PMID 19880844), and no subsequent trial has identified a target that does.

  • Does daprodustat increase heart-failure hospitalisation in people with prior heart failure? Point estimates of 1.37 and 1.52 with p-interaction 0.36 and 0.09 are neither dismissible nor actionable (Cunningham 2024, PMID 38383961).
  • Does intravenous iron in non-dialysis CKD improve anything patients notice? FIND-CKD's endpoint was escalation of anaemia management, not symptoms or survival (Macdougall 2014, PMID 24891437).

  • Why is a cardiovascular event strongly associated with infection in the preceding 30 days in dialysis patients, and is the relationship causal (Macdougall 2020, PMID 32253271)?

  • Why do ESAs remain first-line over HIF-PHIs when pooled long-term data show no MACE difference (Ha 2024, PMID 39186635)? The stated reason is methodological limitation of the HIF-PHI trials rather than observed harm (Del Vecchio 2026, PMID 41604211).

  • How should anaemia be managed in pregnancy, and does SGLT2 inhibitor use or inflammation change the iron and ESA strategy? The 2026 guideline does not address these (Del Vecchio 2026, PMID 41604211).

References

  1. Singh et al. Correction of anemia with epoetin alfa in chronic kidney disease. N Engl J Med. 2006;355(20):2085-2098. PMID 17108343
  2. Drüeke et al. Normalization of hemoglobin level in patients with chronic kidney disease and anemia. N Engl J Med. 2006;355(20):2071-2084. PMID 17108342
  3. Pfeffer et al. A trial of darbepoetin alfa in type 2 diabetes and chronic kidney disease. N Engl J Med. 2009;361(21):2019-2032. PMID 19880844
  4. Singh et al. Daprodustat for the Treatment of Anemia in Patients Undergoing Dialysis. N Engl J Med. 2021;385(25):2325-2335. PMID 34739194
  5. Babitt et al. Executive Summary of the KDIGO 2026 Clinical Practice Guideline for the Management of Anemia in Chronic Kidney Disease. Kidney Int. 2026;109(1):44-56. PMID 41485807
  6. Ju et al. Establishing a Core Outcome Measure for Fatigue in Patients on Hemodialysis. Am J Kidney Dis. 2018;72(1):104-112. PMID 29551585
  7. KDIGO CKD Work Group et al. KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease. Kidney Int. 2024;105(4S):S117-S314. PMID 38490803
  8. Levin et al. Executive summary of the KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease: known knowns and known unknowns. Kidney Int. 2024;105(4):684-701. PMID 38519239
  9. GBD CKD Collaboration et al. Global, regional, and national burden of chronic kidney disease, 1990-2017. Lancet. 2020;395(10225):709-733. PMID 32061315
  10. Cirillo et al. A population-based approach for the definition of chronic kidney disease: CKD Prognosis Consortium. J Nephrol. 2012;25(1):7-12. PMID 22038337
  11. Matsushita et al. Cohort profile: the chronic kidney disease prognosis consortium. Int J Epidemiol. 2013;42(6):1660-1668. PMID 23243116
  12. CKD Prognosis Consortium et al. Estimated GFR, Albuminuria, and Adverse Outcomes: individual-participant data meta-analysis. JAMA. 2023;330(13):1266-1277. PMID 37787795
  13. Inker et al. Relationship of Estimated GFR and Albuminuria to Concurrent Laboratory Abnormalities. Am J Kidney Dis. 2019;73(2):206-217. PMID 30348535
  14. Inker et al. New Creatinine- and Cystatin C-Based Equations to Estimate GFR without Race. N Engl J Med. 2021;385(19):1737-1749. PMID 34554658
  15. Delgado et al. A Unifying Approach for GFR Estimation: Recommendations of the NKF-ASN Task Force on Reassessing the Inclusion of Race in Diagnosing Kidney Disease. Am J Kidney Dis. 2022;79(2):268-288.e1. PMID 34563581
  16. Tangri et al. Multinational assessment of equations predicting kidney failure. JAMA. 2016;315(2):164-174. PMID 26757465
  17. McCullough et al. Cardiovascular toxicity of epoetin-alfa in patients with chronic kidney disease. Am J Nephrol. 2013;37(6):549-558. PMID 23735819
  18. Foley et al. Target hemoglobin trials in chronic kidney disease: design and interpretation issues. Pediatr Nephrol. 2009;24(12):2279-2285. PMID 19221807
  19. Fishbane et al. Anemia treatment in chronic kidney disease accompanied by diabetes mellitus or congestive heart failure. Kidney Int. 2010;77(3):175-177. PMID 20075952
  20. Inrig et al. Effect of hemoglobin target on progression of kidney disease: a secondary analysis of CHOIR. Am J Kidney Dis. 2012;60(3):390-401. PMID 22537421
  21. Yarnoff et al. The Cost-Effectiveness of Anemia Treatment for Persons with Chronic Kidney Disease. PLoS One. 2016;11(7):e0157323. PMID 27404556
  22. Dasgupta et al. Efficacy and safety of daprodustat in patients on peritoneal dialysis in ASCEND-D. Nephrol Dial Transplant. 2025;40(7):1332-1341. PMID 39817409
  23. Singh et al. Analysis of on-treatment cancer safety events with daprodustat versus conventional erythropoiesis-stimulating agents. Nephrol Dial Transplant. 2023;38(8):1890-1897. PMID 36565721
  24. Cunningham et al. Daprodustat and Heart Failure in CKD. J Am Soc Nephrol. 2024;35(5):607-617. PMID 38383961
  25. Chung et al. Erythropoiesis-stimulating agents for anaemia in adults with chronic kidney disease: a network meta-analysis. Cochrane Database Syst Rev. 2023;2(2):CD010590. PMID 36791280
  26. Palmer et al. Darbepoetin for the anaemia of chronic kidney disease. Cochrane Database Syst Rev. 2014;2014(3):CD009297. PMID 24683046
  27. Macdougall IC, et al. Intravenous Iron in Patients Undergoing Maintenance Hemodialysis. N Engl J Med. 2019;380(5):447-458. PMID 30365356
  28. Macdougall IC, et al. Intravenous Iron Dosing and Infection Risk in Patients on Hemodialysis: A Prespecified Secondary Analysis of the PIVOTAL Trial. J Am Soc Nephrol. 2020;31(5):1118-1127. PMID 32253271
  29. Macdougall IC, et al. FIND-CKD: a randomized trial of intravenous ferric carboxymaltose versus oral iron in patients with chronic kidney disease and iron deficiency anaemia. Nephrol Dial Transplant. 2014;29(11):2075-2084. PMID 24891437
  30. Del Vecchio L, 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
  31. Ha JT, et al. Hypoxia-Inducible Factor Prolyl Hydroxylase Inhibitors in Kidney Disease. NEJM Evid. 2024;3(9):EVIDoa2300189. PMID 39186635