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Without intervention, premature cardiovascular disease is virtually certain in progressive chronic kidney disease (CKD). Whatever age the patient, the cardiovascular system in uraemia is senescent and poorly suited to dealing with supraphysiological haemodynamic demands. Anaemia and hypertension are the principal haemodynamic risk factors that can be treated. Many observational studies have shown that anaemia is a risk factor for haemodynamic overload, maladaptive left ventricular growth, left ventricular failure and death. The justification for normal target haemoglobin (Hb) in patients with CKD is still debated. Observational studies of left ventricular size, quality of life, functional status, hospital admission, and survival support higher Hb concentrations (> or =12 g/dl). Intervention trials to date suggest that a physiological approach to anaemia management benefits quality of life, and possibly left ventricular hypertrophy and dilatation. Obviously, avoiding anaemia is the only way to minimize time-averaged, anaemia-related haemodynamic load. Whether this strategy, involving efficient surveillance, early detection, early intervention, and high Hb targets that are independent of the phase of CKD, actually reduces cardiac failure or death remains to be seen.
Nephrol Dial Transplant 2002
PMID:Anaemia: cardiovascular adaptations and maladaptive responses in chronic kidney disease. 1238 55

We retrospectively evaluated the phenomenon of arterial hypotension in peritoneal dialysis (PD) in a large cohort of 633 PD patients from two centers (Toronto Western Hospital, Toronto, Canada, and Division of Nephrology, Democritus University of Thrace, Greece), thus extending our previously reported experience for an additional 6 years (1995-2000). Together, the units had 81 hypotensive patients (12.8%), whose mean age was 63.8 +/- 14.2 years and whose mean duration of peritoneal dialysis was 49.3 +/- 30 months. Based on the underlying pathophysiology, the hypotensive PD patients were divided into four groups: (A) hypovolemia, 32 patients (39.5%); (B) congestive heart failure (CHF), 15 patients (18.5%); (C) receiving antihypertensive medications, 11 patients (13.6%); and (D) "unknown" etiology, 23 patients (28.4%). All patients in the hypovolemic and antihypertensive groups responded well to treatment (volume expansion and discontinuation of antihypertensive medication, respectively), but in the CHF and "unknown" groups, only 40% improved with the appropriate intervention. Patients in the latter two groups showed the poorest prognosis, with an approximate death rate of 65%. The hypovolemic group had better outcomes, which might reflect prompt response to fluid replacement in that group. We conclude that, in PD patients, careful use of antihypertensive medication, the right evaluation of target weight (especially in patients with cardiac failure), and judicious use of hypertonic exchanges may prevent the severe complication of arterial hypotension.
Adv Perit Dial 2002
PMID:Hypotension in patients on chronic peritoneal dialysis: etiology, management, and outcome. 1240 86

The fundamental objective of dialysis is to maintain the dose of solute clearance and ultrafiltration (UF). When peritoneal dialysis (PD) patients cannot maintain the target dose of clearance [weekly Kt/V > 2.0, weekly creatinine clearance (CCr) > 60 L/1.73 m2], the dialysis dose needs to be increased. But the means of increasing the dose only by PD are limited, especially for patients with UF failure (UFF). Combination therapy--PD with hemodialysis (PD + HD)--is the simplest way to solve the problem. The purpose of PD + HD therapy is to support solute clearance and UF when PD alone cannot meet the necessary targets. Acute and transient dialysis cases should be excluded. The general prescription for PD + HD should be 5-6 days of PD weekly and 1 session of HD weekly. For determine the adequacy of PD + HD, we adopted the equivalent renal clearance (EKR), transforming the PD weekly Kt/V and then evaluating total clearance from both modalities. Of our 238 dialysis patients, 31 (13%) use combined therapy. Except for 1 patient that transferred from long-term HD, all of patients had been on PD for more than 60 months, and were experiencing uremic symptoms after decline of residual renal function. In 12 cases, the problem was lack of solute clearance; in 5 cases, it was UFF. High permeability was involved in 5 cases: 4 after long-term PD and 1 from the start of PD. Poor self-management occurred in 9 cases. Contributing factors included hernia, diaphragmatic intercourse, and severe heart failure with strict fluid control. Among the 31 patients, 8 used HD twice weekly. After combination therapy was started, the dialysis dose increased and body fluids became controllable. As a result, uremic symptoms improved and the patients' quality of life increased.
Adv Perit Dial 2002
PMID:Five years' experience of combination therapy: peritoneal dialysis with hemodialysis. 1240 89

Cardiovascular complications are the leading cause of mortality in patients with end-stage renal disease (ESRD). The excess cardiovascular risk and mortality is already demonstrable in early renal disease and in patients with chronic renal failure (CRF), with the highest relative risk of mortality in the youngest patients. The high risk for cardiovascular disease (CVD) results from the additive effect of multiple factors, including hemodynamic overload and several metabolic and endocrine abnormalities more or less specific to uremia. CVD includes disorders of the heart (left ventricular hypertrophy [LVH], cardiomyopathy) and disorders of the vascular system (atherosclerosis, arteriosclerosis), these two disorders being usually associated and interrelated. LVH is the most frequent cardiac alteration in ESRD, resulting from a combined pressure and volume overload. LVH in general is an ominous prognostic sign and an independent risk factor for arrhythmias, sudden death, heart failure, and myocardial ischemia. Regression of LVH needs a combined intervention to reduce hemodynamic overload and is associated with improved prognosis and survival. Clinical studies have shown that damage of large conduit arteries is a major contributing factor for the high incidence of congestive heart failure (CHF), LVH, ischemic heart disease (IHD), sudden death, cerebrovascular accidents, and peripheral artery diseases. Damage to large conduit arteries is principally related to highly calcified occlusive atherosclerotic lesions and to stiffening of large capacitive arteries. These two complications are independent risk factors for survival, and improvement of arterial stiffness is associated with better prognosis and survival. The present review summarizes the most recent works dealing with the pathophysiology of CVD and some aspects of the therapeutic approach.
Semin Dial
PMID:Cardiovascular disease in chronic renal failure: pathophysiologic aspects. 1264 70

Cardiovascular disease (CVD) remains the leading cause of morbidity and mortality in patients with end-stage renal disease (ESRD). Both in dialysis and in transplant patients, CVD remains the leading cause of death. There is accumulating evidence that the increase in CVD burden is present in patients prior to dialysis, due to both conventional risk factors as well as those specific to kidney disease. Of importance is that even in patients with mild kidney disease, the risk of cardiovascular events and death is increased relative to patients without evidence of kidney disease. The new classification system proposed by the National Kidney Foundation as part of the Dialysis Outcomes Quality Initiative (DOQI) process describes the five stages of kidney disease, as well as those complications associated with chronic kidney disease (CKD), in particular cardiovascular risk factors and disease. Patients with kidney disease are deemed to be at highest cardiovascular risk. CVD, defined as the presence of either congestive heart failure (CHF), ischemic heart disease (IHD), or left ventricular hypertrophy (LVH), is prevalent in cohorts with established CKD (8-40%). The prevalence of hypertension, a major risk factor for coronary artery disease (CAD) and LVH is high in patients with CKD (87-90%). At least 35% of patients with CKD have evidence of an ischemic event (myocardial infarction or angina) at the time of presentation to a nephrologist. The prevalence of LVH increases at each stage of CKD, reaching 75% at the time of dialysis initiation, and the modifiable risk factors for LVH include anemia and systolic blood pressure, which are also worse at each stage of kidney disease. Even under the care of nephrologists, a change in cardiac status (worsening of heart failure or anginal symptoms) occurs in 20% of patients. The presence of CVD predicts a faster decline of kidney function and the need for dialysis, after controlling for all other factors including glomerular filtration rate (GFR), age, and the presence of LVH. This article describes the new classification system for staging of CKD, defines and describes CVD in CKD, and reviews the evidence and its limitations with respect to the current understanding of CKD and CVD. Specifically, methodologic issues related to survival and referral bias limit our current understanding of the complex interaction of conventional and nonconventional kidney disease-specific risk factors. We identify the importance of well-conducted studies of patient groups with and without CVD, with and without CKD, in order to better understand the complex physiology so that treatment strategies can be appropriately applied.
Semin Dial
PMID:Clinical epidemiology of cardiovascular disease in chronic kidney disease prior to dialysis. 1264 72

Cardiovascular disease (CVD) is the major cause of death among renal transplant recipients (RTRs), accounting for 17-50% of deaths. Both cardiomyopathy (congestive heart failure [CHF] and left ventricular hypertrophy [LVH]) and ischemic heart disease (IHD) are important complications of renal transplantation, although the morbid impact of cardiomyopathy has been overlooked until recently. Echocardiographic disorders and clinical CHF occur far more frequently in RTRs than in the general population, suggesting that renal transplantation may be a state of accelerated heart failure. In contrast, the incidence of IHD in RTRs is similar to that in the Framingham cohort. Age, diabetes, and gender remain important markers of risk for both disorders. Smoking, hyperlipidemia, and hypertension appear to be the major reversible risk factors for IHD, while anemia and hypertension are major reversible risk factors for cardiomyopathy. Definitive evidence on optimal intervention is lacking. Clinical trials are needed to define optimum targets for treatment of these risk factors, especially hypertension and anemia.
Semin Dial
PMID:Clinical epidemiology of cardiac disease in renal transplant recipients. 1264 73

Patients with end-stage renal disease (ESRD) are at extreme cardiovascular risk. At least half of all patients starting dialysis therapy have overt cardiovascular disease (CVD). In addition, recent studies suggest annual incidence rates for new-onset cardiac failure, peripheral vascular disease, ischemic heart disease (IHD), and stroke of approximately 7%, 7%, 5%, and 1%, respectively. High-level exposure to traditional risk factors, such as smoking and dyslipidemia, hemodynamic overload factors, such as anemia and hypertension, and a myriad of metabolic factors related to uremia are all likely to play a role. There has been explosive growth in observational studies and a heartening, if less dramatic, increase in risk factor intervention trials, suggesting that risk factor modification can lead to meaningful benefit.
Semin Dial
PMID:Clinical epidemiology of cardiac disease in dialysis patients: left ventricular hypertrophy, ischemic heart disease, and cardiac failure. 1264 74

Left ventricular (LV) volume and pressure overload occur frequently in chronic kidney disease (CKD). Anemia is a risk factor for left ventricular hypertrophy (LVH) and dilatation, heart failure, and death. Normalization of hemoglobin with erythropoietin may prevent LVH and dilatation in CKD, but in patients in later phases of their cardiac disease, this intervention is not of benefit. Increased vascular volume causes hypertension, which in turn causes LVH, cardiac failure, and ischemic heart disease (IHD). Manifestations of arteriosclerosis are associated with adverse cardiac outcomes, and angiotensin converting enzyme (ACE) inhibitors may improve LVH and markers of arteriosclerosis. Aortic stenosis in dialysis patients occurs infrequently, but may deteriorate rapidly. The hemodialysis milieu is the quintessential model of LV overload cardiomyopathy.
Semin Dial
PMID:Hemodynamic cardiovascular risk factors in chronic kidney disease: what are the effects of intervention? 1264 77

Cardiovascular disease (CVD) is a major contributor to the mortality and morbidity of patients who suffer from chronic kidney disease (CKD). Heart failure and ischemic heart disease (IHD) are both highly prevalent in this population. The diagnosis of myocardial dysfunction is usually based on echocardiography. As in the general population, systolic dysfunction is treated with a combination of diuretics, renin-angiotensin system blockade, and beta-receptor antagonists. Diastolic dysfunction is best managed by eliminating the cause. Non-invasive tests for coronary artery disease (CAD) may be less reliable in patients with renal disease compared with nonuremic patients. Medical therapy of IHD in this population is generally similar to that for other patient groups, but surgical revascularization appears to carry a higher risk of complications with poorer clinical outcomes. The choice of revascularization procedure (coronary artery bypass grafting versus percutaneous transluminal angioplasty) should be based on the specific coronary anatomy of a given patient as well as a consideration of other comorbid factors.
Semin Dial
PMID:Management of heart failure and coronary artery disease in patients with chronic kidney disease. 1264 82

Cholesterol embolic disease is a devastating complication of atherosclerosis. Universally recommended treatment is lacking thus far. Recent data suggest that a therapeutic protocol aimed at specifically combating three causes of mortality, recurrent bouts of cholesterol embolism, cardiac failure, and cahexia, were associated with a favorable clinical outcome. As for drug therapy, corticosteroid has been reported to be beneficial in reducing local and general inflammatory responses. Concerning apheresis, combined therapy consisting of plasma exchange and low to intermediate-dose corticosteroid therapy has been shown to be effective in multivisceral cholesterol embolism. Low density lipoprotein (LDL) apheresis has been reported to be beneficial for cholesterol embolism-induced damage to the skin and brain.
Ther Apher Dial 2003 Aug
PMID:Apheresis in the treatment of cholesterol embolic disease. 1288 28


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