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Improvement of heart failure after renal transplantation
Journal of the American College of Cardiology © 2005 by the American College of Cardiology Foundation Published by Elsevier Inc.
EDITORIAL COMMENT
Improvement of Heart Failure After Renal Transplantation The Complex Maze of Cardio-Renal Interaction* Hector O. Ventura, MD, FACC, Mandeep R. Mehra, MD, FACC New Orleans, Louisiana “Learn to see, learn to hear, learn to feel and know by practice alone you can become expert. Medicine is learned at the bedside and not in the classroom.” Sir William Osler (1)
Offering an insightful proposition, Osler correctly surmised the importance of observation in the practice of medicine. Despite rapid medical advances in the last century, observation and reasoning remain integral guiding principles for the practice of medicine. In this issue of the Journal, Wali et al. (2) report an observational study of 103 patients with symptomatic systolic heart failure (HF) accompanying endstage kidney disease that underwent renal transplantation. Contrary to prevailing assumptions of a nihilistic attitude toward such patients, these investigators noted that HF symptoms and ventricular function improved in the vast majority of individuals, an effect notably achieved with a low perioperative morbidity and mortality. Thus, this study dispels two widely prevalent myths. First, most clinicians decry such patients as too high-risk to undergo kidney transplantation and second, that the HF is unlikely to improve and will necessarily be responsible for determining the clinical fate after renal transplantation. See page 1051 Nearly two centuries ago, Richard Bright (3) associated kidney and cardiovascular disease when he wrote “the obvious structural changes in the heart [in patients with shrunken kidneys] have consisted chiefly of hypertrophy with or without valve disease; and, what is most striking, out of 52 cases of hypertrophy, no valvular disease whatsoever could be detected in 34.” More recently, clinical and epidemiological studies demonstrated that cardiac disease is a frequent complication of advanced chronic kidney disease and the major cause of death in patients on renal replacement therapy (1,4 –7). Greaves and Sharpe (8) have shown that when compared to age-matched controls, dialysisdependent patients exhibit a 3.5-fold higher mortality. *Editorials published in the Journal of the American College of Cardiology reflect the views of the authors and do not necessarily represent the views of JACC or the American College of Cardiology. From the Cardiomyopathy and Heart Transplantation Center, Ochsner Clinic Foundation, New Orleans, Louisiana.
Vol. 45, No. 7, 2005 ISSN 0735-1097/05/$30.00 doi:10.1016/j.jacc.2004.12.060
Atherosclerosis and HF are highly prevalent among patients on renal replacement therapy, and the latter is an important predictor of mortality (6 – 8). Stack et al. (9) have shown that the diagnosis of HF is recorded in 36% of patients undergoing dialysis therapy. In this analysis, the prevalence of HF was the greatest among diabetics, and, in addition, patients with HF had a higher prevalence of coronary artery disease, cerebrovascular disease, and peripheral vascular disease. Another study by Harnett et al. (7) demonstrated that independent risk factors for the development of HF in patients with end-stage renal disease (ESRD) at the time of initiation on dialysis were systolic dysfunction, diabetes mellitus, older age, and ischemic heart disease. Clinical symptoms of HF recurred in 56% of the patients during dialysis, and this recurrence was linked with the presence of ischemia and systolic dysfunction, anemia, hypoalbuminemia, and hypertension during dialysis. More importantly, the median survival of patients with HF at baseline was 36 months compared to 62 months in patients without HF. Recently, an analysis of the U.S. Renal Data System Dialysis Morbidity and Mortality Study (DMMS) Wave 2 demonstrated that HF is a major risk factor for hospitalization and is associated with an 83% mortality at three years after a hospitalization for HF, similar to that following myocardial infarction (80%) (10,11). Renal transplantation has become standard of care for patients with end-stage kidney disease because of the improvement in surgical techniques and the introduction of new and more powerful immunosuppressive agents (12). Wolfe et al. (13) compared the outcomes of patients awaiting transplantation on dialysis with patients who received kidney transplantation and demonstrated that after three to four years of follow-up, kidney transplantation reduced the risk of death overall by 68%. Moreover, kidney transplantation has been shown to be more cost-effective than dialysis in the long term (14). Cardiovascular disease is the leading cause of death in patients after kidney transplantation; however, its rate is lower than patients on dialysis. The cumulative incidence of coronary heart disease, cerebrovascular disease, and peripheral vascular disease 15 years after renal transplantation has been estimated at 23%, 15%, and 15%, respectively (12). Several studies have demonstrated regression of left ventricular hypertrophy and improvement of left ventricular function after successful kidney transplantation (15–17). Ferreira et al. (15) prospectively studied 24 patients with ESRD in whom 24-h ambulatory blood pressure monitoring and echocardiography were performed before and at 3, 6, and 12 months after renal transplantation. The authors demonstrated that at one year, patients with successful kidney transplantation had a significant decrease in blood pressure, prevalence of left ventricular hypertrophy and left ventricular dilatation, and an improvement in left ventricular function. Moreover, another study (16) demonstrated that regression of left ventricular hypertrophy continues
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beyond the first year after renal transplantation, persisting into the third and fourth years after transplantation. Failure to regress was associated with older age, hypertension, high pulse pressure in normal-sized hearts, and low pulse pressure in dilated hearts. De Lima et al. (17) performed carotid ultrasound and echocardiograms to evaluate the impact of renal transplantation on the morphological and functional characteristics of the carotid arteries and heart in a group of end-stage renal failure patients without overt cardiovascular disease. Twenty-two patients were evaluated 2 to 3 weeks after renal transplantation, and again 12 and 40 months after transplant. The authors demonstrated that successful renal transplantation improves, but does not cause, complete regression of the cardiovascular alterations of end-stage kidney disease. Only intima-media thickness was normalized by transplantation, whereas left ventricular mass index and carotid and ventricular distensibility improved but remained abnormal. Interestingly, they also conclude that, in this group of patients, the duration of dialysis, weight gain, high blood pressure, and high hematocrit adversely affect the rate of change of post-transplant cardiovascular hypertrophy (17). The hypothesis of an improvement in HF after kidney transplantation has been explored in small case series (15,18,19) and in a study utilizing data from the U.S. Renal Data System (20). The latter included 11,369 patients with ESRD due to diabetes that were placed on a renal and kidney pancreas transplant list from July 1994 to June 1997. In comparison to patients maintained on dialysis, those who underwent renal transplantation had a lower incidence of HF hospitalizations. Although clinically important, this study did not include a systematic evaluation of left ventricular function. On the contrary, the strengths of the investigation by Wali et al. (2) lies in the large patient numbers, comprehensive nature of preoperative evaluation, and systematic collection of data on left ventricular function by multiple gated acquisition (MUGA) scans. During follow-up after kidney transplant, MUGA scans were repeated at six months, one year, and at the last evaluation of the follow-up period. Additionally, these investigators determined that a longer duration of dialysis in patients with HF was detrimental for improvement in ventricular function after renal transplantation. Unfortunately, the current study only reports on left ventricular ejection fraction and does not detail other cardiac structural or volumetric parameters to definitively determine whether these favorable changes were truly accompanied by remodeling of the ventricle. This is important because shifts in ejection fraction can occur simply in response to hemodynamic alterations in preload. Nevertheless, the clinical implications of the study lend credence to the notion that renal transplantation can be performed safely in patients with advanced stages of HF due to left ventricular dysfunction. The mechanisms by which renal transplantation normalizes ventricular function remain a matter of speculation and were not evaluated in the Wali et al. (2) study. It is
JACC Vol. 45, No. 7, 2005 April 5, 2005:1061–3
increasingly recognized that the heart and kidney rely closely upon each other for physiological health. Some have dubbed aberrations in this close knit circuit to represent the “cardio-renal syndrome” (21). Even subclinical alterations in renal function possess prognostic implications in patients with ventricular dysfunction (22,23). Conversely, the uremic environment characterized by metabolic aberrations has been shown to be deleterious to cardiac structure and function (24). Thus, studies have linked the development of secondary parathyroidism and anemia as important correlates of functional cardiac decline in patients with end-stage kidney disease (25,26). Similarly, the inflammatory milieu that accompanies uremia is also thought to be a pathophysiological candidate linked to cardiac dysfunction (27). Indeed, case reports exist wherein parathyroidectomy is associated with recovery from ventricular failure in patients on renal replacement therapy (28). Furthermore, the therapeutic use of erythropoietin in HF with accompanying renal insufficiency has been demonstrated to improve ventricular function (29). Thus, it is tempting to speculate that the improvement of renal function after kidney transplantation and consequent resurrection of metabolic abnormalities might be responsible for the resolution of HF, even beyond the hemodynamic effects of blood pressure and volume control. It is interesting that Wali et al. (2) noted trends in improvement of parathyroid hormone levels in those who benefited compared to increases in this hormone in the cohort that showed no improvement in ventricular function. Much work is needed to better understand the reasons underlying the observed benefits on HF after renal transplantation. The importance of insightful observations such as the one reported herein is depicted in the sayings of William Osler. He wrote: “There is no more difficult art to acquire than the art of observation, and for some men it is quite as difficult to record an observation in brief and plain language” (1). Reprint requests and correspondence: Dr. Hector O. Ventura, Ochsner Clinic Foundation, 1514 Jefferson Highway, New Orleans, Louisiana 70121. E-mail: [email protected].
REFERENCES 1. Bean RB, compiler. Sir William Osler: Aphorisms From His Bedside Teachings and Writings. 3rd edition. Springfield, IL: Charles C. Thomas Co., 1968. 2. Wali RK, Wang GS, Gottlieb SS, et al. Effect of kidney transplantation on left ventricular systolic dysfunction and congestive heart failure in patients with end-stage renal disease. J Am Coll Cardiol 2005;45: 1051– 60. 3. Bright R. Cases and observations illustrative of renal disease accompanied with the secretion of albuminous urine. Guy’s Hosp Reports 1836;1:338 – 400. 4. Renal Data System (U.S. RDS 2003 Annual Report Data. Bethesda, MD: National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases, 2003. 5. Go AS, Chertow GM, Fan D, McCulloch CE, Hsu CY. Chronic kidney disease and the risk of death, cardiovascular events and hospitalization. N Engl J Med 2004;351:1296 –305. 6. Collins AJ. Impact of congestive heart failure and other cardiac diseases on patients outcomes. Kidney Int Suppl 2002:53–7.
JACC Vol. 45, No. 7, 2005 April 5, 2005:1061–3 7. Harnett JD, Foley R, Kent GM, Barre PE, Murray D, Parfey PS. Congestive heart failure in dialysis patients; prevalence, incidence, prognosis and risk factors. Kidney Int 1995;47:884 –90. 8. Greaves SC, Sharpe DN. Cardiovascular disease in patients with end-stage renal failure. Aus NZ J Med 1992;22:153– 8. 9. Stack AG, Bloembergen WE. A cross-sectional study of the prevalence and clinical correlates of congestive heart failure among incident U.S. dialysis patients. Am J Kidney Dis 2001;38:992–1000. 10. Trespalacios FC, Taylor AJ, Agodoa LY, Abbot KC. Incident acute coronary syndrome in chronic dialysis patients in the United States. Kidney Int 2002;62:1799 – 805. 11. Trespalacios FC, Taylor AJ, Agodoa LY, Bakris GL, Abbot KC. Heart failure as a cause for hospitalization in chronic dialysis patients. Am J Kidney Dis 2003;41:1267–77. 12. Magee CC, Pascual M. Update in renal transplantation. Arch Intern Med 2004;164:1373– 88. 13. Wolfe RA, Ashby VB, Milford EL, et al. Comparison of mortality in all patients on dialysis, patients on dialysis awaiting transplantation, and recipients of a first cadaveric transplant. N Engl J Med 1999;341:1725–30. 14. Laupacis A, Keown P, Pus N, et al. A study of the quality of life and cost-utility of renal transplantation. Kidney Int 1996;50:235– 42. 15. Ferreira SR, Moises VA, Tavares A, Pacheco-Silva A. Cardiovascular effects of successful renal transplantation: a 1-year sequential study of left ventricular morphology and function, and 24-hour blood pressure profile. Transplantation 2002;74:1580 –7. 16. Rigatto C, Foley RN, Kent GM, Guttmann R, Parfrey PS. Long-term changes in left ventricular hypertrophy after renal transplantation. Transplantation 2000;70:570 –5. 17. De Lima JJ, Vieira ML, Viviani LF, et al. Long-term impact of renal transplantation on carotid artery properties and on ventricular hypertrophy in end-stage renal failure patients. Nephrol Dial Transplant 2002;4:645–51. 18. Parfrey PS, Harnett JD, Foley RN, et al. Impact of renal transplantation on uremic cardiomyopathy. Transplantation 1995;60:908 –14.
Ventura and Mehra Editorial Comment
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19. Burt RK, Gupta-Burt S, Suki WN, Barcenas CG, Ferguson JJ, Van Buren CT. Reversal of left ventricular dysfunction after renal transplantation. Ann Intern Med 1989;111:635– 40. 20. Abbott KC, Hypolite IO, Hshieh P, et al. The impact of renal transplantation on the incidence of congestive heart failure in patients with end-stage renal disease due to diabetes. J Nephrol 2001;14:369 – 76. 21. Bongartz LG, Cramer MJ, Braam B. The cardiorenal connection. Hypertension 2004;43:e14. 22. Gottlieb SS, Abraham W, Butler J, et al. The prognostic importance of different definitions of worsening renal function in congestive heart failure. J Card Fail 2002;8:136 – 41. 23. Dries DL, Exner DV, Domanski MJ, Greenberg B, Stevenson LW. The prognostic implications of renal insufficiency in asymptomatic and symptomatic patients with left ventricular systolic dysfunction. J Am Coll Cardiol 2000;35:681–9. 24. London GM. Cardiovascular disease in chronic renal failure: pathophysiologic aspects. Semin Dial 2003;16:85–94. 25. Horl WH. The clinical consequences of secondary hyperparathyroidism: focus on clinical outcomes. Nephrol Dial Transplant 2004;19 Suppl 5:V2– 8. 26. Pozzoni P, Pozzi M, Del Vecchio L, Locatelli F. Epidemiology and prevention of cardiovascular complication in chronic kidney disease patients. Semin Nephrol 2004;24:417–22. 27. Yao Q, Axelsson J, Heimburger O, Stenvinkel P, Lindholm B. Systemic inflammation in dialysis patients with end-stage renal disease: causes and consequences. Minerva Urol Nefrol 2004;56: 237– 48. 28. Nagashima M, Hashimoto K, Shinsato T, et al. Marked improvement of left ventricular function after parathyroidectomy in a hemodialysis patient with secondary hyperparathyroidism and left ventricular dysfunction. Circ J 2003;67:269 –72. 29. Smith KJ, Bleyer AJ, Little WC, Sane DC. The cardiovascular effects of erythropoietin. Cardiovasc Res 20031;59:538 – 48.
EDITORIAL COMMENT
Improvement of Heart Failure After Renal Transplantation The Complex Maze of Cardio-Renal Interaction* Hector O. Ventura, MD, FACC, Mandeep R. Mehra, MD, FACC New Orleans, Louisiana “Learn to see, learn to hear, learn to feel and know by practice alone you can become expert. Medicine is learned at the bedside and not in the classroom.” Sir William Osler (1)
Offering an insightful proposition, Osler correctly surmised the importance of observation in the practice of medicine. Despite rapid medical advances in the last century, observation and reasoning remain integral guiding principles for the practice of medicine. In this issue of the Journal, Wali et al. (2) report an observational study of 103 patients with symptomatic systolic heart failure (HF) accompanying endstage kidney disease that underwent renal transplantation. Contrary to prevailing assumptions of a nihilistic attitude toward such patients, these investigators noted that HF symptoms and ventricular function improved in the vast majority of individuals, an effect notably achieved with a low perioperative morbidity and mortality. Thus, this study dispels two widely prevalent myths. First, most clinicians decry such patients as too high-risk to undergo kidney transplantation and second, that the HF is unlikely to improve and will necessarily be responsible for determining the clinical fate after renal transplantation. See page 1051 Nearly two centuries ago, Richard Bright (3) associated kidney and cardiovascular disease when he wrote “the obvious structural changes in the heart [in patients with shrunken kidneys] have consisted chiefly of hypertrophy with or without valve disease; and, what is most striking, out of 52 cases of hypertrophy, no valvular disease whatsoever could be detected in 34.” More recently, clinical and epidemiological studies demonstrated that cardiac disease is a frequent complication of advanced chronic kidney disease and the major cause of death in patients on renal replacement therapy (1,4 –7). Greaves and Sharpe (8) have shown that when compared to age-matched controls, dialysisdependent patients exhibit a 3.5-fold higher mortality. *Editorials published in the Journal of the American College of Cardiology reflect the views of the authors and do not necessarily represent the views of JACC or the American College of Cardiology. From the Cardiomyopathy and Heart Transplantation Center, Ochsner Clinic Foundation, New Orleans, Louisiana.
Vol. 45, No. 7, 2005 ISSN 0735-1097/05/$30.00 doi:10.1016/j.jacc.2004.12.060
Atherosclerosis and HF are highly prevalent among patients on renal replacement therapy, and the latter is an important predictor of mortality (6 – 8). Stack et al. (9) have shown that the diagnosis of HF is recorded in 36% of patients undergoing dialysis therapy. In this analysis, the prevalence of HF was the greatest among diabetics, and, in addition, patients with HF had a higher prevalence of coronary artery disease, cerebrovascular disease, and peripheral vascular disease. Another study by Harnett et al. (7) demonstrated that independent risk factors for the development of HF in patients with end-stage renal disease (ESRD) at the time of initiation on dialysis were systolic dysfunction, diabetes mellitus, older age, and ischemic heart disease. Clinical symptoms of HF recurred in 56% of the patients during dialysis, and this recurrence was linked with the presence of ischemia and systolic dysfunction, anemia, hypoalbuminemia, and hypertension during dialysis. More importantly, the median survival of patients with HF at baseline was 36 months compared to 62 months in patients without HF. Recently, an analysis of the U.S. Renal Data System Dialysis Morbidity and Mortality Study (DMMS) Wave 2 demonstrated that HF is a major risk factor for hospitalization and is associated with an 83% mortality at three years after a hospitalization for HF, similar to that following myocardial infarction (80%) (10,11). Renal transplantation has become standard of care for patients with end-stage kidney disease because of the improvement in surgical techniques and the introduction of new and more powerful immunosuppressive agents (12). Wolfe et al. (13) compared the outcomes of patients awaiting transplantation on dialysis with patients who received kidney transplantation and demonstrated that after three to four years of follow-up, kidney transplantation reduced the risk of death overall by 68%. Moreover, kidney transplantation has been shown to be more cost-effective than dialysis in the long term (14). Cardiovascular disease is the leading cause of death in patients after kidney transplantation; however, its rate is lower than patients on dialysis. The cumulative incidence of coronary heart disease, cerebrovascular disease, and peripheral vascular disease 15 years after renal transplantation has been estimated at 23%, 15%, and 15%, respectively (12). Several studies have demonstrated regression of left ventricular hypertrophy and improvement of left ventricular function after successful kidney transplantation (15–17). Ferreira et al. (15) prospectively studied 24 patients with ESRD in whom 24-h ambulatory blood pressure monitoring and echocardiography were performed before and at 3, 6, and 12 months after renal transplantation. The authors demonstrated that at one year, patients with successful kidney transplantation had a significant decrease in blood pressure, prevalence of left ventricular hypertrophy and left ventricular dilatation, and an improvement in left ventricular function. Moreover, another study (16) demonstrated that regression of left ventricular hypertrophy continues
1062
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beyond the first year after renal transplantation, persisting into the third and fourth years after transplantation. Failure to regress was associated with older age, hypertension, high pulse pressure in normal-sized hearts, and low pulse pressure in dilated hearts. De Lima et al. (17) performed carotid ultrasound and echocardiograms to evaluate the impact of renal transplantation on the morphological and functional characteristics of the carotid arteries and heart in a group of end-stage renal failure patients without overt cardiovascular disease. Twenty-two patients were evaluated 2 to 3 weeks after renal transplantation, and again 12 and 40 months after transplant. The authors demonstrated that successful renal transplantation improves, but does not cause, complete regression of the cardiovascular alterations of end-stage kidney disease. Only intima-media thickness was normalized by transplantation, whereas left ventricular mass index and carotid and ventricular distensibility improved but remained abnormal. Interestingly, they also conclude that, in this group of patients, the duration of dialysis, weight gain, high blood pressure, and high hematocrit adversely affect the rate of change of post-transplant cardiovascular hypertrophy (17). The hypothesis of an improvement in HF after kidney transplantation has been explored in small case series (15,18,19) and in a study utilizing data from the U.S. Renal Data System (20). The latter included 11,369 patients with ESRD due to diabetes that were placed on a renal and kidney pancreas transplant list from July 1994 to June 1997. In comparison to patients maintained on dialysis, those who underwent renal transplantation had a lower incidence of HF hospitalizations. Although clinically important, this study did not include a systematic evaluation of left ventricular function. On the contrary, the strengths of the investigation by Wali et al. (2) lies in the large patient numbers, comprehensive nature of preoperative evaluation, and systematic collection of data on left ventricular function by multiple gated acquisition (MUGA) scans. During follow-up after kidney transplant, MUGA scans were repeated at six months, one year, and at the last evaluation of the follow-up period. Additionally, these investigators determined that a longer duration of dialysis in patients with HF was detrimental for improvement in ventricular function after renal transplantation. Unfortunately, the current study only reports on left ventricular ejection fraction and does not detail other cardiac structural or volumetric parameters to definitively determine whether these favorable changes were truly accompanied by remodeling of the ventricle. This is important because shifts in ejection fraction can occur simply in response to hemodynamic alterations in preload. Nevertheless, the clinical implications of the study lend credence to the notion that renal transplantation can be performed safely in patients with advanced stages of HF due to left ventricular dysfunction. The mechanisms by which renal transplantation normalizes ventricular function remain a matter of speculation and were not evaluated in the Wali et al. (2) study. It is
JACC Vol. 45, No. 7, 2005 April 5, 2005:1061–3
increasingly recognized that the heart and kidney rely closely upon each other for physiological health. Some have dubbed aberrations in this close knit circuit to represent the “cardio-renal syndrome” (21). Even subclinical alterations in renal function possess prognostic implications in patients with ventricular dysfunction (22,23). Conversely, the uremic environment characterized by metabolic aberrations has been shown to be deleterious to cardiac structure and function (24). Thus, studies have linked the development of secondary parathyroidism and anemia as important correlates of functional cardiac decline in patients with end-stage kidney disease (25,26). Similarly, the inflammatory milieu that accompanies uremia is also thought to be a pathophysiological candidate linked to cardiac dysfunction (27). Indeed, case reports exist wherein parathyroidectomy is associated with recovery from ventricular failure in patients on renal replacement therapy (28). Furthermore, the therapeutic use of erythropoietin in HF with accompanying renal insufficiency has been demonstrated to improve ventricular function (29). Thus, it is tempting to speculate that the improvement of renal function after kidney transplantation and consequent resurrection of metabolic abnormalities might be responsible for the resolution of HF, even beyond the hemodynamic effects of blood pressure and volume control. It is interesting that Wali et al. (2) noted trends in improvement of parathyroid hormone levels in those who benefited compared to increases in this hormone in the cohort that showed no improvement in ventricular function. Much work is needed to better understand the reasons underlying the observed benefits on HF after renal transplantation. The importance of insightful observations such as the one reported herein is depicted in the sayings of William Osler. He wrote: “There is no more difficult art to acquire than the art of observation, and for some men it is quite as difficult to record an observation in brief and plain language” (1). Reprint requests and correspondence: Dr. Hector O. Ventura, Ochsner Clinic Foundation, 1514 Jefferson Highway, New Orleans, Louisiana 70121. E-mail: [email protected].
REFERENCES 1. Bean RB, compiler. Sir William Osler: Aphorisms From His Bedside Teachings and Writings. 3rd edition. Springfield, IL: Charles C. Thomas Co., 1968. 2. Wali RK, Wang GS, Gottlieb SS, et al. Effect of kidney transplantation on left ventricular systolic dysfunction and congestive heart failure in patients with end-stage renal disease. J Am Coll Cardiol 2005;45: 1051– 60. 3. Bright R. Cases and observations illustrative of renal disease accompanied with the secretion of albuminous urine. Guy’s Hosp Reports 1836;1:338 – 400. 4. Renal Data System (U.S. RDS 2003 Annual Report Data. Bethesda, MD: National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases, 2003. 5. Go AS, Chertow GM, Fan D, McCulloch CE, Hsu CY. Chronic kidney disease and the risk of death, cardiovascular events and hospitalization. N Engl J Med 2004;351:1296 –305. 6. Collins AJ. Impact of congestive heart failure and other cardiac diseases on patients outcomes. Kidney Int Suppl 2002:53–7.
JACC Vol. 45, No. 7, 2005 April 5, 2005:1061–3 7. Harnett JD, Foley R, Kent GM, Barre PE, Murray D, Parfey PS. Congestive heart failure in dialysis patients; prevalence, incidence, prognosis and risk factors. Kidney Int 1995;47:884 –90. 8. Greaves SC, Sharpe DN. Cardiovascular disease in patients with end-stage renal failure. Aus NZ J Med 1992;22:153– 8. 9. Stack AG, Bloembergen WE. A cross-sectional study of the prevalence and clinical correlates of congestive heart failure among incident U.S. dialysis patients. Am J Kidney Dis 2001;38:992–1000. 10. Trespalacios FC, Taylor AJ, Agodoa LY, Abbot KC. Incident acute coronary syndrome in chronic dialysis patients in the United States. Kidney Int 2002;62:1799 – 805. 11. Trespalacios FC, Taylor AJ, Agodoa LY, Bakris GL, Abbot KC. Heart failure as a cause for hospitalization in chronic dialysis patients. Am J Kidney Dis 2003;41:1267–77. 12. Magee CC, Pascual M. Update in renal transplantation. Arch Intern Med 2004;164:1373– 88. 13. Wolfe RA, Ashby VB, Milford EL, et al. Comparison of mortality in all patients on dialysis, patients on dialysis awaiting transplantation, and recipients of a first cadaveric transplant. N Engl J Med 1999;341:1725–30. 14. Laupacis A, Keown P, Pus N, et al. A study of the quality of life and cost-utility of renal transplantation. Kidney Int 1996;50:235– 42. 15. Ferreira SR, Moises VA, Tavares A, Pacheco-Silva A. Cardiovascular effects of successful renal transplantation: a 1-year sequential study of left ventricular morphology and function, and 24-hour blood pressure profile. Transplantation 2002;74:1580 –7. 16. Rigatto C, Foley RN, Kent GM, Guttmann R, Parfrey PS. Long-term changes in left ventricular hypertrophy after renal transplantation. Transplantation 2000;70:570 –5. 17. De Lima JJ, Vieira ML, Viviani LF, et al. Long-term impact of renal transplantation on carotid artery properties and on ventricular hypertrophy in end-stage renal failure patients. Nephrol Dial Transplant 2002;4:645–51. 18. Parfrey PS, Harnett JD, Foley RN, et al. Impact of renal transplantation on uremic cardiomyopathy. Transplantation 1995;60:908 –14.
Ventura and Mehra Editorial Comment
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19. Burt RK, Gupta-Burt S, Suki WN, Barcenas CG, Ferguson JJ, Van Buren CT. Reversal of left ventricular dysfunction after renal transplantation. Ann Intern Med 1989;111:635– 40. 20. Abbott KC, Hypolite IO, Hshieh P, et al. The impact of renal transplantation on the incidence of congestive heart failure in patients with end-stage renal disease due to diabetes. J Nephrol 2001;14:369 – 76. 21. Bongartz LG, Cramer MJ, Braam B. The cardiorenal connection. Hypertension 2004;43:e14. 22. Gottlieb SS, Abraham W, Butler J, et al. The prognostic importance of different definitions of worsening renal function in congestive heart failure. J Card Fail 2002;8:136 – 41. 23. Dries DL, Exner DV, Domanski MJ, Greenberg B, Stevenson LW. The prognostic implications of renal insufficiency in asymptomatic and symptomatic patients with left ventricular systolic dysfunction. J Am Coll Cardiol 2000;35:681–9. 24. London GM. Cardiovascular disease in chronic renal failure: pathophysiologic aspects. Semin Dial 2003;16:85–94. 25. Horl WH. The clinical consequences of secondary hyperparathyroidism: focus on clinical outcomes. Nephrol Dial Transplant 2004;19 Suppl 5:V2– 8. 26. Pozzoni P, Pozzi M, Del Vecchio L, Locatelli F. Epidemiology and prevention of cardiovascular complication in chronic kidney disease patients. Semin Nephrol 2004;24:417–22. 27. Yao Q, Axelsson J, Heimburger O, Stenvinkel P, Lindholm B. Systemic inflammation in dialysis patients with end-stage renal disease: causes and consequences. Minerva Urol Nefrol 2004;56: 237– 48. 28. Nagashima M, Hashimoto K, Shinsato T, et al. Marked improvement of left ventricular function after parathyroidectomy in a hemodialysis patient with secondary hyperparathyroidism and left ventricular dysfunction. Circ J 2003;67:269 –72. 29. Smith KJ, Bleyer AJ, Little WC, Sane DC. The cardiovascular effects of erythropoietin. Cardiovasc Res 20031;59:538 – 48.