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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A pandemic of obesity is contributing importantly to the prevalence of the metabolic syndrome characterized by hypertension, insulin resistance, and hyperlipidemia. In turn, the metabolic syndrome is contributing to vascular disease and the accelerating epidemic of chronic renal failure. Currently, pharmacological approaches to attenuate obesity and its cardiovascular/renal sequelae are limited. The purpose of this study was to determine the effects of 2-hydroxyestradiol, a metabolite of 17beta-estradiol with minimal estrogenic activity, on the development of obesity, the metabolic syndrome, and heart, vascular, and renal dysfunction in obese ZSF1 rats, a well-characterized genetic model of obesity and the metabolic syndrome with concomitant heart, vascular, and kidney disease. ZSF1 rats were treated, beginning at 12 weeks of age, for 26 weeks with vehicle or 2-hydroxyestradiol (10 microg/kg/h). At baseline and after 24 weeks of treatment, animals were placed in metabolic cages, and food intake, water intake, urine output, and urinary excretion of proteins and glucose were determined. Next, in fasting animals, plasma cholesterol was measured, an oral glucose tolerance test was conducted, and total glycated hemoglobin levels were determined. At the end of the study, animals were anesthetized and instrumented for assessment of heart performance, renal hemodynamics, and mesenteric vascular reactivity. 2-Hydroxyestradiol attenuated the development of obesity and improved endothelial function, decreased nephropathy, decreased the severity of diabetes, lowered arterial blood pressure, and reduced plasma cholesterol. 2-Hydroxyestradiol may be an important lead for the development of safe and effect drugs to attenuate obesity and its metabolic, vascular, and renal sequelae.
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PMID:2-Hydroxyestradiol attenuates the development of obesity, the metabolic syndrome, and vascular and renal dysfunction in obese ZSF1 rats. 1171 85

Hyperlipidemia is a common occurance in patients with chronic renal failure (CRF) and has been the subject of many clinical and experimental studies. Despite this, the role of lipogenesis in the development of hyperlipidemia is still obscure. The present study is based on a rat model of CRF involving a two-stage subtotal nephrectomy. In this study, we measured the activity of fatty acid synthase (FAS). This is the rate-limiting enzyme of lipogenesis and is present in liver and white adipose tissue (WAT). Using isotopic methods, we also determined the rate of lipogenesis in vivo in liver and WAT. In both liver and WAT, the results of the analyses were similar. In the uremic rats, there was a tendency for the FAS activity to rise. However, the difference was not statistically significant. Furthermore, there was no increase in the rate of lipogenesis in vivo in either tissue. In summary, the results of our study confirm the thesis that lipogenesis does not play a role in the development of hypertriglyceridemia seen in an experimental CRF in rats.
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PMID:Lipogenesis in experimental chronic renal failure in rats. 1172 8

Ischemic renal disease (IRD) is a frequent cause of end-stage renal disease. Its prevalence is mainly known from autopsy or retrospective arteriographic studies. This prospective study was conducted in 115 subjects selected from 732 patients with advanced chronic renal failure (CRF). Only patients with clinical features suggestive of IRD were selected for this study. In addition to detailed clinical and laboratory evaluation, captopril renal scintigraphy was performed in selected cases. All subjects underwent renal arteriography and all were followed up for 18.4 +/- 11.4 months. Renovascular disease was seen in 15 patients and significant bilateral renal artery disease leading to IRD was observed in 13 (11.3%). Hence the prevalence of IRD in the advanced CRF patients was 1.7%. The majority of patients with IRD (8 [61%]) were above 46 years of age and there were more men than women (10:3). Atherosclerotic renovascular disease was the most common (10 [77%]), even though arthritis (1 [7.6%]), and fibromuscular dysplasia (2 [15.3%]) were also observed. Serum creatinine at time of presentation was significantly higher in patients with IRD (784 +/- 292, p = 0.043) compared to those who did not have IRD (359 +/- 126). Corrective procedures were performed in 5 patients. After treatment the improvement in serum creatinine in patients with IRD at 3 and 6 months (166 +/- 32 and 173 +/- 47, respectively) was significantly different (p < or = 0.05) compared to those who were not treated (610 +/- 194 and 645 +/- 220, respectively). Hyperlipidemia, coronary artery disease and peripheral vascular disease were more prevalent in patients who had IRD compared to those with renal failure. The incidence of diabetes mellitus were similar in both groups. This study denotes a lower prevalence of IRD in the advanced CRF population; they had more severe renal failure at presentation but specific corrective treatment delayed progression of renal disease significantly.
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PMID:Ischemic renal disease in Kuwait. 1186 39

The prevalance of hyperlipidemia in chronic renal failure (CRF) patients is higher than in general population. Secondary amyloidosis is a common cause of CRF in Turkey. In this study, 25 patients with CRF due to secondary renal amyloidosis (amyloid-CRF), 15 patients with CRF without amyloidosis-CRF and 17 healthy controls were studied for serum lipid parameters. The mean serum lipoprotein (a) [LP(a)] level in the patients with amyloid-CRF was significantly higher than in the controls (p < 0.01). The mean serum apolipoprotein B (Apo B), apolipoprotein E (Apo E) and triglyceride levels in the patients with amyloid-CRF were very significantly higher than in the controls (p < 0.001). The mean serum total cholesterol, low-density lipoprotein (LDL) levels in the patients with amyloid-CRF were higher than in the controls (p < 0.05). The mean serum apo AI levels in the patients with amyloid-CRF was very significantly lower than in the controls (p < 0.001). The mean serum high-density lipoprotein (HDL) in the patients with amyloid-CRF was lower than in the controls (p < 0.05). The mean serum Lp (a), Apo AI, Apo B and Apo E levels in the patients with amyloid-CRF were significantly higher than in the patients with CRF (p < 0.01). The mean serum total cholesterol, trigliserides, LDL and HDL levels in the patients with amyloid-CRF were higher than in the patients with CRF (p < 0.05). There was not any correlation with serum lipid parameters and serum albumin and urine protein levels (p > 0.05). Our study suggests that serum lipid parameters are abnormal and might be the risk factor of atherosclerotic vascular disease and contribute to renal disease progression in the patients with secondary renal amyloidosis and lipid abnormalities were different from CRF with various etiology, without amyloidosis.
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PMID:Lipoprotein abnormalities in patients with secondary renal amyloidosis. 1198 51

Kidney mesangial cells (MCs) and vascular smooth muscle cells (VSMCs) are closely related in terms of origin, microscopic anatomy, histochemistry, and contractility. This relationship suggests a similarity between kidney glomerular sclerosis and atherosclerosis. Vitamin E appears beneficial in the prevention and treatment of coronary disease and also inhibits the proliferation of VSMCs in vitro. We used vitamin E and probucol to treat glomerular sclerosis and MC-proliferative glomerulonephritis (GN) in two animal models of glomerular disease. Using rats, a remnant kidney model accelerated with hyperlipidemia was employed to reflect progressive glomerular sclerosis leading to chronic renal failure, and an anti-thymocyte serum treatment was used to model acute MC-proliferative GN. Supplemental dietary antioxidants suppress MC proliferation and glomerular sclerosis in models of glomerular disease in rats. These results suggest that treatment with antioxidants may be a promising intervention to prevent progression of kidney disease.
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PMID:Effects of antioxidants on kidney disease. 1204 53

One of the aims of transplantation is to restore the potential for a full life to individuals with ESRD. To obtain this strategies that allow better and longer allograft function and a reduction in adverse events that lead to premature death are required. To this end, the recommendations below showed reduce cardiovascular disease and help present and future transplant recipients live a full life. Focusing on traditional risk factors (hypertension, hyperlipidemia, discontinuation of smoking, and prevention and treatment of diabetes mellitus) in patients at risk and striving for the recommended targets will have the greatest clinical benefit. These strategies should begin in the pre-dialysis and dialysis phases in order to reduce the cumulative burden of disease. Failing this, early and hopefully pre-emptive transplantation should be the goal.
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PMID:Cardiovascular risk reduction in renal transplantation. Strategies for success. 1207 Apr 54

Cardiovascular, cerebrovascular and peripheral vascular development are the largest cause-specific reason for morbidity and mortality in end-stage renal disease (ESRD) patients. The high prevalence of cardio- and cerebrovascular death may be explained by multiple factors present in patients with progressive renal disease, including hypertension, hyperlipidemia, hyperhomocysteinemia, diabetes mellitus, and hyperparathyroidism. Experimental studies have provided in vivo and in vitro data to support the notion that lipid abnormalities contribute to glomerular and interstitial injury of the renal parenchyma. Hyperchlolesterolemia and increased low-density lipoprotein (LDL) cholesterol are prevalent in patients with the nephrotic syndrome. Plasma high-density lipoprotein (HDL) cholesterol is decreased, and reverse cholesterol transport is impaired in hemodialysis (HD) and pre-ESRD patients. Chronic renal failure patients treated with HD have an increased prevalence of intermediate-density lipoprotein (IDL), and lipoprotein(a). The findings in diabetic patients corresponded with those in nondiabetic patients with renal failure, but diabetic patients have higher apoliprotein C-III and apoliprotein E concentrations. Impaired lipid metabolism is common in patients receiving peritoneal dialysis (PD). In most ESRD patients treated with peritoneal dialysis hypercholesterolemia and hyperglyceridemia are found. Wide panels of therapeutic interventions aimed at correcting the lipid abnormalities that may develop in chronic renal patients as well as in ESRD patients are currently available. Although some novel pharmacological agents are remarkably effective in returning the lipid abnormalities to normal, there is still no convincing evidence based on long-term prospective studies, that would clearly demonstrate a significant reduction of cardiovascular morbidity and mortality of ESRD patients. The therapeutic approaches, which may be considered, include mainly dietary and life-style modifications, selective use of some technical components of dialysis systems, and the judicious prescriptions of lipid-lowering drugs.
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PMID:Lipid abnormalities in chronic renal failure, nephrotic syndrome and dialysis. 1239 21

Hypertriglyceridemia associated with chronic renal failure (CRF) and elevated plasma concentration of very-low-density lipoprotein (VLDL) are thought to be a consequence of the depressed lipoprotein lipase and hepatic lipase activities and impaired clearance of lipoproteins. However, there is some evidence that the lipoproteins overproduction might also contribute to hypertriglyceridemia in CRF. This study was performed to test the hypothesis that the increased rate of lipogenesis consequent to upregulation of fatty acid synthase (FAS), a key lipogenic enzyme, gene expression could contribute to overproduction of triacylglycerols and to hypertriglyceridemia in CRF. FAS activity, FAS protein mass (Western blot analysis), and FAS mRNA level (Northern blot analysis) in liver and epididymal white adipose tissue (WAT) were measured in male Wistar rats 6 weeks after subtotal (5 of 6) nephrectomy or sham operation. Moreover, the rate of lipogenesis in WAT was determined. The CRF group showed significant increase in FAS gene expression (measured as activity, mRNA, and protein abundance) in both liver and WAT. This was associated with the increase in the lipogenesis rate and with the increase in plasma triacylglycerol and VLDL concentrations. Our results suggest that not only decreased removal, but also an increase of triacylglycerol production could contribute, in part, to the CRF-associated hyperlipidemia. Upregulation of FAS gene expression, shown in this report for the first time, reveals another factor involved in disturbed lipid metabolism in CRF. It seems that elevated plasma insulin and cytokine concentration could play an important role in the mechanism responsible for the increased FAS gene expression in CRF.
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PMID:Upregulation of fatty acid synthase gene expression in experimental chronic renal failure. 1248 75

Atheromatous embolism is a systemic disease resulting from cholesterol crystal embolization in many organs, including the kidneys. To characterize atheroembolic renal disease (AERD), we retrospectively evaluated 11 patients with acute renal failure after vascular surgery, vascular radiology investigations, and anticoagulation at Miyazaki Medical College from 1994 to 2001. The diagnosis of cholesterol atheromatous embolism was confirmed by tissue examination or clinical grounds. The patients were all elderly men (average age of 66.8 years) with a history of hypertension (55%), diabetes mellitus (45%), hyperlipidemia (45%), and coronary artery disease (18%). Seven patients had livedo reticularis, and 4 had blood eosinophilia. Clinically, 7 patients were managed conservatively and 5 of them improved, whereas 4 patients required dialysis and developed chronic renal failure or died. The serum creatinine levels of the improved patients were significantly lower (1.28+/-0.3 mg/dl, p < 0.005) than the non-improved ones (7.70+/-3.6). The number of eosinophils was significantly higher in the improved patients (576+/-295 /ml, p < 0.05) than in the non-improved ones (208+/-206). However, no significant difference was observed in the levels of serum cholesterol and C-reactive protein among these patients. Since the population at risk for AERD is growing, we should recognize this disease as a cause of acute renal failure.
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PMID:Atheroembolic renal disease: clinical findings of 11 cases. 1256 May 89

Nephrotic syndrome is a clinical and laboratory syndrome caused by the increased permeability of the glomerular capillary wall for macromolecules. Nephrotic syndrome is a potentially life-threatening state and persistent nephrotic syndrome has a poor prognosis with a high risk of progression to end-stage renal failure and a high risk of cardiovascular complications due to severe hyperlipidemia. Pathogenesis of increased glomerular permeability in different glomerular diseases has not been fully elucidated. Recently, identification of the mutated genes for some podocyte proteins (nephrin, podocin, alpha-actinin-4) in rare familial forms of nephrotic syndrome shed has new light on the molecular mechanisms of glomerular permselectivity. Gradually it becomes apparent that sporadic mutations of podocyte proteins (e.g., podocin) may be present even in some patients with acquired nephrotic syndrome. Expression of other podocyte proteins may change during the course of experimental nephrotic syndrome, possibly as a response to podocyte damage resulting either in apoptosis or stimulation of proliferation and some form of repair, including glomerular sclerosis. Better understanding of these mechanisms could clearly also have therapeutic implications. Glomerular permeability factors are believed to play a role in some noninflammatory glomerular diseases, mainly minimal change disease and focal segmental glomerulosclerosis, but their molecular identification remains elusive, possibly due to the nonhomogeneous nature of the underlying diseases. As an example, focal segmental glomerulosclerosis possibly can be caused by the sporadic mutation of some genes for podocyte proteins, increased production of glomerular permeability factor (possibly by T lymphocytes), or the loss of inhibitors of glomerular permeability factors in nephrotic urine. Clearly the factors causing increased glomerular permeability and factors perpetuating glomerular sclerosis are not necessarily the same. Proteinuria does not seem to be only the consequence of glomerular damage, but it may possibly cause tubular damage and initiate interstitial fibrosis and thus contribute to the progression of chronic renal failure in proteinuric renal diseases. Recent insights into the mechanisms of tubular protein reabsorption may give new tools for preventing the progression of chronic renal disease. Cubilin inhibitors could potentially ameliorate tubular and interstitial damage in patients with heavy proteinuria refractory to treatment. Nephrotic hyperlipidemia is accompanied with increased risk of cardiovascular complications and should be treated in all patients with persistent nephrotic syndrome. The putative positive effect of hypolipidemic drugs (namely statins) on the cardiovascular risk and potentially also on the rate of progression of chronic renal failure remains to be demonstrated in prospective controlled studies. Recent progress in understanding podocyte biology in rare inherited glomerular diseases gives the chance to understand in the near future the molecular pathogenesis of increased glomerular permeability in the much more common acquired forms of nephrotic syndrome.
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PMID:Pathobiochemistry of nephrotic syndrome. 1261 8


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