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Results for “Chronic kidney disease”

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At least 19 recordsLinked to original sources

PubMed2007

Mineral metabolism and mortality in patients with chronic kidney disease.

Chronic kidney disease is associated with profound alterations in mineral metabolism. A growing body of evidence, based largely on observational studies, indicates that patient mortality is associated with altered mineral metabolism. Evidence is reviewed concerning the association between mortality and high concentrations of serum phosphorus, calcium, calcium-phosphate product, and parathyroid hormone. In addition, mortality may be independently associated with dialysate calcium concentration, type of phosphate binder therapy, and use of vitamin D analogs. Practices related to management of altered mineral metabolism may prove to be a promising means of improving outcomes for patients with chronic kidney disease.

Calcium↗

PubMed2006

Metabolic syndrome and chronic kidney disease.

Chronic kidney disease is fast becoming a worldwide epidemic. In the US, the prevalence of chronic kidney disease is 11%. Its increase in the recent years has mirrored the rising trend of obesity, hypertension and diabetes, which are all components of the metabolic syndrome. Metabolic syndrome comprises of 5 components: impaired fasting glucose, abdominal obesity, hypertriglyceridemia, hypertension and low high density lipoprotein cholesterol. While it is a well known cardiovascular risk factor in the general population, its effects in chronic kidney disease and dialysis populations has not been fully elucidated. While the number of people requiring renal replacement therapy is increasing globally, many of those with chronic kidney disease also suffer from cardiovascular morbidity and mortality. This review discusses the interaction between chronic kidney disease and metabolic syndrome, and the impact of the two on the cardiovascular risk in patients with chronic kidney disease.

Cardiovascular Diseases↗

PubMed2005

Detection and evaluation of chronic kidney disease.

Chronic kidney disease affects approximately 19 million adult Americans, and its incidence is increasing rapidly. Diabetes and hypertension are the underlying causes in most cases of chronic kidney disease. Evidence suggests that progression to kidney failure can be delayed or prevented by controlling blood sugar levels and blood pressure and by treating proteinuria. Unfortunately, chronic kidney disease often is overlooked in its earliest, most treatable stages. Guidelines from the National Kidney Foundation's Kidney Disease Outcomes Quality Initiative (KDOQI) recommend estimating glomerular filtration rate and screening for albuminuria in patients with risk factors for chronic kidney disease, including diabetes, hypertension, systemic illnesses, age greater than 60 years, and family history of chronic kidney disease. The glomerular filtration rate, calculated by using a prediction equation, detects chronic kidney disease more accurately than does the serum creatinine level alone; the glomerular filtration rate also is used for disease staging. In most clinical situations, analysis of random urine samples to determine the albumin-creatinine or protein-creatinine ratio has replaced analysis of timed urine collections. When chronic kidney disease is detected, an attempt should be made to identify and treat the specific underlying condition(s). The KDOQI guidelines define major treatment goals for all patients with chronic kidney disease. These goals include slowing disease progression, detecting and treating complications, and managing cardiovascular risk factors. Primary care physicians have an important role in detecting chronic kidney disease early, in instituting measures to slow disease progression, and in providing timely referral to a nephrologist.

Age Distribution↗

PubMed2005

The role of statins in chronic kidney disease.

Chronic kidney disease is associated with cardiovascular event rates that are at least as high as in patients with established atherosclerotic cardiovascular disease or in those with diabetes mellitus. Chronic kidney disease is therefore considered a cardiovascular disease risk equivalent. Treatment of dyslipidemia, which is very common in this population and reflects the pattern seen in the metabolic syndrome, reduces cardiovascular events in patients with chronic kidney disease. Thus, patients with chronic kidney disease should be evaluated and treated for dyslipidemia. Dyslipidemia is a risk factor for the development of impaired kidney function. Dyslipidemia is also associated with progressive renal disease in subjects with no overt renal disease, as well as those with diabetic and nondiabetic kidney disease. Although definitive randomized controlled trials are lacking, the collective evidence suggests that treatment of dyslipidemia is associated with less decline in renal function. The use of potent statins in high doses can lead to transient proteinuria via impairment of proximal tubular receptor--mediated endocytosis, in a dose-dependent manner. Over the long term, however, the use of statins results in a reduction in proteinuria and in the rate of decline of renal function. Several large definitive trials that are currently underway to examine the safety and efficacy of statins in cardiovascular and renal protection should provide more definitive answers on the role of these drugs in this very high risk population.

Arteriosclerosis↗

PubMed2005

[Early diagnosis of chronic kidney diseases].

Chronic kidney diseases frequently progress to end-stage renal failure over a period of several years. Ultimately, the glomerular filtration apparatus and tubulus are destroyed to such an extent that renal replacement therapy is required. This process may last longer than 10 years. To avoid loss of renal function, chronic kidney diseases should be diagnosed as early as possible so that therapeutic measures are initiated in time. Medications which prevent or delay progression to end-stage renal failure, e.g. ACE inhibitors and AT(1) blockers, are more effective if started early in the course of renal disease. A significant number of patients with chronic kidney disease are still diagnosed too late and are without adequate therapy so that chances for prevention and/or delay of chronic kidney disease are missed.

Chronic Disease↗

PubMed2001

Patients, populations and policy: patient outcomes in chronic kidney disease.

Chronic kidney disease represents an interesting illustration for evaluating an epidemic of chronic illness, the impact of care processes and technology on health outcomes, the impact of financial incentives and cost containment on health outcomes, and the choices society must consider in responding to a chronic illness. The evidence suggests that strong economic pressures exist in the care of chronic kidney disease and that cost containment is important. The results in large part reflect the impact of economic pressures on clinical decision making in the absence of good evidence on outcomes. To improve clinical decision making we need valid evidence linking specific processes of care to patient outcomes. Specific processes amenable to study include the provision of preventive services, physician and nurse technical and interpersonal care and adherence to clinical practice guidelines. The ESRD Quality Study (EQUAL) currently underway and supported by the National Institutes of Diabetes and Digestive and Kidney Diseases, may help to guide physicians and centers in caring for their patients with chronic kidney disease. This investigation examines the relation between process of care and outcomes and expands outcomes measure to include disease-specific quality-of-life measures and patient satisfaction and accounts for case mix using the Index of Co-Existent Disease, a measure of the extent of different comorbid diseases as well as their severity (18,19,20). Better data on how processes of care are linked to health outcomes can inform decision making and allow educated cost cutting and quality maintenance.

Costs and Cost Analysis↗

PubMed2006

Oxidants in chronic kidney disease.

Chronic kidney disease is a worldwide public health problem that affects approximately 10% of the US adult population and is associated with a high prevalence of cardiovascular disease and high economic cost. Chronic renal insufficiency, once established, tends to progress to end-stage kidney disease, suggesting some common mechanisms for ultimately causing scarring and further nephron loss. This review defines the term reactive oxygen metabolites (ROM), or oxidants, and presents the available experimental evidence in support of the role of oxidants in diabetic and nondiabetic glomerular disease and their role in tubulointerstitial damage that accompanies progression. It concludes by reviewing the limited human data that provide some proof of concept that the observations in experimental models may be relevant to human disease.

Animals↗

PubMedDate not supplied

Management of pediatric patients with chronic kidney disease.

Chronic kidney disease in children is associated with complications that require nursing interventions in both the inpatient and outpatient settings. Given the progressive nature of the disease and the complexity of the treatment regimen, it is important that nurses be comfortable implementing acute and preventive care strategies and facilitating the coordination of care. In addition, the need for multiple therapies can be distressing for patients and theirfamilies, further supporting the role of the nurse in patient and family education and decision making regarding the plan of care. In this review, we discuss the pertinent issues of pediatric chronic kidney disease in the context of a case study to promote better understanding of real-world nursing practice.

Anemia↗

PubMedDate not supplied

Management of pediatric patients with chronic kidney disease.

Chronic kidney disease in children is associated with complications that require nursing interventions in both the inpatient and outpatient settings. Given the progressive nature of the disease and the complexity of the treatment regimen, it is important that nurses be comfortable implementing acute and preventive care strategies and facilitating the coordination of care. In addition, the need for multiple therapies can be distressing for patients and their families, further supporting the role of the nurse in patient and family education and decision making regarding the plan of care. In this review, we discuss the pertinent issues of pediatric chronic kidney disease in the context of a case study to promote better understanding of real-world nursing practice.

Aftercare↗

PubMed2004

Outcomes associated with hypogonadism in men with chronic kidney disease.

Chronic kidney disease is commonly accompanied by disturbances in the hypothalamic-pituitary-gonadal axis. Such disturbances in men give rise to hypogonadism and low circulating testosterone levels. The deficiency in testosterone can contribute to clinical outcomes such as sexual dysfunction, decreased bone mineralization, malnutrition and decreased muscle mass, and anemia. The administration of androgens to nonuremic hypogonadal men is usually effective in treating such outcomes. By contrast, the response to therapy in uremic men tends to be much less predictable. This variability in response is not surprising, because these same clinical outcomes can be the result of other aspects of the uremic state or the comorbid conditions that are frequently present in men with chronic kidney disease. Although further studies are needed, testosterone therapy may prove most useful as an adjunct to other more general therapies designed to address the uremic state.

Chronic Disease↗

PubMed2005

Treatment of hypertension in chronic kidney disease.

Chronic kidney disease (CKD) is a major public health problem in the United States. It is estimated that nearly 20 million Americans have some degree of chronic kidney disease defined as an estimated glomerular filtration rate of less than sixty milliliters per minute or evidence of kidney damage by imaging study, biopsy, biochemical testing or urine tests with an estimated glomerular filtration rate more than sixty milliliters per minute. Hypertension is present in more than 80% of patients with CKD and contributes to progression of kidney disease toward end stage (ESRD) as well as to cardiovascular events such as heart attack and stroke. In fact the risk for cardiovascular death in this patient population is greater than the risk for progression to ESRD. Proteinuria is an important co-morbidity in hypertensives with CKD and increase risk of disease progression and cardiovascular events. Treatment of hypertension is therefore imperative. The National Kidney Foundation clinical practice guidelines recommend a blood pressure goal of <130 mmHg systolic and <80 mmHg diastolic for all CKD patients. Recent post-hoc analyses of the Modification of Diet in Renal Disease study indicate that lower blood pressure may provide long-term kidney protection in patients with nondiabetic kidney disease. Specifically a mean arterial pressure <92 mmHg (e.g. 120/80 mmHg) as compared to 102-107 mmHg (e.g. 140/90 mmHg) is associated with reduced risk for ESRD. In most cases achieving this goal requires both non-pharmacologic and pharmacologic intervention. Dietary sodium restriction to no more than 2 grams daily is important. In addition, moderate alcohol intake, regular exercise, weight loss in those with a body mass index greater than 25 kg/M(2) and reduced amount of saturated fat help to reduce blood pressure. The first line pharmacologic intervention should be an angiotensin converting enzyme inhibitor or angiotensin II type 1 receptor blocker in those with diabetes or non-diabetics with more than 200 mg protein/gram creatinine on a random urine sample. For non-diabetics with less than 200 mg protein/gram creatinine on a random urine sample, no specific first-line drug class is recommended. After initial dosing with an ACEi, ARB or other drug, a diuretic should be added to the regimen. Thereafter, beta-blockers, calcium channel blockers, apha blockers and alpha 2 agonists (e.g. clonidine) and finally vasodilators (e.g. minoxidil) should be added to achieve blood pressure goal. Combinations of ACEi and ARB are helpful in reducing proteinuria and may also lower blood pressure further in some some cases. Blood pressure should be monitored closely in hypertensive patients with CKD and both clinic and home blood pressure measurements may help the clinician adjust treatment.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed2005

Traditional and nontraditional cardiovascular risk factors in chronic kidney disease.

Chronic kidney disease (CKD) is public health problem, with as many as 20 million individuals affected in the United States. Patients with CKD should be considered in the highest-risk group for development of cardiovascular disease (CVD), and aggressive treatment of traditional and nontraditional risk factors should be instituted. Additional randomized controlled trials are urgently needed to evaluate potential treatments in this population. This article focuses attention on the major modifiable cardiovascular risk factors in CKD.

Cardiovascular Diseases↗

PubMedDate not supplied

[Can cardiovascular calcifications be prevented in chronic kidney disease?].

Chronic kidney disease, with special regard to hemodialysis patients, develop frequent and widespread cardiac and vascular calcifications. In the heart calcifications are mainly located in the coronary arteries and in the valvular structures. There is a strict relation between cardiovascular mortality in CKD and the extent of cardiac and vascular calcifications. Therefore it is important to evaluate the causes of extraskeletal calcifications for the evaluation of the possibility of prevention. The importance of hyperphosphatemia, of hypercalcemia and of the increased CAxP product as a cause of cardiac calcification has been clearly underlined. However the mechanism of calcification, initially considered a physico-chemical precipitation, has been investigated with the conclusion that the process is mediated by cellular differentiation and production of factors favoring mineralization in the extracellular milieu. Increased serum phosphate levels are able to induce a transformation of vascular smooth muscle cells into osteoblast-like cells, able to produce factors known to be pro-mineralizing agents in the bone tissue. Further studies have revealed the importance of a number of inhibitors of calcification of cardiovascular structures, like Fetuin-A, MGP, Osteopontin, Osteoprotegerin. Therefore at present the calcification process of vascular tissue is considered to be linked to a balance between inducers and inhibitors of calcium-phosphate deposits. Prevention of cardiac calcifications is at present mainly based of optimal control of serum phosphate and reduction of calcium load through the use of non-calcium containing phosphate binders. Treatment with statins for prevention and treatment of atherosclerosis is also an important means of decreasing the size and number of atherosclerotic plaques, where a portion of the calcification process develops.

Calcinosis↗

PubMed2005

Chinese herbal medicine in the treatment of chronic kidney disease.

Chronic kidney disease (CKD) is a worldwide public health issue with poor outcomes and high cost. There is growing evidence that some of the adverse outcomes of CKD can be prevented or delayed by early treatment using angiotensin II-converting enzyme inhibitors and angiotensin II-receptor blockers. A great amount of the world's population has been using traditional Chinese herbal medicine (TCHM) for treatment of CKD and has accumulated their experience for years. In this article, the knowledge and the therapeutic principles of traditional Chinese medicine in the treatment of CKD are briefly reviewed. The efficacy of several TCHMs, supported by either clinical evidence or experimental studies, is presented. The future direction for the study of Chinese herbal medicines in CKD is discussed.

Angelica↗

PubMed2005

Strategies to retard the progression of chronic kidney disease.

Chronic kidney disease (CKD) is a common and, in advanced cases, highly morbid disorder. The most severe form of CKD is end-stage renal disease (ESRD), in which the patient requires some form of renal replacement therapy to survive. The increasing incidence, prevalence, and costs of ESRD are major national health care concerns; interventions that may prevent or slow the progression of CKD towards ESRD are extremely important and the focus of this article.

Anemia↗

PubMed2006

Cardiometabolic syndrome and chronic kidney disease.

Chronic kidney disease (CKD) is increasingly recognized as a major risk factor for end-stage renal disease (ESRD), cardiovascular (CV) disease, and CV-related premature death. More than 8 million people in the United States have CKD; therefore, preventive stratiegies should be directed at identifying risk factors for this condition. There is growing evidence implicating the cardiometabolic syndrome, a clustering of CV risk factors that include obesity, insulin resistance, compensatory hyperinsulinemia, dysglycemia, atherogenic dyslipidemia, and hypertension. Factors mediating this relationship include increased glomerular filtration, increased vascular permeability, oxidative and endoplasmic reticulum stress, activation of the renin-angiotensin system, and inappropriate secretion of growth factors. The consequences are microalbuminuria, a marker of inflammation and endothelial dysfunction, renal vascular proliferation, extracellular matrix expansion, and CKD. Prevention of CKD should be directed at controlling all components of the cardiometabolic syndrome, with the ultimate goal of reducing the burden imposed by ESRD.

Albuminuria↗

PubMed2006

Arterial stiffness and enlargement in mild-to-moderate chronic kidney disease.

Chronic kidney disease (CKD) is associated with an increased risk of cardiovascular morbidity and mortality. Arterial stiffness and remodeling have been well documented in patients with end-stage renal disease, but little is known about arterial phenotype in CKD patients with moderate reduction in glomerular filtration rate (GFR). In total, 95 patients (58+/-15 years, mean+/-s.d.) with CKD and GFR measured by renal clearance of (51)Cr-ethylenediaminetetraacetate were compared to 121 hypertensive patients without CKD (59+/-11 years), and 57 normotensive subjects (56+/-6 years). Common carotid artery diameter, intima-media thickness (IMT), distensibility, and Young's elastic modulus were noninvasively determined with a high-definition echotracking system. Patients with CKD had a significantly larger carotid internal diameter than in hypertensives and normotensives (6.32+/-1.05, 5.84+/-0.74, and 5.50+/-0.64 m x 10(-3), respectively; P<0.001), resulting in 25% and 11% increases in circumferential wall stress, respectively, since no significant difference in IMT was observed. Carotid distensibility and elastic modulus did not significantly differ between CKD and hypertensives; normotensives had significantly higher distensibility and lower elastic modulus than CKD and hypertensive patients. Carotid-femoral pulse wave velocity was significantly higher in CKD patients than in hypertensives and normotensives. In multivariate analyses either involving the entire population or restricted to CKD patients, GFR was independently and strongly related to carotid diameter and elastic modulus. Arterial enlargement and increased arterial stiffness occur in parallel with the decline in renal function in patients with mild-to-moderate CKD.

Adult↗

PubMedDate not supplied

[Left ventricular hypertrophy in chronic kidney disease].

Chronic kidney disease (CKD) is associated with increased cardiovascular (CV) risk. Left ventricular (LV) hypertrophy (LVH), together with coronary artery disease, has been considered the main target of intervention. LVH is highly prevalent in CKD even in early stages, as compared to general non-selected population. This is mainly due to the multifactorial pathogenesis of LVH in renal patients where both haemodynamic and non-haemodynamic stimuli synergically act inducing either an increase in left ventricular mass or an LV dilation. Anaemia and arterial hypertension seem to be the most important factors. Interventional studies have shown that partial correction of anaemia through epoetin, together with an arterial hypertension successful therapy through renin-angiotensin system acting drugs, such as ACE-inhibitors, were able to induce a LVH regression in CKD. Indeed, the unfavourable outcome in patients with both CKD and LVH, whose survival is reduced and incidence of fatal and non-fatal CV events increased, can be reversed if LVH is regressed by therapy. The most promising strategy in CKD seems to be LVH early diagnosis through echocardiography, the correct screening of risk factors, a LVM longitudinal monitoring through echo, as well as starting treatment in the early stages of CKD, with the aim of improving general and CV prognosis for these patients.

Anemia↗