Improving Cardiovascular Health Through Personalized Treatment


Cardioprotective Dialysis: Improving Cardiovascular Health Through More Personalized Treatment

September 21, 2020 • 6 min read


By taking a more personalized approach to renal replacement therapy (RRT), it is possible to reduce the very high incidence of cardiovascular disease and death among kidney disease patients. Specific strategies include thorough cardiac screening and risk assessment, evaluation of individual lifestyle factors, consideration of various treatment options such as home-based therapies, and ongoing attention to the manageable complications of dialysis. Detecting and controlling fluid overload and hypertension, cardiac arrhythmia, cardiac remodeling, and vascular calcification can significantly improve the cardiovascular health of individual patients.

Cardiovascular disease (CVD) is the leading cause of morbidity and mortality in chronic kidney disease (CKD) patients.1 CVD is highly prevalent in 30 to 50 percent of late-stage CKD patients starting dialysis and steadily increases up to 60 to 70 percent of CKD patients on maintenance dialysis.2,3 From a pathophysiological perspective, 60 to 80 percent of CKD patients at stage 5 begin dialysis, or renal replacement therapy (RRT), with hypertension and fluid overload, major risk factors for cardiac disease.4,5,6 The percentage remains between 30 and 70 percent in prevalent stabilized dialysis patients (Figure 1).3,7,8,9,10,11 Furthermore, the relative risk of death from cardiovascular events is between 10 and 30 times higher in late-stage CKD population compared with the general population.12,13

Figure 1 | Pathophysiological mechanisms involved in uremic cardiomyopathy development

CVD should not be considered as an intractable fatality of CKD patients but rather should encourage exploration of solutions to efficiently fight this plague.14 CVD results from multiple factors that may be  classified as non-modifiable or modifiable.15,16 Nonmodifiable factors include age, gender, ethnicity, genetics, and comorbid condition. Modifiable factors include dialysis option, treatment schedule and protocol, practice patterns, quality care management, and lifestyle-related factors such as diet, environment, and treatment observance.


Modifiable CVD factors can be addressed through RRT that focuses on five common manageable complications: correcting fluid overload and hypertension, detecting and preventing cardiac arrhythmia, reversing cardiac remodeling, detecting and preventing vascular calcification, and adjusting RRT to patient risk stratification (Figure 2, Figure 3).17

Figure 2 | Five essential actions to reduce cardiac mortality in CKD5 dialysis patients

Figure 3 | Goal-oriented patient care


Extra-cellular fluid overload (FO) is a major source of morbidity of hemodialysis (HD) patients. In a retrospective cohort study using US Renal Data System data, it has been shown that severe fluid overload, such as pulmonary edema and congestive heart failure, is a significant cause of hospital admission and 30-day re-admission.18 This observation suggests that fluid volume is not adequately managed in maintenance HD patients, worsening during the transition period from the hospital to the dialysis unit. Interestingly, according to a 2004 Dialysis Outcomes and Practice Patterns Study (DOPPS) report including 16,720 prevalent HD patients (1996-2002), 46 percent of United States and 25 percent of HD patients present with congestive heart failure suggesting exposure to chronic FO.19 Long-term exposure to FO and hypertension trigger cardiac remodeling, contributing to heart failure in dialysis patients.21,22 This kidney/cardiac cross-talk has been identified as a typical example of a self-aggravating process.22

Restoring sodium mass balance, volume, and blood pressure control are critical to minimizing dialysis patient cardiac risk. A comprehensive, precise approach to managing fluid volume and hemodynamic status of dialysis patients should rely on a four-step approach, with specific adaptations according to dialysis modality.33,34

  1. Adjust dry weight probing and dialysis treatment prescription.32,35
  2. Manage instrumentation and/or imaging.36,37,38
  3. Track cardiac biomarkers CA125, BNP, NT-proBNP, copeptin, and troponin I or T.39,40,41,42,43,44
  4. Introduce machine learning algorithms to support physician, patient, and caregiver decision making.45,46,47


Cardiac arrhythmia (CA) and sudden cardiac death (SCD) account for 26.9 percent of mortality in CKD5 HD patients.2 Although CKD patients are at increased risk for arrhythmias, the underlying mechanisms of CA and their association with SCD are not completely understood.48,49 Several explanations have been proposed, but they are likely facilitated by cardiac structural changes. CKD5 HD patients often present with a histopathology referred to as “uremic cardiomyopathy,” a finding that includes varying degrees of left ventricular hypertrophy and dilation, systolic and diastolic dysfunction, and fibrosis—which predispose the patient to arrhythmias.

Intermittent HD treatments may also trigger arrhythmias through the interaction of cardiac ischemia and electrolyte shifts. Additional factors may be implicated such as profound anemia, hypoxemia, and clearance of cardiac medications. Comparatively, the risk of triggering arrhythmia during PD is reduced and may offer a therapeutic alternative for arrhythmic-prone patients.

Clinically significant arrhythmias are common in HD patients, and bradycardia and asystole—rather than ventricular tachycardia—may be key causes of sudden death in HD patients. Dialysis practices have a strong impact on incidence, type, and severity of arrhythmias. Therefore, new treatment approaches to prevent arrhythmias and SCD are critical.


Cardiac remodeling is a strong determinant of cardiac outcome, including heart failure, arrhythmias, and sudden death in CKD5 HD patients, resulting mainly from hemodynamic load (fluid overload, hypertension) and unload (fluid depletion, ischemic injury) imposed by intermittent HD.61,62 Cardiac remodeling may also be influenced by:

  • Uremic toxins and uremic milieu, such as FGF23, PTH, oxidative stress, and inflammation.
  • Neurohormonal activation and other factors involved in treatment of dialysis patients, including access flow rate, anemia, iron status, and ESA.63,64,65,66,67

Other factors unrelated to remodeling may also affect cardiac structure and influence the course of heart disease, including ischemic heart disease, arrhythmias, and valvular disease.

Slowing or reversing cardiac remodeling should be a priority goal in dialysis patient heart management.63,68 In this context, three complementary approaches to systematically modulate cardiac remodeling may prove beneficial: mechanical, pharmacological, and biological interventions. 

Mechanical intervention relies on a strict control of both volume and pressure, a “volume first” policy.69 Pharmacological intervention introduces the use of cardiac agents—such as betaadrenergic blockers, ACE inhibitors, AR blockers, and aldosterone antagonists—when fluid volume and pressure are corrected.26,68,70 These cardiac agents may provide additional benefits by slowing or reversing cardiac structure abnormalities and by improving hemodynamic function. Biological intervention focuses on improving tolerance and enhancing RRT modality efficiency by revisiting treatment options, schedule, and time.71,72,73

Precise cardiac management of CKD5 dialysis patients should be performed in close collaboration with a cardiology team in conjunction with cardiac monitoring and biomarkers.


Vascular and valvular calcifications are major risk factors for CKD5 dialysis patients. Arterial medial calcification is responsible for increased vascular stiffness, while arterial intima calcification facilitates plaque rupture.74,75 Valvular calcification is responsible for aortic stenosis.76 Calcification modifies cardiac structure and functionality, resulting in heart failure. Vascular calcification is an active, complex process caused by uremic bone metabolic disorders, regulatory failure of the calcificationinhibitory system, and active phenotypic change in vascular smooth muscle cells (VSMCs) into osteoblast-like cells.77,78 Monitoring vascular calcification process or risk should be part of best clinical practices.

Several therapeutic interventions have shown interesting results in delaying vascular calcification. They include introducing noncalcium-containing phosphate binders, low-dose active vitamin D, and calcimimetics; supplementing magnesium; enhancing RRT efficiency; and adjusting dialysate composition.83 Delaying or reducing vascular calcification is feasible by combining several approaches; however, questions remain about if these risk reduction measures correlate with better cardiac outcomes for dialysis patients; further studies are necessary.


RRT must trend away from “one size fits all” to a more personalized and customized approach.84 In other words, dialysis treatment should fit patient needs, patient risk, and patient perception rather than the reverse as it is currently applied. This is the clinical meaning of patient-centered care. In that perspective, choice of dialysis modality should result from shared decision making involving patient, physician, and main stakeholders where various treatment options are discussed in terms of benefits and risks.85 Ultimately, the nephrologist will identify patient medical risks, evaluate personal motivations and feasibility, as well as assess individual capabilities for self-care treatment.86

Cardiac risk screening and profile stratification are paramount best clinical practices in managing dialysis patients. A baseline cardiovascular screening should be performed upon initiation of dialysis, with regular annual screenings scheduled to monitor changes in cardiac structure, carotid and supra aortic arteries, thoracic and abdominal aorta, and peripheral arterial limbs.87 A more precise cardiac assessment relying on cardiac structural and functional characteristics is required for dialysis patients suitability, including electrocardiography, echocardiography, vascular calcification score or pulse wave velocity, and cardiac biomarkers.88 Depending on the specific patient risk and baseline cardiac screening, additional cardiac explorations might be indicated.

Based on patient assessment and shared decision-making processes, a personalized dialysis modality suited to patient expectations might be identified with a high degree of success. Several studies have shown that empowering patients enhances their trust and consequently facilitates the use of self-treatment options, increases treatment adherence, and improves outcomes.86,102,103,104 Furthermore, it is commonly recognized that more frequent dialysis, longer treatment time, specific modalities, or home-based therapies may further improve patient perception and cardiac outcomes.89 RRT customization and adjustment should include patient-centered goals and experience as quality care indicators.17,84,90,91

The nephrology team continues to be responsible for regularly monitoring dialysis treatment performances and tolerance, revising and readjusting prescription and modality as medically necessary. In brief, the shared decision process and patient empowerment may enhance RRT value with a higher quality of life by improving outcomes. Rapidly expanding technological tools—including digital medicine, connected devices, and the support of artificial intelligence—have demonstrated additional means to improve patient outcomes by providing reliable quality control tools for care teams.92 New metrics focused on patient needs, such as patient-reported outcome measures (PROM) or patient-reported experience measures (PREM), will further enrich the panel of clinical performance measures. Several recent studies have shown the strong predictive value of PROM tools, particularly when they are digitally supported or web based.93,94,95

Cardiac burden should not be considered as an intractable fatality of advanced CKD patients on maintenance renal replacement therapy (PD, HD, kidney transplant), but rather should encourage exploration of effective RRT solutions to halt this frustrating and devastating process.96,97,98,99,100,101 Through customized, personalized RRT, it is possible to not only address CKD-CVD but also manage patient risk, preference, and perception for every patient, every day.

Meet The Experts

Senior Chief Scientist, Fresenius Medical Care

Senior Chief Scientist, Fresenius Medical Care


  1. Rayner HC, Pisoni RL, Bommer J, et al. Mortality and hospitalization in haemodialysis patients in five European countries: results from the Dialysis Outcomes and Practice Patterns Study (DOPPS). Nephrol Dial Transplant 2004;19(1):108-20.
  2. United States Renal Data System (USRDS). “Mortality,” chap. 5, vol. 2, 2018 annual data report,
  3. Cozzolino M, Mangano M, Stucchi A, et al. Cardiovascular disease in dialysis patients. Nephrol Dial Transplant 2018;33(Suppl 3):iii28-iii34.
  4. Vrtovsnik F, Verger C, Van Biesen W, et al. The impact of volume overload on technique failure in incident peritoneal dialysis patients. Clinical Kidney Journal, Dec. 22, 2019,
  5. Banerjee D, Ma JZ, Collins AJ, Herzog CA. Long-term survival of incident hemodialysis patients who are hospitalized for congestive heart failure, pulmonary edema, or fluid overload. Clin J Am Soc Nephrol 2007;2(6):1186-90.
  6. Sarafidis PA, Persu A, Agarwal R, et al. Hypertension in dialysis patients: a consensus document by the European Renal and Cardiovascular Medicine (EURECA-m) working group of the European Renal Association-European Dialysis and Transplant Association (ERA-EDTA) and the Hypertension and the Kidney working group of the European Society of Hypertension (ESH). Nephrol Dial Transplant 2017;32(4):620-40.
  7. Antlanger M, Hecking M, Haidinger M, et al. Fluid overload in hemodialysis patients: a cross-sectional study to determine its association with cardiac biomarkers and nutritional status. BMC Nephrology 2013;14:266.
  8. Kalantar-Zadeh K, Regidor DL, Kovesdy CP, et al. Fluid retention is associated with cardiovascular mortality in patients undergoing long-term hemodialysis. Circulation 2009;119(5):671-9.
  9. Dasgupta I, Thomas GN, Clarke J, et al. Associations between hemodialysis facility practices to manage fluid volume and intradialytic hypotension and patient outcomes. Clin J Am Soc Nephrol 2019;14(3):385-93.
  10. Guo Q, Yi C, Li J, et al. Prevalence and risk factors of fluid overload in Southern Chinese continuous ambulatory peritoneal dialysis patients. PloS One 2013;8(1):e53294.
  11. Zoccali C, Moissl U, Chazot C, et al. Chronic fluid overload and mortality in ESRD. J Am Soc Nephrol 2017;28(8):2491-7.
  12. Foley RN, Parfrey PS, Sarnak MJ. Clinical epidemiology of cardiovascular disease in chronic renal disease. Am J Kidney Dis 1998;32(5 Suppl 3):S112-9.
  13. Sarnak MJ, Foley RN. Cardiovascular mortality in the general population versus dialysis: a glass half full or empty? Am J Kidney Dis 2011;58(1):4-6.
  14. Ahmadmehrabi S, Tang WHW. Hemodialysis-induced cardiovascular disease. Semin Dial 2018;31(3):258-67.
  15. Sarnak MJ, Levey AS. Cardiovascular disease and chronic renal disease: a new paradigm. Am J Kidney Dis 2000;35(4 Suppl 1):S117-31.
  16. Levin A. Identification of patients and risk factors in chronic kidney disease—evaluating risk factors and therapeutic strategies. Nephrol Dial Transplant 2001;16(Suppl 7):57-60.
  17. Reuben DB, Tinetti ME. Goal-oriented patient care—an alternative health outcomes paradigm. N Engl J Med 2012;366(9):777-9.
  18. Plantinga LC, King LM, Masud T, et al. Burden and correlates of readmissions related to pulmonary edema in US hemodialysis patients: a cohort study. Nephrol Dial Transplant 2018;33(7):1215-23.
  19. Goodkin DA, Young EW, Kurokawa K, et al. Mortality among hemodialysis patients in Europe, Japan, and the United States: case-mix e.ects. Am J Kidney Dis 2004;44(5 Suppl 2):16-21.
  20. Van Biesen W, Verger C, Heaf J, et al. Evolution over time of volume status and PD-related practice patterns in an incident peritoneal dialysis cohort. Clin J Am Soc Nephrol 2019;14(6):882-93.
  21. Herzog CA, Asinger RW, Berger AK, et al. Cardiovascular disease in chronic kidney disease. A clinical update from Kidney Disease: Improving Global Outcomes (KDIGO). Kidney Int 2011;80(6):572-86.
  22. Sarnak MJ, Levey AS, Schoolwerth AC, et al. Kidney disease as a risk factor for development of cardiovascular disease: a statement from the American Heart Association Councils on Kidney in Cardiovascular Disease, High Blood Pressure Research, Clinical Cardiology, and Epidemiology and Prevention. Hypertension 2003;42(5):1050-65.
  23. Lorell BH, Carabello BA. Left ventricular hypertrophy: pathogenesis, detection, and prognosis. Circulation 2000;102(4):470-9.
  24. Konstam MA, Kramer DG, Patel AR, et al. Left ventricular remodeling in heart failure: current concepts in clinical significance and assessment. JACC Cardiovasc Imaging 2011;4(1):98-108.
  25. Lazzeroni D, Rimoldi O, Camici PG. From left ventricular hypertrophy to dysfunction and failure. Circ J 2016;80(3):555-64.
  26. Zannad F, Rossignol P. Cardiorenal syndrome revisited. Circulation 2018;138(9):929-44.
  27. García-Donaire JA, Ruilope LM. Cardiovascular and renal links along the cardiorenal continuum. Int J Nephrol 2011;2011:975782.
  28. Canaud B, Chazot C, Koomans J, Collins A. Fluid and hemodynamic management in hemodialysis patients: challenges and opportunities. J Bras Nefrol 2019 Oct-Dec;414(4).
  29. McIntyre CW. Recurrent circulatory stress: the dark side of dialysis. Semin Dial 2010;23(5):449-51.
  30. Buchanan C, Mohammed A, Cox E, et al. Intradialytic cardiac magnetic resonance imaging to assess cardiovascular responses in a short-term trial of hemodiafiltration and hemodialysis. J Am Soc Nephrol 2017;28(4):1269-77.
  31. Abu-Alfa AK, Burkart J, Piraino B, et al. Approach to fluid management in peritoneal dialysis: a practical algorithm. Kidney Int Suppl 2002(81):S8-16.
  32. Gilford S. Managing fluid control in the peritoneal dialysis population. Clin J Am Soc Nephrol 2019;14(6):783-4.
  33. Pinter J, Chazot C, Stuard S, et al. Sodium, volume and pressure control in stage 5 chronic kidney disease dialysis patients: a new tryptic to improve cardiac outcome. Nephrol Dial Transplant 2020;accepted.
  34. Flythe JE. Turning the tide: improving fluid management in dialysis through technology. J Am Soc Nephrol 2017;28(8):2260-2.
  35. Agarwal R, Weir MR. Dry-weight: a concept revisited in an e.ort to avoid medication-directed approaches for blood pressure control in hemodialysis patients. Clin J Am Soc Nephrol 2010;5(7):1255-60.
  36. Ekinci C, Karabork M, Siriopol D, et al. E.ects of volume overload and current techniques for the assessment of fluid status in patients with renal disease. Blood Purif 2018;46(1):34-47.
  37. Beaubien-Souligny W, Kontar L, Blum D, et al. Meta-analysis of randomized controlled trials using tool-assisted target weight adjustments in chronic dialysis patients. Kidney Int Rep 2019;4(10):1426-34.
  38. Loutradis C, Sarafidis PA, Ekart R, et al. The e.ect of dry-weight reduction guided by lung ultrasound on ambulatory blood pressure in hemodialysis patients: a randomized controlled trial. Kidney Int 2019;95(6):1505-13.
  39. Davies SJ, Davenport A. The role of bioimpedance and biomarkers in helping to aid clinical decision-making of volume assessments in dialysis patients. Kidney Int 2014;86(3):489-96.
  40. Savoj J, Becerra B, Kim JK, et al. Utility of cardiac biomarkers in the setting of kidney disease. Nephron 2019;141(4):227-35.
  41. Wang AY, Lai KN. Use of cardiac biomarkers in end-stage renal disease. J Am Soc Nephrol 2008;19(9):1643-52.
  42. Niizuma S, Iwanaga Y, Yahata T, Miyazaki S. Renocardiovascular biomarkers: from the perspective of managing chronic kidney disease and cardiovascular disease. Front Cardiovasc Med 2017;4:10.
  43. Sen T, Aksu T, Yilmaz MB. Carbohydrate antigen-125 is a mirror of both left and right sides of the heart. Tex Heart Inst J 2012;39(4):603-4.
  44. Kouris NT, Zacharos ID, Kontogianni DD, et al. The significance of CA125 levels in patients with chronic congestive heart failure. Correlation with clinical and echocardiographic parameters. Eur J Heart Fail 2005;7(2):199-203.
  45. Santoro A, Ferramosca E, Mancini E. Biofeedback-driven dialysis: where are we? Contrib Nephrol 2008;161:199-209.
  46. Hayes W, Allinovi M. Beyond playing games: nephrologist vs machine in pediatric dialysis prescribing. Pediatr Nephrol 2018;33(10):1625-7.
  47. Barbieri C, Cattinelli I, Neri L, et al. Development of an artificial intelligence model to guide the management of blood pressure, fluid volume, and dialysis dose in end-stage kidney disease patients: proof of concept and first clinical assessment. Kidney Dis (Basel) 2019;5(1):28-33.
  48. Samanta R, Chan C, Chauhan VS. Arrhythmias and sudden cardiac death in end stage renal disease: epidemiology, risk factors, and management. Can J Cardiol 2019;35(9):1228-40.
  49. Kalra PA, Green D, Poulikakos D. Arrhythmia in hemodialysis patients and its relation to sudden death. Kidney Int 2018;93(4):781-3.
  50. El Hage N, Jaar BG, Cheng A, et al. Frequency of arrhythmia symptoms and acceptability of implantable cardiac monitors in hemodialysis patients. BMC Nephrol 2017;18(1):309.
  51. Charytan DM, Foley R, McCullough PA, et al. Arrhythmia and sudden death in hemodialysis patients: protocol and baseline characteristics of the monitoring in dialysis study. Clin J Am Soc Nephrol 2016;11(4):721-34.
  52. Schneditz D. Temperature and thermal balance in hemodialysis. Semin Dial 2001;14(5):357-64.
  53. Pun PH, Middleton JP. Dialysate potassium, dialysate magnesium, and hemodialysis risk. J Am Soc Nephrol 2017;28(12):3441-51.
  54. Karaboyas A, Zee J, Brunelli SM, et al. Dialysate potassium, serum potassium, mortality, and arrhythmia events in hemodialysis: results from the dialysis outcomes and practice patterns study (DOPPS). Am J Kidney Dis 2017;69(2):266-77.
  55. Lin YH, Lin C, Ho YH, et al. Heart rhythm complexity impairment in patients undergoing peritoneal dialysis. Sci Rep 2016;6:28202.
  56. Peer G, Korzets A, Hochhauzer E, et al. Cardiac arrhythmia during chronic ambulatory peritoneal dialysis. Nephron 1987;45(3):192-5.
  57. Kocak G, Azak A, Huddam B, et al. Influence of intraperitoneal volume on QT dispersion in patients with continuous ambulatory peritoneal dialysis: acute cardiac impact of peritoneal dialysis. Ren Fail 2011;33(6):568-71.
  58. O’Lone EL, Visser A, Finney H, Fan SL. Clinical significance of multi-frequency bioimpedance spectroscopy in peritoneal dialysis patients: independent predictor of patient survival. Nephrol Dial Transplant 2014;29(7):1430-7.
  59. Orihuela O, de Jesús Ventura M, Ávila-Díaz M, et al. E.ect of icodextrin on heart rate variability in diabetic patients on peritoneal dialysis. Perit Dial Int 2014;34(1):57-63.
  60. Ivarsen P, Povlsen JV, Jensen JD. Increasing fill volume reduces cardiac performance in peritoneal dialysis. Nephrol Dial Transplant 2007;22(10):2999-3004.
  61. Cokkinos DV, Belogianneas C. Left ventricular remodelling: a problem in search of solutions. Eur Cardiol 2016;11(1):29-35.
  62. Kehat I, Molkentin JD. Molecular pathways underlying cardiac remodeling during pathophysiological stimulation. Circulation 2010;122(25):2727-35.
  63. Io H, Suzuki Y. Strategy for prevention of left ventricular remodeling in predialysis and dialysis patients. Contrib Nephrol 2018;196:13-21.
  64. Toblli JE, Cao G, Rivas C, et al. Intravenous iron sucrose reverses anemia-induced cardiac remodeling, prevents myocardial fibrosis, and improves cardiac function by attenuating oxidative/nitrosative stress and inflammation. Int J Cardiol 2016;212:84-91.
  65. Palazzuoli A, Silverberg DS, Iovine F, et al. E.ects of beta-erythropoietin treatment on left ventricular remodeling, systolic function, and B-type natriuretic peptide levels in patients with the cardiorenal anemia syndrome. Am Heart J 2007;154(4):645.e9-.e6.45E15.
  66. Faul C, Amaral AP, Oskouei B, et al. FGF23 induces left ventricular hypertrophy. J Clin Invest 2011;121(11):4393-408.
  67. Grabner A, Schramm K, Silswal N, et al. FGF23/FGFR4-mediated left ventricular hypertrophy is reversible. Sci Rep 2017;7(1):1993.
  68. Frigerio M, Roubina E. Drugs for left ventricular remodeling in heart failure. Am J Cardiol 2005;96(12A):10L-8L.
  69. Agarwal R, Flynn J, Pogue V, et al. Assessment and management of hypertension in patients on dialysis. J Am Soc Nephrol 2014;25(8):1630-46.
  70. Papademetriou V, Toumpourleka M, Imprialos KP, et al. The role of mineralocorticoid receptor antagonists in heart failure with reduced ejection fraction. Curr Pharm Des 2018;24(46):5517-24.
  71. Jaber BL, Lee Y, Collins AJ, et al. E.ect of daily hemodialysis on depressive symptoms and postdialysis recovery time: interim report from the FREEDOM (Following Rehabilitation, Economics and Everyday-Dialysis Outcome Measurements) Study. Am J Kidney Dis 2010;56(3):531-9.
  72. Peters SA, Bots ML, Canaud B, et al. Haemodiafiltration and mortality in endstage kidney disease patients: a pooled individual participant data analysis from four randomized controlled trials. Nephrol Dial Transplant 2016;31(6):978-84.
  73. FHN Trial Group. In-center hemodialysis six times per week versus three times per week. N Engl J Med 2010;363(24):2287-2300.
  74. London GM, Cohn JN. Prognostic application of arterial sti.ness: task forces. Am J Hypertens 2002;15(8):754-8.
  75. Guérin AP, London GM, Marchais SJ, Metivier F. Arterial sti.ening and vascular calcifications in end-stage renal disease. Nephrol Dial Transplant 2000;15(7):1014-21.
  76. Raggi P, Bellasi A, Gamboa C, et al. All-cause mortality in hemodialysis patients with heart valve calcification. Clin J Am Soc Nephrol 2011;6(8):1990-5.
  77. Moe SM, Chen NX. Pathophysiology of vascular calcification in chronic kidney disease. Circ Res 2004;95(6):560-7.
  78. Mizobuchi M, Towler D, Slatopolsky E. Vascular calcification: the killer of patients with chronic kidney disease. J Am Soc Nephrol 2009;20(7):1453-64.
  79. Adragao T, Pires A, Birne R, et al. A plain x-ray vascular calcification score is associated with arterial sti.ness and mortality in dialysis patients. Nephrol Dial Transplant 2009;24(3):997-1002.
  80. Pasch A, Block GA, Bachtler M, et al. Blood calcification propensity, cardiovascular events, and survival in patients receiving hemodialysis in the EVOLVE trial. Clin J Am Soc Nephrol 2017;12(2):315-22.
  81. Dahle DO, Asberg A, Hartmann A, et al. Serum calcification propensity is a strong and independent determinant of cardiac and all-cause mortality in kidney transplant recipients. Am J Transplant 2016;16(1):204-12.
  82. Bostom A, Pasch A, Madsen T, et al. Serum calcification propensity and fetuin-A: biomarkers of cardiovascular disease in kidney transplant recipients. Am J Nephrol 2018;48(1):21-31.
  83. Ter Meulen KJ, Dekker MJE, Pasch A, et al. Citric-acid dialysate improves the calcification propensity of hemodialysis patients: a multicenter prospective randomized cross-over trial. PLoS One 2019;14(12):e0225824.
  84. Chan CT, Blankestijn PJ, Dember LM, et al. Dialysis initiation, modality choice, access, and prescription: conclusions from a Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference. Kidney Int 2019;96(1):37-47.
  85. Couchoud CG, Beuscart JB, Aldigier JC, et al. Development of a risk stratification algorithm to improve patient-centered care and decision making for incident elderly patients with end-stage renal disease. Kidney Int 2015;88(5):1178-86.
  86. Shinkman R. Is “empowered dialysis” the key to better outcomes? NEJM Catalyst 2018 Mar 15;4(2).
  87. Rakhit DJ, Armstrong KA, Beller E, et al. Risk stratifi cation of patients with chronic kidney disease: results of screening strategies incorporating clinical risk scoring and dobutamine stress echocardiography. Am Heart J 2006;152(2):363-70.
  88. Tabriziani H, Baron P, Abudayyeh I, Lipkowitz M. Cardiac risk assessment for end-stage renal disease patients on the renal transplant waiting list. Clin Kidney J 2019;12(4):576-85.
  89. Tentori F, Zhang J, Li Y, et al. Longer dialysis session length is associated with better intermediate outcomes and survival among patients on in-center three times per week hemodialysis: results from the Dialysis Outcomes and Practice Patterns Study (DOPPS). Nephrol Dial Transplant 2012;27(11):4180-8.
  90. Morena M, Jaussent A, Chalabi L, et al. Treatment tolerance and patient-reported outcomes favor online hemodiafi ltration compared to high-fl ux hemodialysis in the elderly. Kidney Int 2017;91(6):1495-1509.
  91. Black N, Burke L, Forrest CB, et al. Patient-reported outcomes: pathways to better health, better services, and better societies. Qual Life Res 2016;25(5):1103-12.
  92. Sanders SF, Terwiesch M, Gordon WJ, Stern AD. How artifi cial intelligence is changing health care delivery. NEJM Catalyst 2019 Oct 17;5(5).
  93. Wetmore JB, Gilbertson DT, Liu J, Collins AJ. Improving outcomes in patients receiving dialysis: the Peer Kidney Care Initiative. Clin J Am Soc Nephrol 2016;11(7):1297-1304.
  94. Anker SD, Agewall S, Borggrefe M, et al. The importance of patient-reported outcomes: a call for their comprehensive integration in cardiovascular clinical trials. Eur Heart J 2014;35(30):2001-9.
  95. Arnedt JT. PROMIS™ of improved tools for assessing sleep and wake function: commentary on “Development of short forms from the PROMIS™ sleep disturbance and sleep-related impairment item banks.” Behav Sleep Med 2011;10(1):25-7.
  96. Foley RN, Parfrey PS, Sarnak MJ. Clinical epidemiology of cardiovascular disease in chronic renal disease. Am J Kidney Dis 1998;32(5 Suppl 3):S112-19. doi:10.1053/ ajkd.1998.v32.pm9820470.
  97. Sarnak MJ, Levey AS, Schoolwerth AC, et al. Kidney disease as a risk factor for development of cardiovascular disease: a statement from the American Heart Association Councils on Kidney in Cardiovascular Disease, High Blood Pressure Research, Clinical Cardiology, and Epidemiology and Prevention. Hypertension 2003;42(5):1050-65. doi:10.1161/01.HYP.0000102971.85504.7c.
  98. Krediet RT, Balafa O. Cardiovascular risk in the peritoneal dialysis patient. Nat Rev Nephrol 2010;6(8):451-60. doi:10.1038/nrneph.2010.68.
  99. Wyld MLR, De La Mata NL, Masson P, et al. Cardiac mortality in kidney transplant patients: a population-based cohort study 1988-2013 in Australia and New Zealand. Transplantation 2020 Mar 10. doi:10.1097/TP.0000000000003224.
  100. Weiner DE, Carpenter MA, Levey AS, et al. Kidney function and risk of cardiovascular disease and mortality in kidney transplant recipients: the FAVORIT trial. Am J Transplant 2012;12(9):2437-45. doi:10.1111/j.1600-6143.2012.04101.x.
  101. Meier-Kriesche HU, Schold JD, Srinivas TR, et al. Kidney transplantation halts cardiovascular disease progression in patients with end-stage renal disease. Am J Transplant 2004;4(10):1662-68. doi:10.1111/j.1600-6143.2004.00573.x.
  102. Lin MY, Liu MF, Hsu LF, Tsai PS. E. ects of self-management on chronic kidney disease: a meta-analysis. Int J Nurs Stud 2017;74:128-37. doi:10.1016/j.ijnurstu.2017.06.008.
  103. Subramanian L, Quinn M, Zhao J, et al. Coping with kidney disease—qualitative findings from the Empowering Patients on Choices for Renal Replacement Therapy (EPOCH-RRT) study. BMC Nephrol 2017;18(1):119. doi: 10.1186/s12882-017-0542-5.
  104. Schatell D, Witten B. Dialysis patient empowerment: what, why, and how. Nephrol News Issues 2005;19(9):37-9.