Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recovery of the patients after transplantation of non-renal organs may be complicated by multi-faceted chronic renal failure (CKD) which is regarded as an independent risk factor of graft dysfunction and mortality. The occurrence of CKD in non-renal transplant recipients depends mainly on a type of transplanted organ, immunosuppressive protocol and pre-transplant kidney dysfunction. Several concomitant diseases including arterial hypertension, dyslipidemia, diabetes mellitus, hepatitis or perioperative renal injury may contribute to chronic kidney disease. Current data suggest that a problem of kidney insufficiency in non-renal organ transplant recipients may still be underscored. Clinicians ought be aware that renal dysfunction should be added to a list of major post-transplant complications.
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PMID:Chronic renal failure in non-renal organ transplant recipients. 1661 70

Dyslipidemia is one of the possible risk factors for advanced atherosclerosis in patients with chronic renal failure. Abnormal phospholipid metabolism may play an important role in the progression of atherosclerosis in patients with renal failure. The aim of this study was to determine specific characteristics of plasma and erythrocyte phospholipid content and fatty acid composition in 37 patients with chronic renal failure on hemodialysis (HD). The results were compared with the characteristics of healthy subjects. Briefly, plasma triglyceride (p < 0.001), total cholesterol (p < 0.05), and total phospholipids (p < 0.01) levels were significantly higher and HDL-cholesterol level significantly lower (p < 0.01) in HD patients. Plasma phosphatidylcholine and phosphatidylethanolamine concentration were significantly higher (p < 0.001) in HD patients. The plasma phospholipid fatty acids composition indicated significantly (p < 0.01) higher level of oleic (18:1 n-9) and lower levels of eicopentaenoic (20:5 n-3 EPA) and docosahexaenoic (22:6 n-3 DHA) acids (p < 0.05). However, in HD patients, the relative concentration of plasma phospholipid n-6 polyunsaturated fatty acid (PUFA) was significantly lower (p < 0.05). The fatty acid composition of erythrocyte phospholipid in HD patients was modified with EPA and DHA levels significantly lowered (p < 0.05). Our results demonstrate an abnormal phospholipid metabolism and deficiency of n-3 PUFA in plasma and erythrocyte phospholipids in hemodialyzed patients.
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PMID:Plasma and erythrocyte phospholipid fatty acids composition in Serbian hemodialyzed patients. 1670 92

Self blood pressure measurements (home BP) and/or ambulatory BP measurements are recommended in mild to moderate hypertension (140/90 - 179/109 mmHg) in order to confirm sustained hypertension and identify white coat and masked hypertension. The evaluation of target organ damages (TOD) has to be integrated in cardiovascular risk estimate and taken into account in the management of hypertensive patients. Beside echocardiography, there is a place for the screening of microalbuminuria in non diabetic hypertensive patients, but these investigations should not be performed systematically. Arterial stiffness evaluation and carotid intima-media thickness quantification are not yet recommended. Cardiovascular risk (CV risk) estimate plays a pivotal role in the therapeutic decision and strategy. The cardiovascular risk grade is based on [1] the list of cardiovascular risk factors (same list AFSSAPS recommendations on dyslipidemia), [2] the presence or absence of TOD and [3] cardiovascular complications: "low", "medium", and "high" CV risk. Lifestyle modifications are recommended in all hypertensive patients. Five antihypertensive drugs are recommended for first line therapy: beta-blockers, thiazide diuretics, ACEIs, ARA II and CCBs (and fixed low dose combinations with AFSSAPS agreement for first line). In order to initiate the treatment, Evidence-based therapy (according to clinical trials conducted in different clinical situations), certain comorbid conditions (compelling indications), efficacy and side-effects in a previous experience, and the cost are the determinants of the first choice. Most hypertensive patients require more than one agent to achieve target blood pressure and for second line therapy the recommended combinations are: betablockers-diuretics, ACEIs-diuretics, ARAII-diuretics, betablockers-CCBs (DHP), ACEIs-CCBs, ARA II-CCBs and CCBs-diuretics. The delay to establish a combination therapy depend on CV risk. The BP goals are those recommended by ESH-ESC 2003: BP<140/90 mmHg in all, BP<130/80 mmHg in diabetic patients and in patients with chronic renal failure. Beside lowering BP, the reduction in proteinuria <500 mg/24 h is a new goal in these high risk patients. These guidelines provide a tool for every day practice and applicability should be evaluated.
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PMID:[French as 2005-recommendations on the management of arterial hypertension]. 1740 53

Secondary dyslipidemias may develop as a result of other diseases or some major exogenous influences. The most common are secondary dyslipidemias due to the following diseases: poorly controlled diabetes mellitus, hypothyreosis, hyperfunction of suprarenal glands, cholestasis, chronic renal diseases (chronic renal failure, nephrotic syndrome), acute infectious diseases. A very common cause of secondary dyslipidemia is abuse of alcohol. Also some drugs may induce dyslipidemias: corticosteroids, immunosuppressive drugs, less frequently also thiazide diuretics and non-selective beta-blockers. Secondary dyslipidemia is physiologic during pregnancy. If causal treatment of secondary dyslipidemia is possible, hypolipidemic drugs are not indicated. The decision to initiate treatment with hypolipidemic drugs depends on the degree of risk of a fatal cardiovascular event rather than on the blood lipids level. When hypolipidemic treatment is indicated, the choice of the drug and its dose also depends on the type of the primary disease and its severity.
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PMID:[Secondary dyslipidemias and their treatment]. 1757 73

Accelerated cardiovascular disease is a frequent complication of renal disease. Chronic kidney disease promotes hypertension and dyslipidemia, which in turn can contribute to the progression of renal failure. Furthermore, diabetic nephropathy is the leading cause of renal failure in developed countries. Together, hypertension, dyslipidemia, and diabetes are major risk factors for the development of endothelial dysfunction and progression of atherosclerosis. Inflammatory mediators are often elevated and the renin-angiotensin system is frequently activated in chronic kidney disease, which likely contributes through enhanced production of reactive oxygen species to the accelerated atherosclerosis observed in chronic kidney disease. Promoters of calcification are increased and inhibitors of calcification are reduced, which favors metastatic vascular calcification, an important participant in vascular injury associated with end-stage renal disease. Accelerated atherosclerosis will then lead to increased prevalence of coronary artery disease, heart failure, stroke, and peripheral arterial disease. Consequently, subjects with chronic renal failure are exposed to increased morbidity and mortality as a result of cardiovascular events. Prevention and treatment of cardiovascular disease are major considerations in the management of individuals with chronic kidney disease.
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PMID:Chronic kidney disease: effects on the cardiovascular system. 1760 56

An abnormal lipid profile is very frequent in patients with kidney disease due to the well-known nephrotoxicity of lipids. During progression of chronic kidney disease, the excretion of triglycerides, LDL and proteins increases while the glomerular filtration rate declines. Blood lipoproteins and lipids are modulated depending on the type of treatment: hemodialysis, CAPD or renal transplant. We analyzed many studies on dyslipidemia in patients with kidney disease by comparing different therapies. The use of statins reduces protein excretion and hyperlipidemia as well as progression of chronic renal failure with a direct effect on mesangial cell proliferation. A decrease in total cholesterol and LDL occurs in hemodialysis patients, a decrease in LDL and an increase in HDL occur in CAPD patients, and a decrease in LDL and triglycerides is observed in renal transplant recipients; in the latter, graft survival increases without there being any relevant correlation with immunosuppressive treatment. In conclusion, we found that statins are useful to contrast the progression of chronic kidney disease and atherosclerosis in hemodialysis and CAPD patients and to reduce chronic allograft nephropathy in renal transplant recipients.
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PMID:[Dyslipidemia and the risk of kidney disease]. 1792 41

The transcription factor peroxisome proliferator-activated receptor (PPAR) alpha plays an important role in lipid homeostasis. In this study, we examined whether the down-regulation of PPAR-alpha gene expression is associated with dyslipidemia in a rat model of chronic renal failure (CRF). Rats with laboratory-induced uremia by 5/6 nephrectomy were bled at 2 weeks and 10 weeks after the nephrectomy to produce conditions. For the sake of convenience, the rats observed at postoperative week 2 were defined as acute renal failure (ARF) and those observed at week 10 were defined as CRF. Lipids in lipoprotein fractions were measured by high-performance liquid chromatography. The abundance of PPAR-alpha messenger RNA (mRNA) in the liver was measured by reverse transcriptase-polymerase chain reaction. Serum creatinine and blood urea nitrogen levels rose with the progression of renal failure, but the total protein levels remained constant. Serum triglyceride in ARF rats remained unchanged from the level in sham-operated control rats, whereas that in CRF rats was 66% higher than the control level. Serum cholesterol was elevated 1.5-fold in ARF rats and 2-fold in CRF rats compared with the sham-operated counterparts. As with triglyceride, very low-density lipoprotein remained unchanged in ARF rats but rose substantially in CRF rats. All of the major lipoprotein fractions were elevated in CRF rats. These lipid and lipoprotein changes were significantly associated with creatinine and blood urea nitrogen levels. The PPAR-alpha mRNA expression in the liver was unchanged in ARF rats but was 44% lower in CRF rats. The PPAR-alpha mRNA expression was inversely correlated with serum creatinine and lipids in the overall rats. Our results indicate that PPAR-alpha mRNA expression is down-regulated in the liver of CRF rats and that this down-regulation may play a crucial role in the development of dyslipidemia.
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PMID:Decreased peroxisome proliferator-activated receptor alpha gene expression is associated with dyslipidemia in a rat model of chronic renal failure. 1799 26

The receptor for advanced glycation end-products (RAGE) is involved in microvascular and macrovascular complications in diabetes. The expression of RAGE is up-regulated in atherosclerotic plaques of diabetic animals, and the augmentation of atherosclerosis in diabetic mice is inhibited by the competition of RAGE. An endogenous secretory RAGE (esRAGE) was identified as a novel splice variant carrying all of the extracellular domains, but devoid of the transmembrane and intracytoplasmic domains. The esRAGE is released from the cells, to bind advanced glycation end-products, and this is capable of neutralizing the actions of advanced glycation end-products on endothelial cells in culture. The adenoviral overexpression of esRAGE restores the impairment of vascular dysfunction in diabetes, suggesting that esRAGE may be an important inhibitor of RAGE signaling in vivo, and may be useful for the prevention of diabetic vascular complications. In 203 age-matched and sex-matched type 2 diabetic and 134 nondiabetic subjects, plasma esRAGE levels were inversely associated with carotid or femoral atherosclerosis. In patients with end-stage renal disease (ESRD), plasma esRAGE levels are higher than in those without ESRD. In a cohort of 206 patients (including 171 nondiabetic patients) with chronic renal failure who were followed for a median of 111 months, the cumulative incidence of cardiovascular death by Kaplan-Meier estimation was significantly higher in subjects in the lowest tertile of plasma esRAGE than in those in the middle or highest tertile. Compared with the lowest tertile of plasma esRAGE, the hazards ratios for the highest and middle tertile were 0.40 (95% confidence interval, 0.18 to 0.89) and 0.26 (95% confidence interval, 0.10 to 0.66), respectively. The higher risk at the lower level of esRAGE was still significant even after adjustment for body mass index, hypertension, dyslipidemia, and vascular complications, and was confounded only by age and diabetes. Thus, we postulate that plasma esRAGE is a potential protective factor and a novel biomarker against the occurrence of cardiovascular disease in ESRD.
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PMID:Endogenous secretory receptor for advanced glycation end-products and cardiovascular disease in end-stage renal disease. 1808 49

Dyslipidemia complicates renal function leading to disturbances of major homeostatic organs in the body. Here we examined the effect of chronic renal dysfunction induced by uninephrectomy on fat redistribution and lipid peroxidation in rats treated with an angiotensin-converting enzyme (ACE) inhibitor (lisinopril) for up to 10 months. Uninephrectomized rats developed fat redistribution and hypercholesterolemia typical of chronic renal failure when compared with sham-operated rats or lisinopril-treated uninephrectomized rats. The weight of the peri-renal fat was significantly less in the untreated compared to the lisinopril-treated uninephrectomized rats or those rats with a sham operation. We also found that there was a shift of heat-protecting unilocular adipocytes to heat-producing multilocular fat cells in the untreated uninephrectomized rats. Similarly in these rats we found a shift of subcutaneous and visceral fat to ectopic fat with excessive lipid accumulation and lipofuscin pigmentation. Lisinopril treatment prevented fat redistribution or transformation and lipid peroxidation. This study shows that ACE inhibition may prevent the fat anomalies associated with chronic renal dysfunction.
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PMID:Fat redistribution and adipocyte transformation in uninephrectomized rats. 1914 58

Acute and especially chronic renal failure (CRF) are relatively common and important risk factor for morbidity and mortality in patients after heart, lung, liver or intestine transplantation. Numerous factors contribute to the development of CRF in this group of patients, like treatment with calcineurin inhibitors and other nephrotoxic drugs in the perioperative period, hemodynamical changes during and after the surgery, preexistent renal disease, hypertension, diabetes mellitus, dyslipidemia and anemia. Pretransplant evaluation of renal function is mandatory to predict which patients have increased risk for development of CRF. In the posttransplantation course it is necessary to timely diagnose and treat renal failure, while patients with insufficient renal function have 4.55-fold increased risk of death compared to patients with normal renal function. Special problem is diagnostic approach to patients with suspected chronic renal disease who are candidates for transplantation of other parenhimatose organs. Diagnostic value of serum creatinine and estimation of renal function based on its value is very limited. Gold diagnostic standard is radioisotope estimation of glomerular filtration, but this method is not widely available. It seems that this problem may be solved with the use of cystatin C, but this approach needs to be validated in large studies. Numerous different immunosuppressive drugs available on the market enable individualization of immunosuppression. Different drugs combinations may have less nephrotoxic potential, but one must be careful because of the possible risk of organ rejection with the change of immunosuppression. Use of angiotensin convertase enzyme inhibitors and/or angiotensin receptor blockers, statins with drugs for control of hyperglycemia, may prevent or postpone development of CRF. Although technical advances of contemporary hemodialysis machines and peritoneal dialysis equipment enable well tolerated dialysis even in critically ill patients, renal transplantation remains the method of choice for treatment of patients with transplanted parenhimatous organ that developed CRF.
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PMID:[Chronic renal failure after heart, lung, liver, or intestine transplantation]. 1857 34


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