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Medical Associates  ·  Department of Nephrology ← Maintenance Hemodialysis module  ·  urinenephrology.org
Clinical Mastery Series  ·  Maintenance Hemodialysis

Adequacy, Nutrition, Depression, and Cognition — and What Quality Metrics Miss

Kt/V, albumin, protein-energy wasting, depression and cognitive screening, and the gap between a metric that predicts and a metric that helps
Andrew Bland, MD, FACP, FAAP UICOMP · UDPA · Butler COM Reviewed September 2026 15 min read

Bottom Line

Part of the Maintenance Hemodialysis mastery module. This page condenses sections 8.2, 8.5, and 8.6 of the full white paper, Screening and Health Maintenance in Maintenance Hemodialysis.

  • Kt/V is a process metric. Check spKt/V monthly and keep it at or above 1.4 per session for thrice-weekly dialysis.1 In the HEMO randomized trial (n = 1,846), a higher dose did not reduce mortality (RR 0.96, 95% CI 0.84–1.10).2 Kt/V tells you whether the prescription was delivered, not whether the patient is getting healthier.
  • Albumin is an inflammation signal first. In Owen's 1993 analysis, albumin predicted mortality 21 times more powerfully than the urea reduction ratio.3 Inflammation, not protein intake, drives most albumin decline, and low albumin predicts death mainly when CRP is also high. Measure CRP with albumin.4,5,6
  • Protein-energy wasting is common and lethal. It affects 28–54% of dialysis patients, and malnutrition carries a pooled mortality HR of 1.49 (1.53 on hemodialysis).7,8
  • Screen for depression and cognitive impairment. Depression affects 20–40% of hemodialysis patients and cognitive impairment 30–80%. Use the PHQ-9 at initiation and at least annually, and the MoCA or MMSE at initiation and periodically.9,10
  • Quality metrics predict, but correcting them has not helped. Kt/V (HEMO), hemoglobin (the Normal Hematocrit Trial), and PTH (EVOLVE) all failed the randomized test.2,11,12 High-volume hemodiafiltration, which targets middle molecules rather than urea, reduced all-cause mortality in CONVINCE (ARR 4.6%, NNT 22 over a median 30 months).13

1. Dialysis Adequacy: What Kt/V Measures

The monitoring standard

  • Single-pool Kt/V: monthly; target ≥ 1.4 per session for thrice-weekly hemodialysis (KDOQI 2015).1
  • Urea reduction ratio: an alternative adequacy metric; target ≥ 70%.
  • Residual kidney function: assess periodically in patients who still make urine. It contributes to total solute clearance and may allow a reduced dialysis prescription.

How the adequacy paradigm was built

The Kt/V story rests on an observational study and a small randomized trial. Owen and colleagues (1993) analyzed 13,473 hemodialysis patients and found that a urea reduction ratio below 60% was associated with higher mortality. That paper launched the adequacy movement. The same data showed that serum albumin was a 21-fold more powerful predictor of mortality than the urea reduction ratio.3 The National Cooperative Dialysis Study (1981) established that clearly inadequate dialysis increases hospitalization. It set a floor; it did not show that exceeding the minimum improves outcomes.14 The step from "very low Kt/V is harmful" to "higher Kt/V is better" is the assumption the HEMO trial was designed to test.

HEMO: the definitive negative trial

HEMO was a 2×2 factorial randomized trial in 1,846 prevalent hemodialysis patients. It compared a standard dose (achieved eKt/V 1.16, spKt/V 1.32) with a high dose (achieved eKt/V 1.53, spKt/V 1.71), and low-flux with high-flux membranes. All-cause mortality did not differ between the dose groups (RR 0.96, 95% CI 0.84–1.10), and neither did the composites of cardiac hospitalization or death, infection hospitalization or death, or albumin decline or death. High-flux membranes showed no benefit in the primary analysis.2

Why more Kt/V does not help

Kt/V measures urea clearance. Urea is small, freely diffusible, and cleared easily, but the solutes most suspected of driving uremic toxicity are not urea.

Toxin classExamplesMolecular weightClearance
Small water-soluble (what Kt/V measures)Urea, creatinine60–113 DaExcellent with conventional hemodialysis
Middle moleculesβ2-microglobulin, FGF-23, IL-61,000–50,000 DaPoor with conventional hemodialysis; improved with hemodiafiltration
Protein-bound uremic toxinsp-Cresyl sulfate, indoxyl sulfate, TMAO100–300 Da (bound)Minimal regardless of dose

A secondary analysis of HEMO samples found that the higher dose did not meaningfully lower non-urea solutes: p-cresyl sulfate showed no reduction, and methylguanidine only a 22% reduction.15 The intervention that raised Kt/V did not clear the solutes Kt/V was supposed to represent.

Warning — low Kt/V is a marker of sickness

Low Kt/V is not only a sign of too little dialysis. Muscle wasting lowers urea generation, obesity enlarges the volume of distribution, missed treatments reflect depression and non-adherence, and poor access flow delivers less clearance. Raising the number by lengthening treatment or increasing blood flow does not make the patient less sick when the underlying drivers are malnutrition, inflammation, and cardiovascular disease.

Kt/V still earns its place. It detects access dysfunction, recirculation, and treatment non-adherence, all of which are actionable. Its value is as a check that the machine delivered what was prescribed.

2. Albumin: A Stronger Predictor, a Harder Target

Albumin predicts death far better than Kt/V. A meta-analysis of 29 cohort studies (11,063 dialysis patients) found that malnutrition, assessed by GNRI, MIS, SGA, ISRNM criteria, or anthropometry, carried a pooled mortality HR of 1.49 (95% CI 1.36–1.64). The hemodialysis subgroup showed HR 1.53 (95% CI 1.38–1.70). The effect was larger in patients over 60 (HR 1.87) and in studies with follow-up of 36 months or less (HR 1.62).8 In a retrospective hemodialysis cohort, albumin below 3.5 g/dL carried HR 1.84.16

The clinical question is not whether low albumin predicts death. It is what drives it, and whether raising it helps.

Driver of low albuminMechanismDoes correcting it help?
Chronic inflammation (primary driver)IL-6, TNF-α, and CRP increase hepatic albumin catabolism and decrease synthesis; the acute-phase response redirects hepatic protein production toward CRP, fibrinogen, and ferritinPotentially, by addressing infection, access problems, and membrane biocompatibility, but no RCT targeting inflammation has shown an albumin-mediated mortality benefit
Protein-energy wastingInadequate intake; anorexia from uremic toxins, depression, and dialysis-day fatigueIntradialytic parenteral nutrition raises albumin modestly but has not shown a mortality benefit in RCTs
Dialysate protein loss0–2 g of albumin per high-flux session; more with post-dilution hemodiafiltration17Minimal impact; losses are modest relative to synthesis
Metabolic acidosisMuscle catabolism through the ubiquitin-proteasome pathwayCorrection improves nutritional markers; no mortality RCT
Volume overloadProposed dilution and hepatic congestion, although kinetic studies found that plasma-volume expansion does not contribute to hypoalbuminemia18,19Albumin rises with volume removal, but the rise reflects concentration, not production
Comorbid diseaseHeart failure, liver disease, diabetes, and malignancy each lower albuminAlbumin is the downstream effect, not the cause

Kaysen's kinetic studies set the hierarchy. Falling serum albumin tracks elevated acute-phase proteins (CRP, α1-acid glycoprotein, ceruloplasmin), not markers of protein intake such as the normalized protein catabolic rate. Nutrition mainly affects albumin synthesis, while inflammation increases albumin catabolism, and in well-dialyzed patients inflammation was the principal cause of albumin decline.4,18,19 Low albumin predicts mortality primarily when CRP is also elevated.5,6

Key Point — draw a CRP with every albumin

An albumin of 3.2 g/dL with a CRP of 0.5 mg/L is a nutrition problem. An albumin of 3.2 g/dL with a CRP of 45 mg/L is an inflammation problem. The interventions differ, but quality reporting treats both as "low albumin" in need of supplements. That is why population-level nutrition programs disappoint: they treat inflammation with protein shakes.

Clinical Pearl — the Owen paradox

Owen's 1993 paper is cited as the foundation of Kt/V monitoring, yet its own data showed albumin was 21 times more powerful as a mortality predictor.3 The field built its monitoring around the weaker predictor because Kt/V could be adjusted monthly with the prescription, while albumin reflected an inflammatory process that resisted simple intervention. Convenience of measurement displaced strength of association.

3. Nutritional Assessment and Protein-Energy Wasting

Protein-energy wasting (PEW) affects 28–54% of maintenance dialysis patients (interquartile range across 90 studies)7 and is independently associated with morbidity and mortality, with the pooled mortality HR of 1.49 described above.8

ParameterFrequencySignificance
Serum albuminMonthlyInflammation and nutrition marker; below 3.5 g/dL is associated with increased mortality. Inflammation lowers it independently of nutrition
Prealbumin (transthyretin)As indicatedShorter half-life (2 days) may reflect more recent intake; less standardized
Subjective Global Assessment and nutrition screeningScreening at least every 6 months; a comprehensive dietitian assessment within 90 days of starting dialysis, then annually or as indicated20Validated composite of weight change, intake, GI symptoms, functional capacity, and examination
nPNA (normalized protein nitrogen appearance)MonthlyA complementary marker of protein intake, not read in isolation. KDOQI 2020 sets dietary protein at 1.0–1.2 g/kg/day and gives nPCR no separate target20
BMI and body compositionAt initiation; periodicallyInterpretation is complex: in observational data, higher BMI is associated with better survival on dialysis

The International Society of Renal Nutrition and Metabolism diagnoses PEW when at least one criterion is met in three of four categories:21

  1. Serum chemistry: albumin < 3.8 g/dL, prealbumin < 30 mg/dL, or cholesterol < 100 mg/dL
  2. Body mass: BMI < 23, unintentional weight loss > 5% over 3 months or > 10% over 6 months, or total body fat < 10%
  3. Muscle mass: muscle wasting of 5% over 3 months or 10% over 6 months, mid-arm muscle circumference more than 10% below the 50th percentile of a reference population, or low creatinine appearance
  4. Dietary intake: protein < 0.8 g/kg/day or energy < 25 kcal/kg/day for more than 2 months
Warning

Albumin below 3.5 g/dL is a red flag, but attributing it purely to malnutrition is a mistake. Inflammation lowers albumin through increased catabolism and decreased hepatic synthesis. Supplementing nutrition while ignoring the inflammatory driver misses the pathophysiology. Nutrition on hemodialysis is developed further in Nutrition and protein-energy wasting on HD.

4. Depression and Cognitive Impairment

Depression

Depression affects 20–40% of hemodialysis patients, and some studies using self-report instruments report rates as high as 68%.9 It is independently associated with:9,22,23

  • Higher all-cause mortality (HR approximately 1.5–2.0)
  • More hospitalizations
  • Missed dialysis treatments, themselves a direct predictor of mortality
  • Lower quality of life and treatment adherence
  • A higher likelihood of withdrawing from dialysis

The PHQ-9 is validated in dialysis populations. The two-question PHQ-2 is a rapid screen, and a positive result should trigger the full PHQ-9. Screen at initiation and at least annually; given the prevalence and fluctuating course, screening every 6 months may be warranted.9,22,23

Cognitive impairment

Cognitive impairment is common and underrecognized on hemodialysis, with estimates from 30% to 80% depending on the tool and definition. A 2025 study documented its co-occurrence with depression and significant unmet diagnostic need.10 Four contributors deserve attention:

  • Uremic encephalopathy: deficits from retained uremic toxins, partly reversible with adequate dialysis
  • Vascular cognitive impairment: cerebral small-vessel disease driven by hypertension, diabetes, and uremic vasculopathy
  • Dialysis-related fluctuation: cognition is often worse in the hours after dialysis, from osmotic shifts and hemodynamic instability
  • Dementia: substantially more prevalent in ESKD than in age-matched controls

Consider screening with the Montreal Cognitive Assessment (MoCA) or Mini-Mental State Examination (MMSE) at initiation and periodically, particularly with functional decline, non-adherence, or unexplained behavioral change.

Clinical Pearl — these findings change management

A depressed patient misses sessions. A cognitively impaired patient cannot manage medications, fluid limits, or diet. Screening matters because it changes care: SSRIs can be used in ESKD, with dose adjustment for citalopram and escitalopram, and cognitive impairment may prompt caregiver involvement, a simpler medication regimen, or reassessment of dialysis modality.

5. What Quality Metrics Miss

Kt/V is not unique. Across dialysis quality metrics the same sequence repeats: a strong observational association with mortality, a guideline target, interventions deployed to hit the target, and randomized trials that show no benefit, or harm, from hitting it.

MetricObservational associationInterventional evidenceWhat it most likely represents
Kt/V / URRLow values associated with higher mortality3HEMO (RCT): no benefit from a higher dose.2 ADEMEX (RCT, peritoneal dialysis): no benefit from higher peritoneal clearance24Overall health, nutrition, adherence, and access function
Albumin21-fold stronger predictor than URR;3 HR 1.84 below 3.5 g/dL;16 malnutrition HR 1.53 on hemodialysis8Nutritional supplementation to raise albumin has not shown a mortality benefitAn inflammation marker mistaken for a nutrition target
HemoglobinAnemia associated with higher mortalityNormal Hematocrit Trial (RCT, hemodialysis): halted early; the FDA-filed report showed higher death, RR 1.27.11,25 CHOIR and TREAT (RCTs, non-dialysis CKD): higher targets raised composite cardiovascular events (CHOIR) and stroke (TREAT); CREATE showed no cardiovascular difference.26,27,28 The mortality signal is meta-analytic: RR 1.17 across nine trials29ESA-driven normalization causes harm
PhosphorusHigh phosphorus associated with higher mortalityNo placebo-controlled RCT shows a binder mortality benefit; IMPROVE-CKD (RCT, non-dialysis CKD) negative30Diet, residual function, and bone disease
PTHExtremes associated with higher mortalityEVOLVE (RCT): cinacalcet missed its composite end point, HR 0.93 (95% CI 0.85–1.02), despite lowering PTH12Severity of bone-mineral disease

This is the reverse-causation trap: sick patients have bad numbers, and fixing the numbers does not fix the sickness. The mineral-metabolism rows are developed in CKD-MBD monitoring on HD.

Anemia, briefly

Anemia monitoring now follows the KDIGO 2026 anemia guideline: hemoglobin at least monthly in hemodialysis patients on an ESA, iron studies every 1–3 months, and a hemoglobin target below 11.5 g/dL (1D).31 The hemoglobin row above is the most expensive demonstration in nephrology that making a number normal is not the same as making a patient better. Targets, ESA hyporesponsiveness, iron, HIF-PH inhibitors, and transfusion are covered in Anemia: targets, ESAs, and hyporesponsiveness and Anemia: iron, HIF-PH inhibitors, and transfusion.

What this means for practice

None of this argues for letting patients receive clearly inadequate dialysis. It argues for honesty about what each metric measures:

  1. Monitor Kt/V as a process metric, not an outcome metric. It shows whether the machine delivered the prescription.
  2. Stop treating albumin as a nutrition target. It is an inflammation signal first; pair it with CRP.
  3. Accept the HEMO result. A Kt/V of 1.4 is the minimum. Pushing it from 1.4 to 1.8 has no proven survival benefit and is low-value care.
  4. Remember the hemoglobin lesson. It applies to every dialysis quality metric.
  5. Invest in what HEMO could not test: clearance of middle molecules and control of inflammation.

6. High-Volume Hemodiafiltration

If Kt/V fails because urea is the wrong target, and albumin falls because of inflammation, the logical therapy clears middle molecules and reduces inflammation. High-volume hemodiafiltration (HDF) does both, and two randomized trials have shown the mortality benefit that conventional adequacy trials could not.

TrialDesignKey result
ESHOL (2013)RCT, n = 906; high-efficiency online HDF vs high-flux hemodialysisAll-cause mortality HR 0.70 (95% CI 0.53–0.92); NNT 8 to prevent one death per year. Cardiovascular mortality HR 0.67 (95% CI 0.44–1.02), not significant32
CONVINCE (2023)RCT, n = 1,360; high-dose HDF (≥ 23 L/session) vs high-flux hemodialysisAll-cause mortality 17.3% vs 21.9%; HR 0.77 (95% CI 0.65–0.93); ARR 4.6%, NNT 22 over a median 30 months; mean convection volume 25.3 L13

HEMO asked whether more urea removal helps; it did not. ESHOL and CONVINCE asked whether convective removal of middle molecules helps; it did, at high convective volumes. The dose that matters is convective volume, not Kt/V.

The anti-inflammatory mechanism is supported by CONTRAST. Over 3 years, CRP and IL-6 rose in patients on low-flux hemodialysis but stayed stable on HDF, a difference of approximately 20% per year for CRP and 16% per year for IL-6, most pronounced in anuric patients. Serum albumin fell equally in both arms.33 Proposed contributors are convective clearance of complement factor D, cytokines, and advanced glycation end products; ultrapure dialysate that limits endotoxin exposure; and 30–40% higher β2-microglobulin clearance than high-flux hemodialysis.34

HDF does increase dialysate albumin loss: above 5 g per session with some dialyzers on post-dilution HDF, and up to 24 g in one reported case.17 In a 47-patient crossover study, patients who started HDF with low albumin improved their albumin, plausibly because reduced inflammation let hepatic synthesis recover,35 although in CONTRAST albumin fell equally on HDF and hemodialysis.33 Ward and colleagues asked whether mild hypoalbuminemia is "a price worth paying" for better removal of middle-molecular-weight toxins.36 The ESHOL and CONVINCE mortality data suggest it is. The full treatment of HDF is in High-Volume Hemodiafiltration.

Clinical Pearl — measure HDF by convective volume

HDF is a different modality, not simply "more dialysis." Conventional hemodialysis optimizes diffusive clearance of small solutes; HDF adds convective clearance of middle molecules. Measuring HDF with Kt/V captures the wrong dimension. The relevant dose is convective volume per session, and the mortality benefit appeared at ≥ 23 L. A program that adopts HDF without reaching that volume may see no benefit.13

7. Evidence Gaps

  • No RCT targeting inflammation has shown an albumin-mediated mortality benefit, and nutritional interventions that raise albumin, including intradialytic parenteral nutrition, have not reduced mortality.
  • Correcting metabolic acidosis improves nutritional markers, but no mortality trial exists.
  • The effect of HDF on albumin is inconsistent: albumin improved in a small crossover study but fell equally in both arms of CONTRAST.33,35
  • Depression screening frequency beyond annual is a judgment call; 6-monthly screening may be warranted given the fluctuating course.9,22,23
  • Cognitive impairment estimates range from 30% to 80% because tools and definitions differ, and diagnostic need is largely unmet.10

8. At the Chair

For the dialysis team
  • A falling Kt/V or URR can point to something fixable: shortened or missed treatments, access problems, or recirculation. Report it along with anything you have noticed about the access or the treatment time delivered.
  • Report a falling albumin together with signs of infection, access problems, poor appetite, or weight loss. Low albumin is often inflammation, not only diet.
  • Missed treatments, withdrawal, new forgetfulness, and confusion with medications can signal depression or cognitive impairment. Report them; both are common and both change care.

Chair-side reference: Nursing card N9 — Monthly labs: what they mean and what to report.

References

Claims and references on this page are drawn from the source white paper (Screening and Health Maintenance in Maintenance Hemodialysis), whose reference list was re-verified against PubMed on 2026-09-26. References are renumbered for this page.

  1. Rocco MV, Daugirdas JT, Depner TA, et al. KDOQI Clinical Practice Guideline for Hemodialysis Adequacy: 2015 Update. Am J Kidney Dis. 2015;66(5):884-930. PMID 26498416
  2. Eknoyan G, Beck GJ, Cheung AK, et al. Effect of dialysis dose and membrane flux in maintenance hemodialysis. N Engl J Med. 2002;347(25):2010-2019. PMID 12490682
  3. Owen WF, Lew NL, Liu Y, Lowrie EG, Lazarus JM. The urea reduction ratio and serum albumin concentration as predictors of mortality in patients undergoing hemodialysis. N Engl J Med. 1993;329(14):1001-1006. PMID 8366899
  4. Kaysen GA, Dubin JA, Müller HG, et al. Inflammation and reduced albumin synthesis associated with stable decline in serum albumin in hemodialysis patients. Kidney Int. 2004;65(4):1408-1415. PMID 15086482
  5. Mukai H, Villafuerte H, Qureshi AR, Lindholm B, Stenvinkel P. Serum albumin, inflammation, and nutrition in end-stage renal disease: C-reactive protein is needed for optimal assessment. Semin Dial. 2018;31(5):435-439. PMID 29926516
  6. Alves FC, Sun J, Qureshi AR, et al. The higher mortality associated with low serum albumin is dependent on systemic inflammation in end-stage kidney disease. PLoS One. 2018;13(1):e0190410. PMID 29298330
  7. Carrero JJ, Thomas F, Nagy K, et al. Global prevalence of protein-energy wasting in kidney disease: a meta-analysis of contemporary observational studies from the International Society of Renal Nutrition and Metabolism. J Ren Nutr. 2018;28(6):380-392. PMID 30348259
  8. Rashid I, Sahu G, Tiwari P, et al. Malnutrition as a potential predictor of mortality in chronic kidney disease patients on dialysis: a systematic review and meta-analysis. Clin Nutr. 2024;43(7):1760-1769. PMID 38852509
  9. Yuan C, Chang F, Zhai H. Integrative approaches to depression in end-stage renal disease: insights into mechanisms, impacts, and pharmacological strategies. Front Pharmacol. 2025;16:1559038. PMID 40297143
  10. Gautam S, Kiran UV. Co-occurrence of cognitive dysfunction and depressive disorders in hemodialysis patients: demographic patterns and unmet diagnostic needs. Cureus. 2025;17(12):e99003. PMID 41527644
  11. 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
  12. Chertow GM, Block GA, Correa-Rotter R, et al. Effect of cinacalcet on cardiovascular disease in patients undergoing dialysis. N Engl J Med. 2012;367(26):2482-2494. PMID 23121374
  13. Blankestijn PJ, Vernooij RWM, Hockham C, et al. Effect of hemodiafiltration or hemodialysis on mortality in kidney failure. N Engl J Med. 2023;389(8):700-709. PMID 37326323
  14. Lowrie EG, Laird NM, Parker TF, Sargent JA. Effect of the hemodialysis prescription on patient morbidity: report from the National Cooperative Dialysis Study. N Engl J Med. 1981;305(20):1176-1181. PMID 7027040
  15. Meyer TW, Sirich TL, Fong KD, et al. Kt/Vurea and nonurea small solute levels in the Hemodialysis Study. J Am Soc Nephrol. 2016;27(11):3469-3478. PMID 27026365
  16. Öneç K, Altun G, Sav T. Baseline serum albumin for long-term risk stratification in maintenance hemodialysis patients: a retrospective cohort study. J Clin Med. 2026;15(1):333. PMID 41517580
  17. Cuvelier C, Tintillier M, Migali G, Van Ende C, Pochet JM. Albumin losses during hemodiafiltration: all dialyzers are not created equal — a case report. BMC Nephrol. 2019;20(1):392. PMID 31660886
  18. Kaysen GA. Biological basis of hypoalbuminemia in ESRD. J Am Soc Nephrol. 1998;9(12):2368-2376. PMID 9848794
  19. Kaysen GA, Dubin JA, Müller HG, et al. Relationships among inflammation, nutrition and physiologic mechanisms establishing albumin levels in hemodialysis patients. Kidney Int. 2002;61(6):2240-2249. PMID 12028466
  20. Ikizler TA, Burrowes JD, Byham-Gray LD, et al. KDOQI Clinical Practice Guideline for Nutrition in CKD: 2020 Update. Am J Kidney Dis. 2020;76(3 Suppl 1):S1-S107. PMID 32829751
  21. Fouque D, Kalantar-Zadeh K, Kopple J, et al. A proposed nomenclature and diagnostic criteria for protein-energy wasting in acute and chronic kidney disease. Kidney Int. 2008;73(4):391-398. PMID 18094682
  22. Zhao J, Wu M, Zhang L, et al. Higher levels of depression are associated with increased all-cause mortality in individuals with chronic kidney disease: a prospective study based on NHANES. J Affect Disord. 2025;390:119785. PMID 40609657
  23. Depression in kidney failure patients. In: Handbook of Dialysis Therapy. Springer; 2025:127.
  24. Paniagua R, Amato D, Vonesh E, et al. Effects of increased peritoneal clearances on mortality rates in peritoneal dialysis: ADEMEX, a prospective, randomized, controlled trial. J Am Soc Nephrol. 2002;13(5):1307-1320. PMID 11961019
  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. Singh AK, Szczech L, Tang KL, et al. Correction of anemia with epoetin alfa in chronic kidney disease. N Engl J Med. 2006;355(20):2085-2098. PMID 17108343
  27. Drüeke TB, Locatelli F, Clyne N, 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
  28. Pfeffer MA, Burdmann EA, Chen CY, 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
  29. 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
  30. Toussaint ND, Pedagogos E, Lioufas NM, et al. A randomized trial on the effect of phosphate reduction on vascular end points in CKD (IMPROVE-CKD). J Am Soc Nephrol. 2020;31(11):2653-2666. PMID 32917784
  31. 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
  32. Maduell F, Moreso F, Pons M, et al. High-efficiency postdilution online hemodiafiltration reduces all-cause mortality in hemodialysis patients. J Am Soc Nephrol. 2013;24(3):487-497. PMID 23411788
  33. den Hoedt CH, Bots ML, Grooteman MP, et al. Online hemodiafiltration reduces systemic inflammation compared to low-flux hemodialysis. Kidney Int. 2014;86(2):423-432. PMID 24552852
  34. Canaud B, Vienken J, Ash S, Ward RA. Hemodiafiltration to address unmet medical needs in ESKD patients. Clin J Am Soc Nephrol. 2018;13(9):1435-1443. PMID 29511057
  35. Aichi M, Kuragano T, Iwasaki T, et al. Hemodiafiltration improves low levels of health-related quality of life (QoL) and nutritional conditions of hemodialysis patients. ASAIO J. 2022;68(2):297-302. PMID 34172640
  36. Ward RA, Beck W, Bernardo AA, et al. Hypoalbuminemia: a price worth paying for improved dialytic removal of middle-molecular-weight uremic toxins? Nephrol Dial Transplant. 2019;34(6):901-907. PMID 30102329

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