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• W2022285777 abstract "Cardiovascular disease is the primary cause of morbidity and premature mortality in chronic kidney disease. While it is well established that patients with kidney failure (chronic kidney disease stage 5) are at high risk of cardiovascular disease morbidity and mortality1.Foley R.N. Parfrey P.S. Sarnak M.J. Epidemiology of cardiovascular disease in chronic renal disease.J Am Soc Nephrol. 1998; 9: S16-S23Crossref PubMed Scopus (30) Google Scholar, patients with earlier stages of chronic kidney disease also experience a high rate of fatal and nonfatal cardiovascular events2.Manjunath G. Tighiouart H. Ibrahim H. et al.Level of kidney function as a risk factor for atherosclerotic cardiovascular outcomes in the community.J Am Coll Cardiol. 2003; 41: 47-55Abstract Full Text Full Text PDF PubMed Scopus (663) Google Scholar. Recent guidelines and position statements have therefore defined chronic kidney disease as a cardiovascular risk equivalent, and patients in all stages of chronic kidney disease are considered in the “highest risk group” for development of cardiovascular disease3.Sarnak M.J. Levey A.S. Schoolwerth A.C. 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. 2003; 108: 2154-2169Crossref PubMed Scopus (2675) Google Scholar. We propose that patients with chronic kidney disease are at increased risk for cardiovascular disease for several reasons Figure 1: (1) chronic kidney disease is associated with increased prevalence of traditional and nontraditional cardiovascular disease risk factors; (2) chronic kidney disease is an independent risk factor for cardiovascular disease; (3) many cardiovascular disease risk factors are also risk factors for progression of chronic kidney disease; and (4) the presence of cardiovascular disease may be a risk factor for chronic kidney disease. The interrelationship between cardiovascular and chronic kidney disease, with each contributing to the pathogenesis of the other, leads to a cycle of cardiovascular and kidney disease progression. In the current review we focus on chronic kidney disease stages 1 to 4 and (1) present evidence suggesting that markers of chronic kidney disease, including reduced glomerular filtration rate (GFR) and microalbuminuria, are independent risk factors for cardiovascular disease, (2) describe the spectrum of cardiovascular disease in chronic kidney disease, and (3) discuss the role of traditional and nontraditional risk factors in the development of the different forms of cardiovascular disease. We do not describe management strategies as this is discussed in an accompanying review. An abundance of recent data has demonstrated an association between reduced kidney function and cardiovascular disease morbidity and mortality that persists after adjustment for traditional cardiovascular disease risk factors2.Manjunath G. Tighiouart H. Ibrahim H. et al.Level of kidney function as a risk factor for atherosclerotic cardiovascular outcomes in the community.J Am Coll Cardiol. 2003; 41: 47-55Abstract Full Text Full Text PDF PubMed Scopus (663) Google Scholar,4.Go A.S. Chertow G.M. Fan D. et al.Chronic kidney disease and the risks of death, cardiovascular events, and hospitalization.N Engl J Med. 2004; 351: 1296-1305Crossref PubMed Scopus (8252) Google Scholar. Possible explanations for this association include that reduced GFR (1) is associated with an increased level of non-traditional risk factors that are frequently not adjusted for in analyses, (2) may be a marker of the severity of diagnosed vascular disease or of undiagnosed vascular disease, (3) may be a measure of residual confounding from traditional risk factors, for example, the severity of hypertension, and (4) patients with reduced GFR may not receive the benefits of optimal therapies such as aspirin, beta blockers, angiotensin-converting enzyme (ACE) inhibitors. Prospective studies have established that albumin excretion, at levels well below the current cutoffs used to define microalbuminuria, is an independent predictor of cardiovascular disease outcomes5.Wachtell K. Ibsen H. Olsen M.H. et al.Albuminuria and cardiovascular risk in hypertensive patients with left ventricular hypertrophy: The LIFE Study.Ann Intern Med. 2003; 139: 901-906Crossref PubMed Scopus (466) Google Scholar. Potential reasons for these findings include the following: (1) microalbuminuria may be a marker of generalized endothelial dysfunction and vascular permeability, (2) microalbuminuria may be associated with other traditional and nontraditional cardiovascular disease risk factors, and (3) microalbuminuria may be a precursor for the development of early or incipient kidney disease. In support of the last hypothesis, studies have demonstrated that microalbuminuria is associated with an increased risk for development of albuminuria, an accepted marker of kidney disease6.Mann J.F. Gerstein H.C. Yi Q.L. et al.Development of renal disease in people at high cardiovascular risk: Results of the HOPE randomized study.J Am Soc Nephrol. 2003; 14: 641-647Crossref PubMed Scopus (125) Google Scholar. Manifestations of cardiovascular disease in chronic kidney disease can be broadly classified as those affecting the myocardium and those affecting the blood vessels although these pathophysiologic processes are not mutually exclusive and are in fact closely interrelated Figure 2. As described below, clinical manifestations of myocardial and vascular remodeling include left ventricular hypertrophy (LVH), increased pulse pressure, and ischemic heart disease, all of which are independent risk factors for mortality in patients with kidney failure8.Zoccali C. Benedetto F.A. Mallamaci F. et al.Prognostic impact of the indexation of left ventricular mass in patients undergoing dialysis.J Am Soc Nephrol. 2001; 12: 2768-2774PubMed Google Scholar, 9.Klassen P.S. Lowrie E.G. Reddan D.N. et al.Association between pulse pressure and mortality in patients undergoing maintenance hemodialysis.JAMA. 2002; 287: 1548-1555Crossref PubMed Scopus (341) Google Scholar, 1.Comorbid conditions and correlations with mortality risk among 3,399 incident hemodialysis patients.Am J Kidney Dis. 1992; 20: 32-38PubMed Google Scholar. The pressure and volume overload that are inherent to the abnormalities of homeostasis seen in chronic kidney disease lead to structural alterations of the myocardium11.London G.M. Parfrey P.S. Cardiac disease in chronic uremia: pathogenesis.Adv Ren Replace Ther. 1997; 4: 194-211PubMed Google Scholar. These structural changes include ventricular remodeling that may lead to eccentric or concentric LVH, systolic and diastolic dysfunction, and resultant clinical symptoms of heart failure. Abnormalities of myocardial structure are common in chronic kidney disease. The prevalence of LVH was 30% in a cohort of patients with chronic kidney disease stages 3 and 412.Mcmahon L.P. Roger S.D. Levin A. Development, prevention, and potential reversal of left ventricular hypertrophy in chronic kidney disease.J Am Soc Nephrol. 2004; 15: 1640-1647Crossref PubMed Scopus (75) Google Scholar. In a large cohort derived from a health maintenance organization, the prevalence of heart failure ranged from 5% to 21% among patients with GFR of 15 to 60 mL/min/1.73 m24.Go A.S. Chertow G.M. Fan D. et al.Chronic kidney disease and the risks of death, cardiovascular events, and hospitalization.N Engl J Med. 2004; 351: 1296-1305Crossref PubMed Scopus (8252) Google Scholar. In a community-based cohort of patients with heart failure, 55% had creatinine clearance <59 mL/min13.Mcalister F.A. Ezekowitz J. Tonelli M. et al.Renal insufficiency and heart failure: Prognostic and therapeutic implications from a prospective cohort study.Circulation. 2004; 109: 1004-1009Crossref PubMed Scopus (558) Google Scholar. The hemodynamic and metabolic milieu evident in chronic kidney disease facilitates arterial remodeling. The resultant structural abnormalities include changes in the arterial lumen as well as components of the vessel wall14.London G.M. Marchais S.J. Guerin A.P. et al.Arterial structure and function in end-stage renal disease.Nephrol Dial Transplant. 2002; 17: 1713-1724Crossref PubMed Scopus (200) Google Scholar. Manifestations of intimal disease include atherosclerotic plaque formation and subsequent development of coronary artery disease and ischemic heart disease. Structural changes in the arterial wall such as increased collagen, calcification and extracellular matrix result in arteriosclerosis and arterial stiffening. There is a high prevalence of both atherosclerosis and arteriosclerosis in chronic kidney disease. A coronary angiographic investigation of predialysis patients with chronic kidney disease stage 5 with no history of heart disease noted that 53% of the cohort had significant coronary artery stenosis defined as >50% stenosis [abstract; Ohtake T et al, J Am Soc Nephrol 9:0765, 2005]. In the population-based Atherosclerosis Risk in Communities (ARIC) Study, the prevalence of symptomatic coronary heart disease was 11% among persons with chronic kidney disease versus 4% in those without kidney disease2.Manjunath G. Tighiouart H. Ibrahim H. et al.Level of kidney function as a risk factor for atherosclerotic cardiovascular outcomes in the community.J Am Coll Cardiol. 2003; 41: 47-55Abstract Full Text Full Text PDF PubMed Scopus (663) Google Scholar. There was a significant association between arterial stiffness, estimated as pulse wave velocity, and kidney function in a cohort of patients with mean creatinine clearance of 68.5 mL/min/1.73 m215.Mourad J.J. Pannier B. Blacher J. et al.Creatinine clearance, pulse wave velocity, carotid compliance and essential hypertension.Kidney Int. 2001; 59: 1834-1841Abstract Full Text Full Text PDF PubMed Scopus (214) Google Scholar. The consequences of arteriosclerosis and loss of arterial compliance include increased afterload that in turn causes ventricular hypertrophy thus setting up a cycle of deteriorating myocardial function13.Mcalister F.A. Ezekowitz J. Tonelli M. et al.Renal insufficiency and heart failure: Prognostic and therapeutic implications from a prospective cohort study.Circulation. 2004; 109: 1004-1009Crossref PubMed Scopus (558) Google Scholar. In turn, LVH increases myocardial oxygen demand thus further exacerbating ischemic heart disease. Both traditional and nontraditional risk factors have been implicated in the development of cardiovascular disease in chronic kidney disease. Traditional risk factors are those defined in the Framingham Heart Study and used to predict coronary heart disease outcomes in the general population16.Wilson P.W. D'Agostino R.B. Levy D. et al.Prediction of coronary heart disease using risk factor categories.Circulation. 1998; 97: 1837-1847Crossref PubMed Scopus (7010) Google Scholar. Nontraditional risk factors are uremia-related factors that increase in prevalence as kidney function declines and may contribute to the excess risk of cardiovascular disease seen in chronic kidney disease3.Sarnak M.J. Levey A.S. Schoolwerth A.C. 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. 2003; 108: 2154-2169Crossref PubMed Scopus (2675) Google Scholar Table 1.Table 1Manifestations of cardiovascular disease in chronic kidney disease and associated putative risk factorsPathologyTraditional risk factorsNontraditional risk factorsCardiomyopathyOlder ageAlbuminuriaHypertensionReduced glomerular filtration rateValvular diseaseAnemiaDyslipidemiaInflammationSmokingArteriosclerosisDiabetesExtracellular fluid volume overloadAbnormal calcium/phosphate metabolismAtherosclerosisOlder ageAlbuminuriaMale genderReduced glomerular filtration rateHypertensionAnemiaDiabetesInflammationDyslipidemiaOxidative stressSmokingEndothelial dysfunctionPhysical inactivityHomocysteineLeft ventricular hypertrophyLipoprotein(a)MalnutritionThrombogenic factorsSympathetic activityInsulin resistance/metabolic syndromeArteriosclerosisOlder ageAlbuminuriaMale genderReduced glomerular filtration rateSmokingEndothelial dysfunctionHypertensionAbnormal calcium/phosphate metabolismDiabetesMetabolic syndromeDyslipidemia Open table in a new tab Systolic blood pressure and anemia appear to be important determinants of left ventricular remodeling in patients with kidney disease17.Levin A. Thompson C.R. Ethier J. et al.Left ventricular mass index increase in early renal disease: Impact of decline in hemoglobin.Am J Kidney Dis. 1999; 34: 125-134Abstract Full Text Full Text PDF PubMed Scopus (715) Google Scholar. In addition, several traditional and nontraditional cardiovascular disease factors are implicated in the pathogenesis of LVH in chronic kidney disease. In a cohort of incident dialysis patients from Dialysis Morbidity and Mortality Study (DMMS) Wave 2, age, hypertension, diabetes, smoking, and serum calcium and parathyroid hormone (PTH) levels were correlates of LVH18.Stack A.G. Saran R. Clinical correlates and mortality impact of left ventricular hypertrophy among new ESRD patients in the United States.Am J Kidney Dis. 2002; 40: 1202-1210Abstract Full Text Full Text PDF PubMed Scopus (105) Google Scholar. Limited data exists on determinants of LVH in patients in the earlier stages of chronic kidney disease. In a nested analysis of data from the Australian Predialysis (SLIMHEART) Study, LVH was a product of both increased chamber size as well as wall thickness11.London G.M. Parfrey P.S. Cardiac disease in chronic uremia: pathogenesis.Adv Ren Replace Ther. 1997; 4: 194-211PubMed Google Scholar. In a cross-sectional study of patients with mean creatinine clearance of 25 mL/min, older age, higher systolic blood pressure, lower hemoglobin, and decreased level of kidney function were independent predictors of LVH19.Levin A. Singer J. Thompson C.R. et al.Prevalent left ventricular hypertrophy in the predialysis population: Identifying opportunities for intervention.Am J Kidney Dis. 1996; 27: 347-354Abstract Full Text PDF PubMed Scopus (616) Google Scholar. Similarly, in the ARIC Study, among African Americans with chronic kidney disease stage 3, lower GFR and lower hemoglobin were associated with LVH20.Astor B.C. Arnett D.K. Brown A. et al.Association of kidney function and hemoglobin with left ventricular morphology among African Americans: The Atherosclerosis Risk in Communities (ARIC) study.Am J Kidney Dis. 2004; 43: 836-845Abstract Full Text Full Text PDF PubMed Scopus (56) Google Scholar. More recent data suggest that additional nontraditional factors may be implicated in the development of LVH in kidney disease. In a cross-sectional study of hemodialysis patients, coronary artery calcification score and pulse pressure were independent correlates of LVH21.Yildiz A. Memisoglu E. Oflaz H. et al.Atherosclerosis and vascular calcification are independent predictors of left ventricular hypertrophy in chronic haemodialysis patients.Nephrol Dial Transplant. 2005; 20: 760-767Crossref PubMed Scopus (48) Google Scholar. Markers of oxidative stress, discussed later, were also associated with LVH independent of carotid intima media thickness and number of plaques in a cohort of chronic hemodialysis patients22.Zoccali C. Mallamaci F. Asahia K. et al.Pentosidine, carotid atherosclerosis and alterations in left ventricular geometry in hemodialysis patients.J Nephrol. 2001; 14: 293-298PubMed Google Scholar. There are limited data on traditional atherosclerotic cardiovascular disease factors in chronic kidney disease stages 1 to 4. Much of the existing information is extrapolated from studies in the general population. However, this extrapolation for the most part seems reasonable, as there is no a priori reason to assume that these risk relationships will widely differ in patients in the earlier stages of chronic kidney disease. A few studies have confirmed the importance of traditional cardiovascular disease risk factors, such as diabetes, higher total cholesterol, lower high-density lipoprotein (HDL) cholesterol, smoking, and higher systolic blood pressure, in the development of atherosclerotic cardiovascular disease in chronic kidney disease stages 1 to 423.Culleton B.F. Larson M.G. Wilson P.W. et al.Cardiovascular disease and mortality in a community-based cohort with mild renal insufficiency.Kidney Int. 1999; 56: 2214-2219Abstract Full Text Full Text PDF PubMed Scopus (724) Google Scholar,24.Muntner P. He J. Astor B.C. et al.Traditional and nontraditional risk factors predict coronary heart disease in chronic kidney disease: Results from the Atherosclerosis Risk in Communities Study.J Am Soc Nephrol. 2005; 16: 529-538Crossref PubMed Scopus (375) Google Scholar. Recent studies have suggested that the Framingham risk equation may be inadequate to attribute risk of coronary heart disease in a person with chronic kidney disease25.Longenecker J.C. Coresh J. Powe N.R. et al.Traditional cardiovascular disease risk factors in dialysis patients compared with the general population: The CHOICE Study.J Am Soc Nephrol. 2002; 13: 1918-1927Crossref PubMed Scopus (508) Google Scholar,26.Sarnak M.J. Coronado B.E. Greene T. et al.Cardiovascular disease risk factors in chronic renal insufficiency.Clin Nephrol. 2002; 57: 327-335Crossref PubMed Scopus (177) Google Scholar, although this remains to be evaluated in large prospective studies. A potential explanation for the Framingham equation being inadequate in chronic kidney disease is the presence of nontraditional factors that are not accounted for by this equation. There are few prospective studies or randomized controlled trials evaluating nontraditional factors as risk factors for the development of cardiovascular disease in chronic kidney disease. Available evidence for some of these risk factors is briefly summarized below. We do not discuss anemia, as this is the topic of an accompanying review. Inflammation appears to play an integral part in the pathogenesis of atherosclerosis. The most widely studied marker of inflammation is C-reactive protein (CRP). CRP may not be merely a marker of inflammation but may in fact mediate several key processes in the development of atherosclerosis including plaque initiation, formation, and rupture. In longitudinal analysis, CRP measured at baseline in the Modification of Diet in Renal Disease (MDRD) Study was an independent predictor of all-cause and cardiovascular disease mortality27.Menon V. Greene T. Wang X. et al.C-reactive protein and serum albumin as predictors of all-cause and cardiovascular mortality in patients with chronic kidney disease.Kidney Int. 2005; 68: 766-772Abstract Full Text Full Text PDF PubMed Scopus (299) Google Scholar. In the Nurses Health Study, higher levels of CRP, interleukin-6 (IL-6), and tumor necrosis factor (TNF) receptors I and II were associated with increased odds of coronary events in women with creatinine clearance <74 mL/min28.Knight E.L. Rimm E.B. Pai J.K. et al.Kidney dysfunction, inflammation, and coronary events: A prospective study.J Am Soc Nephrol. 2004; 15: 1897-1903Crossref PubMed Scopus (118) Google Scholar. Other pro- and anti-inflammatory cytokines, including IL-10, and TNF-α may also play a role in the development of cardiovascular disease in chronic kidney disease29.Stenvinkel P. Ketteler M. Johnson R.J. et al.IL-10, IL-6, and TNF alpha: Central factors in the altered cytokine network of uremia. The good, the bad, and the ugly.Kidney Int. 2005; 67: 1216-1233Abstract Full Text Full Text PDF PubMed Scopus (619) Google Scholar. Oxidative stress has been postulated as a common pathway via which other cellular processes such as inflammation and insulin resistance culminate in the pathogenesis of atherosclerosis30.Himmelfarb J. Stenvinkel P. Ikizler T.A. et al.The elephant in uremia: Oxidant stress as a unifying concept of cardiovascular disease in uremia.Kidney Int. 2002; 62: 1524-1538Abstract Full Text Full Text PDF PubMed Scopus (946) Google Scholar. There are, however, very limited data examining oxidative stress markers as cardiovascular disease risk factors in patients with chronic kidney disease. Post hoc analysis of patients with elevated creatinine in the Heart Outcomes and Protection (HOPE) Study did not find a benefit of Vitamin E on cardiovascular disease outcomes31.Mann J.F. Lonn E.M. Yi Q. et al.Effects of vitamin E on cardiovascular outcomes in people with mild-to-moderate renal insufficiency: results of the HOPE study.Kidney Int. 2004; 65: 1375-1380Abstract Full Text Full Text PDF PubMed Scopus (88) Google Scholar; however, the Secondary Prevention with Antioxidants of Cardiovascular Disease in End-Stage Renal Disease (SPACE) trial demonstrated a reduction in cardiovascular disease events with vitamin E32.Boaz M. Smetana S. Weinstein T. et al.Secondary prevention with antioxidants of cardiovascular disease in endstage renal disease (SPACE): Randomised placebo-controlled trial.Lancet. 2000; 356: 1213-1218Abstract Full Text Full Text PDF PubMed Scopus (895) Google Scholar. Similarly, Tepel et al33.Tepel M. Van Der Giet M. Statz M. et al.The antioxidant acetylcysteine reduces cardiovascular events in patients with end-stage renal failure: A randomized, controlled trial.Circulation. 2003; 107: 992-995Crossref PubMed Scopus (334) Google Scholar were able to achieve cardiovascular disease event reduction in patients with kidney failure by administration of acetylcysteine, a putative antioxidant agent33.Tepel M. Van Der Giet M. Statz M. et al.The antioxidant acetylcysteine reduces cardiovascular events in patients with end-stage renal failure: A randomized, controlled trial.Circulation. 2003; 107: 992-995Crossref PubMed Scopus (334) Google Scholar. There is a close correlation between components of the metabolic syndrome and kidney disease; and in fact it has been proposed that albuminuria be considered a component of the metabolic syndrome34.Palaniappan L. Carnethon M. Fortmann S.P. Association between microalbuminuria and the metabolic syndrome: NHANES III.Am J Hypertens. 2003; 16: 952-958Crossref PubMed Scopus (251) Google Scholar. Metabolic syndrome has been linked to increased risk of cardiovascular disease mortality in the general population35.Ford E.S. The metabolic syndrome and mortality from cardiovascular disease and all-causes: findings from the National Health and Nutrition Examination Survey II Mortality Study.Atherosclerosis. 2004; 173: 307-312Abstract Full Text Full Text PDF Scopus (396) Google Scholar but data are lacking in chronic kidney disease. Hyperinsulinemia and insulin resistance are also prevalent in kidney disease and a prospective study of nondiabetic hemodialysis patients demonstrated an association between insulin resistance and cardiovascular disease mortality36.Shinohara K. Shoji T. Emoto M. et al.Insulin resistance as an independent predictor of cardiovascular mortality in patients with end-stage renal disease.J Am Soc Nephrol. 2002; 13: 1894-1900Crossref PubMed Scopus (298) Google Scholar. A novel risk factor that has been the focus of recent investigation in kidney disease is adiponectin. Adiponectin, an adipocyte hormone, is inversely related to several metabolic parameters such as body mass index, glucose, and insulin and has been postulated to be a biomarker for the metabolic syndrome. Decreased plasma levels of adiponectin were associated with increased risk of cardiovascular disease mortality in a cohort of chronic hemodialysis patients37.Zoccali C. Mallamaci F. Tripepi G. et al.Adiponectin, metabolic risk factors, and cardiovascular events among patients with end-stage renal disease.J Am Soc Nephrol. 2002; 13: 134-141Crossref PubMed Google Scholar. High homocysteine (tHcy) appears to be associated with increased cardiovascular disease risk in the general population38.Boushey C.J. Beresford S.A. Omenn G.S. et al.A quantitative assessment of plasma homocysteine as a risk factor for vascular disease. Probable benefits of increasing folic acid intakes.JAMA. 1995; 274: 1049-1057Crossref PubMed Scopus (3431) Google Scholar. Similarly, elevated levels of tHcy may be associated with increased morbidity and mortality from cardiovascular disease in patients with kidney failure39.Mallamaci F. Zoccali C. Tripepi G. et al.Hyperhomocysteinemia predicts cardiovascular outcomes in hemodialysis patients.Kidney Int. 2002; 61: 609-614Abstract Full Text Full Text PDF PubMed Scopus (259) Google Scholar. In contrast, low tHcy levels were associated with hospitalization and mortality in other studies in hemodialysis patients40.Wrone E.M. Hornberger J.M. Zehnder J.L. et al.Randomized trial of folic acid for prevention of cardiovascular events in end-stage renal disease.J Am Soc Nephrol. 2004; 15: 420-426Crossref PubMed Scopus (204) Google Scholar. Data are lacking on the relationship between homocysteine and cardiovascular disease risk in patients in the earlier stages of chronic kidney disease, and whether decreasing homocysteine levels can reduce cardiovascular disease risk in this patient population. As described in a subsequent section, abnormal mineral metabolism can promote arterial calcification, and arterial stiffness, which may lead to LVH and thereby potentiation of atherogenesis. Abnormal endothelium-dependent vasodilation, manifested as impaired brachial artery reactivity, is a predictor of cardiovascular disease events and mortality in patients with kidney failure and this association is independent of arterial stiffness and LVH41.London G.M. Pannier B. Agharazii M. et al.Forearm reactive hyperemia and mortality in end-stage renal disease.Kidney Int. 2004; 65: 700-704Abstract Full Text Full Text PDF PubMed Scopus (112) Google Scholar. Endothelium-dependent vasodilation appears to be impaired in patients with chronic kidney disease42.Thambyrajah J. Landray M.J. Mcglynn F.J. et al.Abnormalities of endothelial function in patients with predialysis renal failure.Heart. 2000; 83: 205-209Crossref PubMed Scopus (171) Google Scholar, although its association with outcomes has not been studied in this population. Endothelial cell apoptosis facilitates atherosclerotic plaque formation in several different ways, including increased vascular permeability, proliferation of smooth muscle cells and macrophages, and platelet activation and aggregation. A prospective study in chronic hemodialysis patients noted that levels of sFas, a marker of apoptosis, were independent predictors of future risk of fatal and nonfatal cardiovascular events43.Troyanov S. Hebert M.J. Masse M. et al.Soluble Fas: A novel predictor of atherosclerosis in dialysis patients.Am J Kidney Dis. 2003; 41: 1043-1051Abstract Full Text Full Text PDF PubMed Scopus (33) Google Scholar. Impaired endothelium-dependent vasodilation is related to carotid wall distensibility in patients with kidney failure, suggesting that endothelial dysfunction may contribute to arterial structural alterations in patients with kidney disease44.Pannier B. Guerin A.P. Marchais S.J. et al.Postischemic vasodilation, endothelial activation, and cardiovascular remodeling in end-stage renal disease.Kidney Int. 2000; 57: 1091-1099Abstract Full Text Full Text PDF PubMed Scopus (110) Google Scholar. A growing body of evidence implicates hyperphosphatemia and elevated calcium phosphate product as contributors to the excess cardiovascular disease risk in kidney failure45.Block G.A. Klassen P.S. Lazarus J.M. et al.Mineral metabolism, mortality, and morbidity in maintenance hemodialysis.J Am Soc Nephrol. 2004; 15: 2208-2218Crossref PubMed Scopus (2080) Google Scholar. Potential pathways include increased large vessel calcification with its associated effects on arterial stiffening, increased pulse pressure, decreased coronary perfusion, and LVH. There are limited data evaluating the relationships of serum levels of phosphorus and calcium phosphate product with cardiovascular disease in earlier stages of chronic kidney disease. A recent analysis of a cohort of United States veterans with chronic kidney disease stage 3 demonstrated that serum phosphorus levels>3.5 mg/dL were independent predictors of all-cause mortality46.Kestenbaum B. Sampson J.N. Rudser K.D. et al.Serum phosphate levels and mortality risk among people with chronic kidney disease.J Am Soc Nephrol. 2005; 16: 520-528Crossref PubMed Scopus (868) Google Scholar. Patients in all stages of chronic kidney disease are at high risk of cardiovascular disease. We have briefly presented available data from studies exploring the mechanisms underlying this excess risk. We acknowledge that this is not an exhaustive review of all the potential risk factors involved in the development of cardiovascular disease in chronic kidney disease. Rather, we have focused on a few with some degree of evidence available and that are potentially modifiable. It needs to be emphasized that causal relationships are yet to be established for many of the risk factors discussed. The implications of our present state of knowledge is that a high suspicion for cardiovascular disease is warranted and that aggressive treatment of traditional risk factors should be instituted in the earlier stages of chronic kidney disease. Additional basic science research, observational studies, and clinical trials, are, however, urgently needed to understand the pathophysiology of cardiovascular disease and to evaluate potential interventions to reduce the burden of cardiovascular disease in chronic kidney disease stages 1 to 4." @default.
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• W2022285777 title "Cardiovascular risk factors in chronic kidney disease" @default.
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