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 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with chronic kidney disease have a higher burden of cardiovascular disease, which increases in a dose-dependent fashion with worsening kidney function. Traditional cardiovascular risk factors, including advanced age, diabetes mellitus, hypertension and dyslipidemia, have an important role in the progression of cardiovascular disease in patients who have a reduced glomerular filtration rate, especially in those with mild-to-moderate kidney disease. In patients with severe kidney disease, nontraditional or 'novel' risk factors, including inflammation, oxidative stress, vascular calcification, a prothrombotic milieu, and anemia, seem to confer additional risk. In this Review, we highlight factors that increase cardiovascular risk in patients with a reduced estimated glomerular filtration rate. In addition, we discuss therapeutic strategies for reducing cardiovascular risk in patients with kidney disease, whose unique atherosclerotic phenotype might require an approach that differs from traditional models developed in populations with normal kidney function. Therapeutic paradigms for patients with chronic kidney disease and cardiovascular risk factors must be evaluated in randomized trials, from which such patients have often been excluded.
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PMID:Cardiovascular risk factors in patients with chronic kidney disease. 1962 Oct 12

There is an ongoing trend of a rapid increment in the frequency of diabetes mellitus, expecially the non-insulin dependent form. By the end of the 2nd millenium 150 million cases were recorded worldwide, while the estimations predicted doubling the number by the year 2030. Numerous chronic complications accompany the disease, among them micro-, as well as macrovascular prevail, affecting small and large blood vessels. This paper provides a literature review on the topic of diabetic nephropathy, the main microvascular complication of diabetic disease. Microalbuminuria is the earliest sign of the diabetic renal involvement, with more than 30 mg and less than 300 mg of albumins in 24 h urine sample. The reduction of renal function begins with albuminuria leaving microalbuminuria level and entering the pathologic proteinuria range. Renal failure advances through the 5 stages, the final fifth occurring fortunately only in a minor proportion of the patients. The final stage ensues in 232 of 100 000 diabetic patients, according to the US data. However, in many developed countries there are 30-40% of new patients entering chronic dialysis treatment for diabetic nephropathy. Pathogenesis of diabetic nephropathy is based on hyperglycemia and distinct hemodynamic changes, glomerular hyperfiltration and high intraglomerular pressure. The important role have oxidative stress, advanced glycation end products, some cytokines, growth factors and sorbitol pathway. Nevertheless, genetic influence is considered by far the most important risk factor for diabetic nephropathy. Heritage determines the susceptibility in one and the protection in another diabetic patient. At the moment of pathologic proteinuria occurrence, glomerular filtration rate begins to decline for 1.2 ml/min/monthly in some patients, making the annual reduction of 7-14 ml/min/1.73 m2 of body surface area. Improving glycemia, blood pressure control, renal anemia correction with rHu-Epo, dyslipidemia control, reduction in protein intake, i.e. management of the nongenetic factors, could slower the renal function loss in some of the patients. Hence, these measures could reduce the proportion of the patients reaching end-stage renal disease, having in mind that morphological and functional changes are reversible only within certain limits. Therefore, the success of kidney protection is better if commenced earlier.
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PMID:[Diabetic nephropathy and prevention of diabetic nephropathy caused chronic renal insufficiency]. 1976 85

Energy and protein metabolism are both altered in chronic kidney disease (CKD) from its early stages. Patients undergoing peritoneal dialysis (PD) use peritoneal solutions with glucose as osmotic agent, which exposes them to an increased glucose load (40-80 g/day) and during PD there is a net loss of proteins through the peritoneum (4-8 g/day). Insulin resistance may lead to a reduction of the anabolic effects of insulin, while its proliferative effects on adipose tissue are potentially enhanced. Insulin resistance is also an important factor in the development of hypertriglyceridemia in PD patients: it increases free fatty acid availability, which then stimulates the release of large triglyceride-rich VLDL. Moreover, inhibitors of lipolytic enzymes (apoC-III, inflammation, oxidative modification and carbamoylation of apolipoproteins) may reduce lipid clearance, contributing to the development of dyslipidemia. Inflammatory molecules also play an important role in regulating glucose metabolism, and the excessive activation of inflammatory pathways may represent a fundamental step in the development of insulin resistance, including an over-expression of cytokines. Frequently, protein intake is reduced in PD because of under-dialysis, glucose load, abdominal discomfort and abnormal hormones levels, leading to a complex "protein-energy malnutrition". Optimization of dialysis dose, correction of acidosis and anemia and nutritional counseling, together with "non-traditional" management strategies, such as the use of PD solutions without glucose, like icodextrin and amino acid based solutions, represent the best strategies to prevent and correct malnutrition in PD patients. The mainstay of therapy is a reduction of glucose-based PD solutions and a correct dietary prescription.
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PMID:Metabolic consequences of peritoneal dialysis treatment. 1985 52

The pathophysiological modifications underlying chronic renal failure seems to be dependent on the insufficiency degree, which will determine the moment to start therapy. As there is yet limited information about animal models of moderate chronic renal failure, we intended to perform a complete characterization of the hematological and cardio-renal alterations induced by partial nephrectomy. Blood samples from control and chronic renal failure rats were collected at 0, 3, 9, and 15 weeks in order to evaluate renal function, hematological parameters, iron metabolism, blood lipids, peripheral sympathetic nervous system, and inflammatory and redox status markers. BP, tissues trophy indexes, and kidney histomorphology were also assessed. Our data are consistent with a sustained moderate degree of chronic renal failure with a quickly compensated modest anaemia, though presenting iron metabolism disturbances. Despite the reasonable degree of functionality of the remnant kidney, as suggested by the anaemia correction and by the kidney hypertrophy and moderate lesions, several important cardiovascular modifications were developed. Our model presented hypertension, dyslipidemia, erythropoietic disturbances, sympathetic activation, and oxidative stress. This model might be a good tool to study the cellular/molecular mechanisms underlying moderate stages of chronic renal failure and to evaluate the therapeutic efficacy for prevention and treatment/correction of cardio-renal anaemia syndromes and complications in early stages.
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PMID:Characterization of a rat model of moderate chronic renal failure--focus on hematological, biochemical, and cardio-renal profiles. 1992 93

Anemia-related blood examinations are included in examinations for periodic health checkups at workplaces designated by the Industrial Safety and Health Law in Japan. The aim of this study was to determine whether there were regional differences in the prevalence of anemia in workers and, if so, to investigate possible reasons for the differences. Relationships between prevalence of anemia found by periodic health checkups and some common factors related to anemia in each prefecture of Japan were investigated by ecological regression analysis using Spearman's rank correlation coefficient. There were regional differences in the prevalence of anemia in the prefectures of Japan (5.2-11.7%), and high prevalence was observed in prefectures in the northeastern district, such as Iwate, Akita and Yamagata Prefectures, and in Fukui, Shimane and Nagasaki Prefectures. Prevalence of anemia in each prefecture was significantly correlated with the prevalence of hypertension, dyslipidemia, liver dysfunction, abnormality in ECG, hyperglycemia or glucosuria at health checkups in each prefecture. Prevalence of anemia in each prefecture was significantly correlated with the percentage of patients receiving therapy for anemia in each prefecture but not with the prevalence of myoma uteri, endometriosis uteri or mortality of uterus cancer in each prefecture. There was also no significant correlation of the prevalence of anemia with the prevalence of iron-deficiency anemia or dietary iron intake in each prefecture. The prevalence of anemia in each prefecture showed significant positive correlations with the ratio of female population to total population and the ratio of female workers to total workers in each prefecture; it also showed a significant negative correlation with the ratio of the number of large-sized workplaces (300 or more workers) to the number of workplaces with 50 or more workers in each prefecture. A considerable regional difference in the prevalence of anemia was found by periodic health checkups at workplaces, and we consider that this difference is not due to regional differences in the incidence of diseases causing genital bleeding in women but to regional differences in the ratio of female workers to total workers and the status of health control at the workplace, which depends on size of the workplace.
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PMID:[Regional differences in prevalence of anemia found by periodic health checkups at workplaces in Japan]. 1994 17

Specific laboratory tests and physical findings are available to the practicing clinician that should raise the suspicion of inflammation. Inflammation is related to specific clinical outcomes. Once identified, changes in clinical practice may affect the level of inflammation in individual and or groups of dialysis patients with the hope that these changes may in turn affect outcome in a positive manner. Standard clinical tests and observations associated with inflammation are hypoalbuminemia, erythropoietin resistance, decreased iron saturation accompanied by high ferritin, frailty, low serum creatinine, reduced total and LDL-cholesterol, and increased C reactive protein (CRP). Inflammation is strongly associated with loss of physical function, dyslipidemia (low LDL- and HDL-cholesterol, increased triglycerides), and anemia that is unresponsive to erythropoietin. Inflammation is associated with cardiovascular events, increased hospitalization, and death. Correctible causes of inflammation are tunneled dialysis catheters, arteriovenous grafts, catheter infection, periodontal disease, poor water quality, and dialyzer incompatibility. Obesity also is a source of cytokines but may be less amenable to treatment. Inflammation is multifactorial in dialysis patients. Some sources are recognizable and correctable, such as vascular access type, clinical infection, and water quality, and some are not. Inflammation is strongly associated with outcome.
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PMID:Biochemistry and biomarkers of inflamed patients: why look, what to assess. 1999 7

Chronic kidney disease (CKD) is a strong risk factor for cardiovascular events and death. Hypertension, dyslipidemia, anemia, vascular calcification, and secondary hyperparathyroidism have all been implicated in the pathogenesis of cardiovascular disease associated with CKD. Numerous trials have been performed assessing the effects of modifying these risk factors on cardiovascular events and on the progression to end-stage renal disease. Many guidelines have been issued. In this article we review the guidelines and the strength of evidence supporting them. Specifically, we discuss blood pressure goals for patients with CKD, the role of renin-angiotensin system blocking agents for blood pressure control and proteinuria reduction, and the evidence for treatment recommendations of dyslipidemia. We review the trials addressing risks and benefits of different hemoglobin targets for treatment of anemia with erythropoietin. The use of phosphate-binding drugs to prevent and treat secondary hyperparathyroidism is likely beneficial, but few data support the use of vitamin D compounds. Supplementation with sodium bicarbonate may be an inexpensive treatment to retard progression to end-stage renal disease. The article concludes with a discussion of the case vignette presented in the previous article.
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PMID:Management of chronic kidney disease: what is the evidence? 2013 75

Nephropathic subjects show an increased tendency to develop cardiovascular diseases, mainly as the consequence of several risk factors including increased oxidative stress, inflammation, physical inactivity, anemia, vascular calcification, and endothelial dysfunction. The alterations in lipid metabolism represent a relatively lesser important cause of genesis and progression of atherosclerosis. Unfortunately, in these patients the atherogenic potential of dyslipidemia may depend more on apolipoproteins than on lipid abnormalities, and may not always be recognized by measurement of plasma lipids alone. The aim of this review was therefore to analyze the main lipid alterations that can occur in nephropathic patients, as well as their causes and their effects on the cardiovascular system. The clinical evidence and recommendations for the use of lipid-regulating drugs in patients with chronic kidney disease, nephrotic syndrome, in patients undergoing hemo- and peritoneal dialysis and in transplanted patients was also reviewed. Moreover, we analyzed the link between dyslipidemia and kidney disease onset and progression and the role of statins in preventing it.
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PMID:Alterations of lipid metabolism in chronic nephropathies: mechanisms, diagnosis and treatment. 2035 96

Diabetic kidney disease (DKD) is the leading cause of end-stage renal disease (ESRD), and one of the most prevalent microvascular complications of both type 1 and type 2 diabetes. Additionally, risk of death is increased at all stages of DKD. As early as the microalbuminuric stage, the death rate approaches 20% per year. Therefore, management strategies should address reducing risk of mortality as well as progression to ESRD. DKD is associated with multiple co-morbidities including hypertension, dyslipidemia, cardiovascular disease, anemia, and bone and mineral metabolism disorders (BMD). Anemia and BMD often occur earlier in the course of DKD than with other forms of chronic kidney disease. Pharmacological and dietary management of hyperglycemia, hypertension, dyslipidemia, anemia, and BMD pose specific challenges in DKD. However, with heightened awareness of risks and a multifactorial management approach, the impact of DKD on micro- and macrovascular complications and death can be reduced.
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PMID:Management of the diabetic patient with advanced chronic kidney disease. 2037 53

Clinical observations revealed an increased prevalence of iron deficiency anemia without chronic bleeding in patients treated with serial low-density lipoprotein (LDL) apheresis. Since several different proteins are adsorbed by LDL apheresis beside pro-atherogenic lipoproteins, we examined the modification of the full blood count, plasma iron, vitamin B12, folic acid, and hemolysis by LDL apheresis. Nineteen patients (55 (50-59) years, 4 female, 15 male) undergoing chronic LDL apheresis due to mixed dyslipidemia (N = 17), homozygous familiar hypercholesterolemia (N = 1) or isolated elevated lipoprotein(a) (N = 1) were included in this study. They were treated with direct adsorption of lipoproteins (DALI; N = 6), heparin-induced LDL-precipitation (HELP; N = 7) or double filtration plasmapheresis (DFPP; N = 6). The patients' full blood count, iron metabolism (plasma iron, ferritin, transferrin, transferrin saturation), vitamins involved in erythropoiesis (vitamin B12 and folic acid), and markers of hemolysis (haptoglobin and free hemoglobin) were analyzed directly before and after LDL apheresis. A single LDL apheresis session significantly decreased the levels (reduction in the median [25(th)-75(th) percentiles] of: ferritin 9.8 [1.3-18] %; P = 0.004), transferrin (12.1 [10.0-15.96] %; P = 0.0005), and vitamin B12 (17.8 [16.2-20.8] %; P = 0.0005). Thereby, transferrin and vitamin B12 were decreased in all (N = 19) and ferritin in 74% (N = 14) of the patients. Twelve out of 19 patients (63.2%) had mild anemia despite iron administration in 14 out of 19 patients (73.7%). LDL apheresis had no significant influence on full blood count, plasma iron, transferrin saturation, folic acid, or hemolysis. Similar changes were observed in all LDL apheresis methods used. LDL apheresis significantly decreases ferritin, transferrin, and vitamin B12, suggesting an influence of serial LDL apheresis on erythropoiesis.
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PMID:Low-density lipoprotein apheresis decreases ferritin, transferrin and vitamin B12, which may cause anemia in serially treated patients. 2043 34


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