Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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

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

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

A 54-year-old man was found to have hypertension at age 32, and a diagnosis of Werner's Syndrome was made at age 36 when he was examined for hyperlipidemia. Diabetes mellitus was found at age 42. Proteinuria appeared at age 49, and microscopic hematuria was seen at age 50. At age 51, serum creatinin level began to rise and atrophy of bilateral kidneys was observed by abdominal CT. There after, the renal function gradually worsened. At age 53, the serum creatinin level rose to 8.3 mg/dl, and systemic edema as well as loss of appetite appeared, resulting in the initiation of hemodialysis. In Werner's syndrome, though arteriosclerosis arises frequently, case reports with chronic renal failure are extremely rare. To investigate the cause of the renal dysfunction, renal biopsy was performed and the samples were histologically examined, revealing the presence of hypertensive glomerular changes. It is, thus, conceivable that hypertension had played a major role in the progression of renal failure in this case.
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PMID:[A report of a case with Werner's syndrome suffering from end-stage renal failure]. 1282 81

Control of ventricular rate by atrioventricular node ablation and pacemaker implantation in patients with drug-refractory atrial fibrillation (AF) is associated with improved left ventricular (LV) function. The objective of this study was to determine the effect of atrioventricular node ablation on long-term survival in patients with AF and LV dysfunction. Survival was determined by the Kaplan-Meier method for 56 study patients with LV ejection fraction (EF) < or =40% who underwent atrioventricular node ablation and pacemaker implantation and 56 age- and gender-matched control patients with AF and LVEF >40%, and age- and gender-matched control subjects from Minnesota. Groups were compared using the log-rank test. In study patients (age 69 +/- 10 years; 45 men), LVEF was 26% +/- 8% and 34% +/- 13% (p <0.001) before and after ablation, respectively. During follow-up (40 +/- 23 months), 23 patients died. Observed survival was worse than that of normal subjects (p <0.001) and control patients (p = 0.005). After ablation, LVEF nearly normalized (> or =45%) in 16 study patients (29%), in whom observed survival was comparable to that of normal subjects (p = 0.37). Coronary artery disease, hyperlipidemia, chronic renal failure, previous myocardial infarction, and coronary artery operation were independent predictors for mortality. Near normalization of LVEF occurred in 29% of study patients, suggesting that AF-induced EF reduction is reversible in many patients. Normal survival in patients with reversible LV dysfunction highlights potential survival benefits of rate control. Poor survival in patients with persistent LV dysfunction confirms the importance of optimal medical therapy.
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PMID:Significant effects of atrioventricular node ablation and pacemaker implantation on left ventricular function and long-term survival in patients with atrial fibrillation and left ventricular dysfunction. 1284 41

Hyperlipidemia is a common problem in solid organ transplant recipients. In this study we evaluated the role of pre-transplant renal replacement therapy on early and late changes of serum lipid levels in children following renal transplantation. In 46 children with chronic renal failure (median age 10.3 years) and 12 children with heart failure (median age 5.0 years), cholesterol and triglycerides were measured before and during follow-up after transplantation. Children with renal failure had significantly higher serum lipids than controls ( n=34, median age 9.2 years) and patients with heart failure. Pre transplantation, cholesterol and triglycerides were significantly lower in the hemodialysis than in the peritoneal dialysis population, whereas conservatively treated children had intermediate levels. After transplantation, serum cholesterol converged towards a mean level of 208 mg/dl and triglyceride levels converged towards a uniform level of 195 mg/dl at 9 months post transplant. The ratio of cholesterol/high-density lipoprotein significantly decreased from 4.7 to 3.8. The pattern of "post-transplant hyperlipidemia" was similar in both renal and cardiac allograft recipients. Hence, the early post-transplant changes of serum lipid pattern are markedly dependent on the mode of pre-transplant renal replacement therapy. Later, serum lipid levels were no longer influenced by prior renal replacement therapy and showed a new pattern of "post-transplant hyperlipidemia" in all children.
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PMID:Serum lipid pattern unifies following renal transplantation in children. 1288 78

Vascular events caused by arteriosclerosis are the major cause of death in patients under hemodialysis (HD). Arteriosclerosis is associated with lipoprotein abnormalities such as increased serum levels of low-density lipoprotein (LDL), especially of modified LDL (M-LDL) and oxidized LDL (Ox-LDL). We examined the relationship between markers of arteriosclerosis, hemostasis, and lipid metabolism in patients with chronic renal failure, hyperlipidemia, and healthy volunteers. In patients under HD, the serum levels of total cholesterol, LDL, and triglyceride (TG) were decreased, but the serum levels of M-LDL were increased compared to HL and healthy volunteers. In patients with CRF, the serum levels of Ox-LDL in patients under HD were lower than in those under continuous ambulatory peritoneal dialysis or conservative therapy. The plasma levels of antithrombin and protein C were significantly lower and the plasma levels of thrombomodulin were significantly higher in patients under HD compared to those under conservative therapy. These data show that patients under HD were more in hypercoagulable state than those under conservative therapy. Among patients under HD, only the plasma levels of von Willebrand factor were significantly increased in patients with more than 30 U/L of Ox-LDL compared to those with less than 30 U/L of Ox-LDL. There was no significant difference in the tests of arteriosclerosis among M-LDL values and Ox-LDL values. These findings suggest that abnormalities of lipid are not the main risk factor for arteriosclerosis disease in patients under HD.
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PMID:Effects of lipid abnormalities on arteriosclerosis and hemostatic markers in patients under hemodialysis. 1450 8

A serum lipoprotein(a) (Lp(a)) is an independent risk factor for cardiac events. It is well known that the patients with chronic renal failure (CRF) have a high concentration of serum Lp(a). The purpose of this study was to indicate the relationship between serum Lp(a) concentration and apoprotein(a) (apo(a)) isoforms under the condition of renal dysfunction. One-hundred thirty patients having hypertension, hyperlipidemia, diabetes mellitus and/or CRF were selected in this study. All patients were divided into two groups according to the level of serum creatinine. Serum Lp(a) concentration in the CRF patients (Cr > 2.0 mg/dl) was significantly higher than that in the controls (Cr < 1.2 mg/dl). Many CRF patients had high molecular weight (HMW)-apo(a). This study showed that the increase in HMW-apo(a) was closely accompanied by the increase in serum creatinine levels, and the serum Lp(a) concentration with HMW-apo(a) was higher according to their creatinine levels.
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PMID:Serum lipoprotein(a) concentration and Apo(a) isoform under the condition of renal dysfunction. 1471 45


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