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Risk Factors for Mortality in Hemodialysis Patients: Two-Year Follow-Up Study

DOI: 10.1155/2013/518945

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Abstract:

Background. End-stage renal disease (ESRD) patients under hemodialysis (HD) have high mortality rate. Inflammation, dyslipidemia, disturbances in erythropoiesis, iron metabolism, endothelial function, and nutritional status have been reported in these patients. Our aim was to identify any significant association of death with these disturbances, by performing a two-year follow-up study. Methods and Results. A large set of data was obtained from 189 HD patients (55.0% male; 66.4 ± 13.9 years old), including hematological data, lipid profile, iron metabolism, nutritional, inflammatory, and endothelial (dys)function markers, and dialysis adequacy. Results. 35 patients (18.5%) died along the follow-up period. Our data showed that the type of vascular access, C-reactive protein (CRP), and triglycerides (TG) are significant predictors of death. The risk of death was higher in patients using central venous catheter (CVC) (Hazard ratio [HR] =3.03, 95% CI = 1.49–6.13), with higher CRP levels (fourth quartile), compared with those with lower levels (first quartile) (HR = 17.3, 95% CI = 2.40–124.9). Patients with higher TG levels (fourth quartile) presented a lower risk of death, compared with those with the lower TG levels (first quartile) (HR = 0.18, 95% CI = 0.05–0.58). Conclusions. The use of CVC, high CRP, and low TG values seem to be independent risk factors for mortality in HD patients. 1. Introduction Patients with end-stage renal disease (ESRD) have a high mortality rate [1, 2] that far exceeds the mortality rate for the non-ESRD population [3]. In the past half-century, the widespread use of hemodialysis (HD) to prolong life of ESRD patients has been a remarkable achievement, preventing death from uremia in these patients. Nowadays this therapy has expanded widely and is being used by an increasing elderly patient population, leading to significant economic consequences to patients and to healthcare systems. Our present knowledge of the mechanisms leading to increased death in this context is incomplete. In the last years, this medical field has known significant technological and pharmacological improvements. Although some evidence may suggest that mortality rate among dialysis patients has decreased over the last few years, actually, patient’s survival is still low. Cardiovascular disease (CVD) has been considered the most common cause of death in these patients [4]. Cardiac arrest and congestive heart failure are more prominent causes of cardiovascular death than acute myocardial infarction in patients with uremia. A higher mortality rate within the

References

[1]  W. M. Vollmer, P. W. Wahl, and C. R. Blagg, “Survival with dialysis and transplantation in patients with end-stage renal disease,” The New England Journal of Medicine, vol. 308, no. 26, pp. 1553–1558, 1983.
[2]  J. P. Held, F. Brunner, M. Odaka, J. R. Garcia, F. K. Port, and D. S. Gaylin, “Five-year survival for end-stage renal disease patients in the United States, Europe, and Japan, 1982 to 1987,” American Journal of Kidney Diseases, vol. 15, no. 5, pp. 451–457, 1990.
[3]  K. J. Jager, B. Lindholm, D. Goldsmith et al., “Cardiovascular and non-cardiovascular mortality in dialysis patients: where is the link?” Kidney International Supplements, vol. 1, pp. 21–23, 2011.
[4]  R. N. Foley, P. S. Parfrey, and M. J. Sarnak, “Clinical epidemiology of cardiovascular disease in chronic renal disease,” American Journal of Kidney Diseases, vol. 32, no. 5, supplement 3, pp. S112–S119, 1998.
[5]  M. J. Sarnak, A. S. Levey, A. C. Schoolwerth 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,” Circulation, vol. 108, no. 17, pp. 2154–2169, 2003.
[6]  A. J. Collins, “Cardiovascular mortality in end-stage renal disease,” American Journal of the Medical Sciences, vol. 325, no. 4, pp. 163–167, 2003.
[7]  P. Stenvinkel, J. J. Carrero, J. Axelsson, B. Lindholm, O. Heimbürger, and Z. Massy, “Emerging biomarkers for evaluating cardiovascular risk in the chronic kidney disease patient: how do new pieces fit into the uremic puzzle?” Clinical Journal of the American Society of Nephrology, vol. 3, no. 2, pp. 505–521, 2008.
[8]  J. Kendrick and M. B. Chonchol, “Nontraditional risk factors for cardiovascular disease in patients with chronic kidney disease,” Nature Clinical Practice Nephrology, vol. 4, no. 12, pp. 672–681, 2008.
[9]  E. Costa, S. Rocha, P. Rocha-Pereira et al., “Cross-talk between inflammation, coagulation/fibrinolysis and vascular access in hemodialysis patients,” Journal of Vascular Access, vol. 9, no. 4, pp. 248–253, 2008.
[10]  American Diabetes Association, “Standards of medical care in diabetes-2009,” Diabetes Care, vol. 32, pp. S13–S61, 2009.
[11]  JNC 6. National High Blood Pressure Education Program, “The sixth report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure,” Archives of Internal Medicine, vol. 157, no. 21, pp. 2413–2446, 1997.
[12]  F. Locatelli, P. Aljama, P. Bárány et al., “Revised European best practice guidelines for the management of anaemia in patients with chronic renal failure,” Nephrology, Dialysis, Transplantation, vol. 19, supplement 2, pp. 1–47, 2004.
[13]  B. A. Cooper, P. Branley, L. Bulfone et al., “A randomized, controlled trial of early versus late initiation of dialysis,” The New England Journal of Medicine, vol. 363, no. 7, pp. 609–619, 2010.
[14]  S. Shastri, N. Tangri, H. Tighiouart et al., “Predictors of sudden cardiac death: a competing risk approach in the hemodialysis study,” Clinical Journal of the American Society of Nephrology, vol. 7, no. 1, pp. 123–130, 2012.
[15]  J. Zimmermann, S. Herrlinger, A. Pruy, T. Metzger, and C. Wanner, “Inflammation enhances cardiovascular risk and mortality in hemodialysis patients,” Kidney International, vol. 55, no. 2, pp. 648–658, 1999.
[16]  R. K. Dhingra, E. W. Young, T. E. Hulbert-Shearon, S. F. Leavey, and F. K. Port, “Type of vascular access and mortality in U.S. hemodialysis patients,” Kidney International, vol. 60, no. 4, pp. 1443–1451, 2001.
[17]  S. Pastan, J. M. Soucie, and W. M. McClellan, “Vascular access and increased risk of death among hemodialysis patients,” Kidney International, vol. 62, no. 2, pp. 620–626, 2002.
[18]  W. F. Owen Jr., N. L. Lew, Y. Liu, E. G. Lowrie, and J. M. Lazarus, “The urea reduction ratio and serum albumin concentration as predictors of mortality in patients undergoing hemodialysis,” The New England Journal of Medicine, vol. 329, no. 14, pp. 1001–1006, 1993.
[19]  K. Kalantar-Zadeh, R. D. Kilpatrick, N. Kuwae et al., “Revisiting mortality predictability of serum albumin in the dialysis population: time dependency, longitudinal changes and population-attributable fraction,” Nephrology Dialysis Transplantation, vol. 20, no. 9, pp. 1880–1888, 2005.
[20]  E. Costa, M. Lima, J. M. Alves et al., “Inflammation, T-cell phenotype, and inflammatory cytokines in chronic kidney disease patients under hemodialysis and its relationship to resistance to recombinant human erythropoietin therapy,” Journal of Clinical Immunology, vol. 28, no. 3, pp. 268–275, 2008.
[21]  E. Costa, B. J. G. Pereira, P. Rocha-Pereira et al., “Role of prohepcidin, inflammatory markers and iron status in resistance to rhEPO therapy in hemodialysis patients,” American Journal of Nephrology, vol. 28, no. 4, pp. 677–683, 2008.
[22]  J. Bazeley, B. Bieber, Y. Li et al., “C-reactive protein and prediction of 1-year mortality in prevalent hemodialysis patients,” Clinical Journal of the American Society of Nephrology, vol. 6, no. 10, pp. 2452–2461, 2011.
[23]  C. Libetta, V. Sepe, P. Esposito, F. Galli, and A. Dal Canton, “Oxidative stress and inflammation: implications in uremia and hemodialysis,” Clinical Biochemistry, vol. 44, no. 14-15, pp. 1189–1198, 2011.
[24]  M. L. V. Jacober, R. L. Mamoni, C. S. P. Lima, B. L. Dos Anjos, and H. Z. W. Grotto, “Anaemia in patients with cancer: role of inflammatory activity on iron metabolism and severity of anaemia,” Medical Oncology, vol. 24, no. 3, pp. 323–329, 2007.
[25]  R. E. Fleming and W. S. Sly, “Hepcidin: a putative iron-regulatory hormone relevant to hereditary hemochromatosis and the anemia of chronic disease,” Proceedings of the National Academy of Sciences of the United States of America, vol. 98, no. 15, pp. 8160–8162, 2001.
[26]  D. M. Wrighting and N. C. Andrews, “Interleukin-6 induces hepcidin expression through STAT3,” Blood, vol. 108, no. 9, pp. 3204–3209, 2006.
[27]  R. M. - Tanner, T. M. Brown, and P. Muntner, “Epidemiology of obesity, the metabolic syndrome, and chronic kidney disease,” Current Hypertension Reports, vol. 14, pp. 152–159, 2012.
[28]  K. Kalantar-Zadeh, K. C. Abbott, A. K. Salahudeen, R. D. Kilpatrick, and T. B. Horwich, “Survival advantages of obesity in dialysis patients,” American Journal of Clinical Nutrition, vol. 81, no. 3, pp. 543–554, 2005.
[29]  R. G. Kalaitzidis and K. C. Siamopoulos, “The role of obesity in kidney disease: recent findings and potential mechanisms,” International Urology and Nephrology, vol. 43, no. 3, pp. 771–784, 2011.
[30]  G. Fantuzzi, “Adipose tissue, adipokines, and inflammation,” Journal of Allergy and Clinical Immunology, vol. 115, no. 5, pp. 911–920, 2005.
[31]  G. Fantuzzi, “Adiponectin and inflammation: consensus and controversy,” Journal of Allergy and Clinical Immunology, vol. 121, no. 2, pp. 326–330, 2008.
[32]  A. N. N. Mertens and P. Holvoet, “Oxidized LDL and HDL: antagonists in atherothrombosis,” FASEB Journal, vol. 15, no. 12, pp. 2073–2084, 2001.

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