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 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Optimization of the management of chronic renal failure (CRF) is aimed at decreasing morbidity and mortality risks of CRF patients, due to the progression of CRF toward end-stage renal disease (ESRD), and to CRF-related complications with functional or life-threatening consequences. The so-called spontaneous progression of CRF toward ESRD depends on factors related to the primary renal disease, and on non-specific factors mainly related to hypertension and renal functional adaptations to nephron loss. Secondary prevention of CRF needs: early identification of primary renal disease, in order to start specific therapies; the treatment of hypertension; dietary advice on protein intake; prevention of events and drug toxicity potentially harmful to renal function. Clinical events appear late in the course of CRF, following several disorders often present for a long time: hypertension, dyslipidemia, phosphocalcic disorders, anaemia, malnutrition). These disorders should be screened for, and treated, as a part of tertiary prevention measures. When dialysis becomes unavoidable, early information and medical preparation of the patient are mandatory, giving the best chances of success to the applied dialysis method. Unfortunately, most CRF patients are referred at a late stage of the disease, when the effects of therapeutic interventions are limited; this results in increased length of hospital stays, increased risk of early dialysis complications, and decreased capacity to be treated at home.
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PMID:[How do we optimize the management of chronic renal failure?]. 1180 90

Premature atherosclerosis is a major cause of morbidity and mortality in end-stage renal disease patients. Dyslipidemia and increased oxidative stress contribute to premature atherogenesis in these patients. The dyslipidemia of end-stage renal disease consists of both quantitative and qualitative abnormalities in serum lipoproteins. Qualitative changes include hypertriglyceridemia (increased remnant lipoproteins), low high-density lipoprotein-cholesterol, and increased lipoprotein (a). In addition to quantitative changes, lipoproteins in end-stage renal disease undergo compositional and qualitative changes that make them pro-atherogenic, such as various modifications of apolipoprotein B, including oxidation, and modification by advanced glycation end-products. The 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors and low-dose fibrates could be effective therapies for lipid disorders. The best evidence for increased oxidative stress in end-stage renal disease is the demonstration of increased plasma F2-isoprostanes. Confirmation of the positive findings with high-dose alpha-tocopherol in the Secondary Prevention with Antioxidants of Cardiovascular Disease in End-stage Renal Disease Study is urgently needed. Clinical trials with statins and other drugs that improve dyslipidemia also need to be undertaken. These therapies could clearly lead to a reduction in cardiovascular morbidity and mortality in these patients.
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PMID:Accelerated atherosclerosis, dyslipidemia, and oxidative stress in end-stage renal disease. 1185 5

Dyslipidemias are common in patients with chronic kidney disease. The causes vary with the stage of kidney disease, the degree of proteinuria, and the modality of end-stage renal disease treatment. Dyslipidemias have been associated with kidney disease progression, and a number of small, randomized, controlled trials of lipid-lowering agents have been conducted. Unfortunately, the results of these trials, although encouraging, have been inconclusive because of the small numbers of patients enrolled. Dyslipidemias may also contribute to the high incidence of cardiovascular disease in patients with chronic kidney disease. This is most likely for patients with chronic renal insufficiency and for kidney transplant recipients. Less certain is the role of dyslipidemias in the pathogenesis of cardiovascular disease among dialysis patients.
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PMID:Hyperlipidemia in kidney disease: causes and consequences. 1198 Dec 63

Dyslipidemia increases the risk of cardiovascular events among individuals with renal disease, and there is a growing body of evidence that it hastens the progression of renal disease itself. Children with nephrotic syndrome or renal transplants have easily recognized hyperlipidemia. Among those with chronic renal insufficiency or end-stage renal disease, detection of dyslipidemia requires more careful analysis and knowledge of normal pediatric ranges. Disordered lipoprotein metabolism results from complex interactions among many factors, including the primary disease process, use of medications such as corticosteroids, the presence of malnutrition or obesity, and diet. The systematic treatment of dyslipidemia in children with chronic renal disease is controversial because conclusive data regarding the risks and benefits are lacking. Hepatic 3-methylglutaryl coenzyme A reductase inhibitors (statins), fibrates, plant stanols, bile acid-binding resins, and dietary manipulation are options for individualized treatment. Prospective investigations are required to guide clinical management.
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PMID:Dyslipidemia in pediatric renal disease: epidemiology, pathophysiology, and management. 1198 Dec 90

Insulin resistance is closely associated with atherosclerosis and cardiovascular mortality in the general population. Patients with end-stage renal disease (ESRD) are known to have insulin resistance, advanced atherosclerosis, and a high cardiovascular mortality rate. We evaluated whether insulin resistance is a predictor of cardiovascular death in a cohort of ESRD. A prospective observational cohort study was performed in 183 nondiabetic patients with ESRD treated with maintenance hemodialysis. Insulin resistance was evaluated by the homeostasis model assessment method (HOMA-IR) using fasting glucose and insulin levels at baseline, and the cohort was followed for a mean period of 67 mo. Forty-nine deaths were recorded, including 22 cardiovascular deaths. Cumulative incidence of cardiovascular death by Kaplan-Meier estimation was significantly different between subjects in the top tertile of HOMA-IR (1.40 to 4.59) and those in the lower tertiles of HOMA-IR (0.28 to 1.39), and the hazard ratio (HR) was 2.60 (95% confidence interval [CI], 1.12 to 6.01; P = 0.026) in the univariate Cox proportional hazards model. In multivariate Cox models, the positive association between HOMA-IR and cardiovascular mortality remained significant (HR, 4.60; 95% CI, 1.83 to 11.55; P = 0.001) and independent of age, C-reactive protein, and presence of preexisting vascular complications. Further analyses showed that the effect of HOMA-IR on cardiovascular mortality was independent of body mass index, hypertension, and dyslipidemia. In contrast, HOMA-IR did not show such a significant association with noncardiovascular mortality. These results indicate that insulin resistance is an independent predictor of cardiovascular mortality in ESRD.
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PMID:Insulin resistance as an independent predictor of cardiovascular mortality in patients with end-stage renal disease. 1208 86

To choose the best possible dialysis technique for those patients with end-stage renal disease continues to be a matter of debate. Even after putting aside the evident influence that economic and geographic factors as well as the health politics may have in the selection of the technique, different studies comparing survival between hemodialysis (HD) and peritoneal dialysis (PD) have shown contradictory results which could be explained by the differing methodological and statistical methods used together with the different influence assigned to the comorbidity found when starting the treatment, a situation that has increased the confusion about this topic. Based on this we performed a retrospective analysis with a follow-up time of seven years including all those patients who started dialytic treatment in our area, with a final number of 3.106 hemodialysis patients and 542 peritoneal dialysis patients. Those patients who were transferred to another treatment technique during the time of the study were excluded. Age higher than 70 years, cardiovascular disease, liver disease, diabetes mellitus and the presence of dyslipidemia were included as comorbidity factors. Peritoneal dialysis patients were younger than those treated by hemodialysis (54.53 vs 60.1 years), but suffered from higher cardiovascular comorbidity and were more often diabetic. The global survival was the same in both groups up to 32 months of treatment. Although no differences were found when comparing those patients without comorbidity factors, those with comorbidity had better survival on hemodialysis. Age higher than 70 years was the only comorbidity factor with statistically significant difference for a better survival in hemodialysis.
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PMID:[Analysis of survival in dialysis: hemodialysis versus peritoneal dialysis and the significance of comorbidity]. 1212 25

This review covers lipids, apolipoproteins, and receptors involved in the dyslipidemia of the nephrotic syndrome in humans and in rat or mouse models of the syndrome. It emphasizes research published during the last decade, though earlier work is cited. The focus is on the biosynthesis and catabolism of the plasma lipoprotein density classes and the role of receptors and enzymes in regulating lipoprotein metabolism in nephrosis. Although the factors responsible for the initiation of the hepatic and peripheral cellular responses to proteinuria and hypoalbuminemia remain elusive, recent work highlights the increased risk of atherosclerosis and the progression of renal disease associated with nephrotic dyslipidemia. Understanding of the role of the kidney in the catabolism of apolipoproteins entering the glomerular filtrate has been enhanced by the discovery of the receptor-mediated uptake of apolipoprotein A-I, the main apoprotein of HDL. The following aspects of lipid and lipoprotein metabolism in relation to nephrosis are discussed, with attention paid to differences between experimental nephrosis and the human nephrotic syndrome:(1) Albumin metabolism (2) Lipoprotein metabolism (3) Receptors (4) LCAT and CETP (5) Hepatic and Lipoprotein Lipase (6) Lipid metabolism (7) Lipiduria (8) Hypotheses and Questions (9) Summary.
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PMID:Lipoprotein metabolism in the nephrotic syndrome. 1213 20

Uremic patients suffer from a secondary form of complex dyslipidemia consisting of quantitative and qualitative abnormalities in serum lipoproteins resulting in altered lipoprotein composition and metabolism. The most prominent are an increase in serum triglyceride levels (due to elevated very-low-density lipoprotein remnants and intermediate-density lipoprotein) and low high-density lipoprotein (HDL) cholesterol. Low-density lipoprotein (LDL) cholesterol is often normal, but the cholesterol may originate from the atherogenic small and dense LDL subclass. The apolipoprotein B-containing part of the lipoprotein may undergo modifications (peptide modification of the enzymatic and advanced glycation end-product, oxidation or glycosylation). Modifications contribute to impaired LDL receptor-mediated clearance from plasma and promote prolonged circulation. HDL particles are structurally altered during states of inflammation. The contribution of this complex and atherogenic form of dyslipidemia to cardiovascular disease in patients with renal disease is at present unclear. Most studies are negative in demonstrating the predictive power of serum lipids for the development of cardiovascular disease. This is most likely due to interference with deteriorating aspects of the activated acute-phase response. Since it is also still unclear whether we have therapeutics available with a sufficient impact on LDL size, remnant lipoprotein lowering and restoration of HDL function, we urgently need specific intervention trials.
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PMID:Uremia-specific alterations in lipid metabolism. 1220 90

Diabetes is a major health problem in the United States. There is a long history of diabetic registries and databases with systematically collected patient information. We examine one such diabetic data warehouse, showing a method of applying data mining techniques, and some of the data issues, analysis problems, and results. The diabetic data warehouse is from a large integrated health care system in the New Orleans area with 30,383 diabetic patients. Methods for translating a complex relational database with time series and sequencing information to a flat file suitable for data mining are challenging. We discuss two variables in detail, a comorbidity index and the HgbA1c, a measure of glycemic control related to outcomes. We used the classification tree approach in Classification and Regression Trees (CART) with a binary target variable of HgbA1c >9.5 and 10 predictors: age, sex, emergency department visits, office visits, comorbidity index, dyslipidemia, hypertension, cardiovascular disease, retinopathy, end-stage renal disease. Unexpectedly, the most important variable associated with bad glycemic control is younger age, not the comorbiditity index or whether patients have related diseases. If we want to target diabetics with bad HgbA1c values, the odds of finding them is 3.2 times as high in those <65 years of age than those older. Data mining can discover novel associations that are useful to clinicians and administrators [corrected].
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PMID:Data mining a diabetic data warehouse. 1223 16

Obesity is the most common nutritional disorder in the United States. Growing evidence suggests that obesity initiates a cascade of disorders including hypertension, diabetes, atherosclerosis, and chronic renal disease, many of which are interdependent. Abnormal kidney function, caused by increased renal tubular reabsorption, initiates volume expansion and increased blood pressure during excess weight gain, and the hypertension and metabolic abnormalities associated with obesity, in turn, contribute to chronic renal disease. Obesity causes cardiac and vascular disease through well-known mediators such as hypertension, type II diabetes, and dyslipidemia, but there is evidence for less well-characterized mediators such as chronic inflammation and hypercoagulation. Although obesity is increasingly recognized as a serious health problem, there are still many unanswered questions about how the multiple disorders associated with excess weight gain interact to cause cardiovascular and renal disease. Also, there are few studies that have examined whether sustained weight loss in obese subjects can reverse these changes. In view of the "epidemic" of obesity in our country and the excess burden of cardiovascular and renal disease in minority populations, addressing these issues is of paramount importance for the Jackson Heart Study, as well as for other national health initiatives.
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PMID:Mechanisms of obesity-associated cardiovascular and renal disease. 1224 Jul 10


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