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:C0242339 (dyslipidemia)
13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

We examined the incidence of renal function deterioration (RFD) in a population of male gout patients and to identify associated risk factors. Subjects who had been regularly followed up for more than 2 years and had visited Chang Gung Memorial Hospital-Kaohsiung Medical Center Rheumatology Clinic between June 1, 2006 and January 31, 2007 were enrolled. Four subjects were excluded as secondary gout was suspected. Group I (Gr I) comprised subjects without RFD and group II (Gr II) comprised subjects with RFD during the follow-up period. RFD was defined as absolute increment in creatinine (Cr) levels over 0.4 mg/dl for subjects with baseline Cr levels <or=1.4 mg/dl or as more than 50% increment of baseline Cr level per 12-month interval in average for subjects with baseline Cr levels >1.4 mg/dl. Clinical parameters were analyzed to study the potential risk factors of RFD. Of 318 male gout patients, 296 (93.1%) were categorized as Gr I, and 22 (6.9%) were categorized as Gr II. The observation periods for Gr I and Gr II were 81.20+/-53.29 and 92.41+/-46.72 months, respectively (p=0.338). Initial Cr levels are similar between the two groups (1.25+/-0.51 vs 1.25+/-0.61, p=0.963). Multiple logistic regression analysis revealed that current age, age at disease onset, disease duration, treatment duration, body weight, height, family history of gout, tophi, urolithiasis, tobacco use, alcohol consumption, history of cerebral vascular accident, hypertension, diabetes mellitus, dyslipidemia, base-line and final Cr, blood urea nitrogen level, serum uric acid level, and body-mass index were not independent risk factors. However, history of ischemic heart disease [IHD; odds ratio (OR) 7.68, 95% confidence interval (CI) 1.99-29.70] and greater waist circumference (WC; OR 1.06, 95% CI 1.01-1.11) were two independent risk factors of RFD. Additionally, the Cox multivariable analysis disclosed that IHD (p<0.001) and greater WC (p=0.011) deteriorated kidney function in these patients. The incidence of RFD in male gout patients is 6.9%. History of IHD and greater WC are two independent risk factors for developing RFD.
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PMID:Ischemia heart disease and greater waist circumference are risk factors of renal function deterioration in male gout patients. 1803 May 16

Hyperlipidemia has been well recognized as a striking feature of nephrotic syndrome and other renal diseases. However, the underlying pathophysiological mechanisms still have not yet been elucidated. In this study, we evaluated acylation-stimulating protein (ASP) and complement component 3 (C3) in children (n=48) with various forms of proteinuric renal disease [nephrotic syndrome, acute poststreptococcal infection glomerulonephritis (APSGN), and lupus nephritis (LN)] in comparison with age- and gender-matched controls (n=279). In children with proteinuric renal disease, various aberrations in plasma lipids were noted, including increased triglyceride, cholesterol, and low-density lipoprotein cholesterol (LDL-C) (all p<0.0001). Whereas C3 was not altered in children with nephrotic syndrome (1.05+/-0.05 g/L vs. 1.29+/-0.04 controls), the decrease was pronounced in children with LN and APSGN (0.42+/-0.11, p<0.05 and 0.30+/-0.06, p<0.001, respectively). Plasma C3 correlated positively with lipid parameters [triglyceride, cholesterol, LDL-C, apolipoprotein B (apoB), high-density lipoprotein cholesterol (HDL-C) and apoA1] and inversely with total protein, blood urea nitrogen, and creatinine. By contrast, plasma ASP was significantly elevated in all proteinuric renal diseases (101.4+/-7.1 nmol/L nephrotic syndrome, 90.9+/-14.1 LN, and 81.8+/-7.2 APSGN vs. 44.3+/-1.5 controls, p<0.05 to p<0.001), and this increase was correlated with changes in lipid parameters (triglycerides and apoA1). In summary, these results demonstrate alterations in C3 and ASP that may contribute to or compensate for dyslipidemia.
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PMID:Increased plasma acylation-stimulating protein in pediatric proteinuric renal disease. 1825 59

Hydroxymethylglutaryl coenzyme A reductase inhibitors (statins) decrease serum cholesterol. Dyslipidemia is believed to be associated with the development of renal dysfunction. It was postulated that statins may reduce the development of renal dysfunction. The effect of statin use on the development of renal dysfunction in 197,551 patients (Department of Veterans Affairs, Veterans Integrated Service Network 16 [VISN16] database) was examined. Of these patients, 29.5% (58,332 patients) were statin users and 70.5% (139,219 patients) were not. Development of renal dysfunction was defined as doubling of baseline creatinine or increase in serum creatinine > or =0.5 mg/dl from the first to last measurement with a minimum of 90 days in between. During 3.1 years of follow-up, 3.4% of patients developed renal dysfunction. After adjustment for demographics, diabetes mellitus, smoking, hypertension, and other medications (mainly angiotensin-converting enzyme inhibitors, calcium channel blockers, and aspirin), use of statins decreased the odds of developing renal dysfunction by 13% (odds ratio [OR] 0.87, 95% confidence interval [CI] 0.82 to 0.92, p <0.0001). The beneficial effect of statins appeared to be independent of the decrease in cholesterol. Other variables that affected the development of renal dysfunction were age (OR 1.04, 95% CI 1.03 to 1.04, p <0.0001), diabetes (OR 1.77, 95% CI 1.68 to 1.86, p <0.0001), hypertension (OR 1.11, 95% CI 1.02 to 1.2, p = 0.0153), and smoking (OR 1.12, 95% CI 1.02 to 1.24, p = 0.0244). In conclusion, statin use may retard the development of renal dysfunction. The beneficial effect of statins in preventing the development of renal dysfunction appears to be independent of their lipid-lowering effect.
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PMID:Effect of statins on the development of renal dysfunction. 1835 17

To evaluate survival after acute myocardial infarction (AMI) in nonagenarians, we conducted a retrospective chart review of 177 consecutive patients > or =90 years of age admitted from 2000 to 2006 with a primary diagnosis of AMI confirmed by peak troponin I > or =1.5 microg/L. Mean follow-up was 3.7 years (range 4 months to 6.7 years). Mean age was 93 years, 34% were men, and 60% were Caucasian. Common co-morbidities included hypertension (67%), dyslipidemia (28%), atrial fibrillation (28%), renal insufficiency (27%), dementia (23%), and previous cerebrovascular events (22%). Mean peak troponin was 20 mug/L (range 1.5 to 183 microg/L). Cardiac catheterization was performed within 48 hours in 42 patients (24%) and after 48 hours in 14 patients (8%); 40 patients (23%) received an intervention. Hospital mortality was 15% (n = 27). Survival at 30 days, 90 days, and 1 year were 78%, 69%, and 47%. Independent predictors of shorter survival time by Cox analysis included body mass index <25 kg/m2 (p <0.001), creatinine > or =2.0 mg/dl (p = 0.001), hemoglobin <11.0 g/dl (p = 0.016), and dementia (p = 0.027). Patients receiving aspirin, clopidogrel, beta blockers, and renin-angiotensin system inhibitors appeared to have a lower mortality. In conclusion, AMI in nonagenarians is associated with high mortality, with over 50% of patients dying within one year of presentation; elevated creatinine and lower hemoglobin are strong predictors of adverse prognosis, and lower body mass index and the presence of dementia add independent prognostic significance.
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PMID:Outcomes of acute myocardial infarction in nonagenarians. 1847 45

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

Dunnigan-type familial partial lipodystrophy (FPLD) is a rare monogenic adipose tissue disorder in which the affected subjects have increased predisposition to insulin resistance and related metabolic complications, such as glucose intolerance, diabetes, dyslipidemia, and hepatic steatosis. Our patient was a 35-year-old female who had been receiving insulin injection therapy for diabetes mellitus and was transferred to our hospital. She was diagnosed with FPLD on the basis of the following symptoms: increase in subcutaneous fat in the face, neck, and upper trunk; loss of subcutaneous fat in the lower limbs and the gluteal region. We found a heterozygous CGG to CAG transition in codon 482 of exon 8 in the gene encoding lamin A/C (LMNA), which leads to an arginine to glutamine substitution (R482Q). At the time of admission, her serum creatinine level was 8.4 mg/dl, and her blood urea nitrogen (BUN) level was 81 mg/dl. Her serum creatinine level was elevated and hemodialysis was performed twice every week. However, she died of cerebral hemorrhage 9 months after hemodialysis. Although it is uncommon for patients with FPLD to exhibit renal dysfunction and require hemodialysis, this case suggests the need for careful analysis of renal function in a patient with FPLD.
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PMID:A case of Dunnigan-type familial partial lipodystrophy (FPLD) due to lamin A/C (LMNA) mutations complicated by end-stage renal disease. 1901 97

Nephrologists should promote the detection of CKD in heart disease patients. The evaluation should include estimation of GFR and detection of microalbuminuria in a recently voided urine sample by the albumin:creatinine ratio. Any patient with stage 3 or 4 CKD and rapid deterioration of GFR should be evaluated by the nephrologist. - Patients with CKD have a high risk of cardiovascular (CV) complications and heart disease patients have a high incidence of CKD and progression is also more rapid (Strength of Recommendation B). The most likely pathophysiological hypothesis is endothelial damage. - The CV risk profile should be established in each patient followed by adequate compliance with control goals for common CV risk factors: smoking, obesity, sedentarism, hypertension, dyslipidemia. Early treatment of anemia and bone mineral disease as CV risk factors requires special mention (Strength of Recommendation B). - Management of these patients will be based on individualization of treatment, close systematic follow-up, and integration between care levels: Specialized care (nephrologists and cardiologists) and primary care. - The cardiorenal syndrome (CRS) is a condition in which both organs are simultaneously affected and their deleterious effects are reinforced in a feedback cycle, with accelerated progression of renal and myocardial damage. Because of its prognostic value, treatment of HF takes precedence over CKD. Most studies on cardiovascular risk and on HF exclude patients with stage 4-5 CKD. We thus do not have sufficient strong evidence and recommendations are based on the extrapolation of data from studies with normal GFR or milder grades of CKD, and on the empirical use of certain treatments. - ARBs and ACEIs are the mainstays of treatment of HF with systolic and diastolic dysfunction, and have been shown to reduce mortality in studies in the general population (Strength of Recommendation A). The may also slow progression of CKD, especially in diabetics. Dual renin-angiotensin blockade with the combined use of lower doses of both drugs has shown promising results for control of CKD progression, but there are no data to recommend its use for control of HF in advanced stages of CKD (stage 4-5) (Strength of Recommendation C). - In these stages of CKD, only loop diuretics have sufficient potency. The therapeutic dose range should be achieved. Lowdose thiazides achieve diuretic synergy. The use of spironolactone and eplerenone has shown benefits in patients with AMI and HF with an ejection fraction < 40% without advanced CKD. They should always be used with strict control of GFR and K+. No benefit has been shown for the use of <<dopamine in diuretic doses>> (may even be harmful) or continuous infusion of furosemide (Strength of Recommendation B). The use of beta-blockers should be increased in these patients. - Treatment-refractory heart failure in the context of stage 3 CKD could be amenable to ultrafiltration techniques. Continuous ambulatory PD could be an alternative treatment to maintain hemodynamic equilibrium while also allowing pharmacological treatments to be prescribed that would not be feasible without dialysis and could even improve myocardial and kidney function (Strength of Recommendation C).
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PMID:[Cardiorenal syndrome]. 1901 35

TREATMENT OF ARTERIAL HYPERTENSION - Blood pressure (BP) should be regularly measured in all patients with CKD (Strength of Recommendation C). - BP control and proteinuria reduction delay progression of CKD (Strength of Recommendation A) and reduce cardiovascular risk (Strength of Recommendation C). Thus, control of both factors should be the treatment objective. - The BP target in patients with CKD should be < 130/80 mmHg, and 125/75 mmHg if proteinuria is > 1 g/24 hours (Strength of Recommendation A). - Lifestyle changes should be made: low-sodium diet (less than 100 mEq/day of sodium or 2.4 g/day of salt); weight reduction if patient is overweight (body mass index 20-25 kg/m2); regular aerobic physical exercise and moderate alcohol intake for BP control and prevention of cardiovascular risk (Strength of Recommendation A). - The choice of the antihypertensive drug in patients with CKD depends on the etiology of CKD, cardiovascular risk, or presence of clinical or subclinical cardiovascular disease (Strength of Recommendation A). - Two or more antihypertensive drugs are usually required to control blood pressure in patients with CKD (Strength of Recommendation B), and will frequently include a diuretic, which in stages 4-5 should be a loop diuretic (Strength of Recommendation B). - Renin-angiotensin-aldosterone system (RAAS) inhibitors are first choice drugs in patients with diabetic nephropathy, patients with non-diabetic nephropathy with a protein/creatinine ratio higher than 200 mg/g, and patients with heart failure (Strength of Recommendation A). The combination of ACEIs and ARBs is indicated for reducing proteinuria that remains high despite treatment with a RAAS inhibitor, provided potassium levels do not exceed 5.5 mEq/L (Strength of Recommendation B). - When RAAS blockers are started or their dose is changed in patients with advanced CKD, kidney function and serum potassium levels should be monitored at least after 1-2 weeks. DIAGNOSIS AND TREATMENT OF DYSLIPIDEMIA - A complete evaluation of the lipid profile including total cholesterol, LDL-C, HDL-C, and triglycerides should be performed in any patient with CKD at baseline and at least annually (Strength of Recommendation B). - In patients with stage 4-5 CKD and LDL-C >or= 100 mg/dL, treatment to decrease levels to < 100 mg/dL should be considered because of their high CV risk. This reduction is recommended in secondary prevention and in primary prevention in diabetic patients. Lipid-lowering treatment is recommended in all other patients, although no evidence showing its benefits is available yet (Strength of Recommendation C). - In patients with stage 4-5 CKD and triglyceride levels >or= 500 mg/dL which are not corrected by treating the underlying cases, treatment with triglyceride-lowering drugs may be considered to reduce the risk of pancreatitis. However, treatment with fibrates should be used with caution, and these drugs should not be associated to statins due to the risk of rhabdomyolysis (Strength of Recommendation C). There is little experience on the efficacy and safety of omega-3 fatty acids for the treatment of hypertriglyceridemia in patients with grade 4-5 CRF, but they may be considered a possibly safer alternative to fibrates (Strength of Recommendation C). SMOKING - Smoking is a cardiovascular risk factor and a risk factor for progression of kidney disease in patients with CRF (Strength of Recommendation B). - Use of active measures to achieve smoking cessation is recommended in patients with CRF (Strength of Recommendation C). HOMOCYSTEINE - Hyperhomocysteinemia has been postulated as a cardiovascular risk factor in the general population and in kidney patients, but the available evidence is not consistent. - There is no evidence that vitamin therapy decreases cardiovascular risk in patients with CRF, and recommendation of routine vitamin measurement and start of vitamin therapy to reduce cardiovascular risk in these patients is therefore questionable (Strength of Recommendation B). LEFT VENTRICULAR HYPERTROPHY - Left ventricular hypertrophy (LVH) is a cardiovascular risk factor in patients with CRF (Strength of Recommendation B). - It is advisable to perform an echocardiogram at baseline and every 12-24 months and to consider treatments allowing for LVH regression (Strength of Recommendation C). The approach to LVH should be early and multifactorial because its reversibility is limited once established (Strength of Recommendation C). - RAAS blockade with ACEIs or ARBs partially reverts LVH in patients with CRF (Strength of Recommendation B). ANTI-PLATELET AGGREGATION - Because of the high cardiovascular risk in patients with CKD, anti-platelet aggregant therapy, especially low-dose aspirin, would be indicated in patients with type 2 diabetes as primary prevention, and in all patients with CKD as secondary prevention. There is however no evidence of the benefits of anti-platelet aggregant therapy in primary prevention in patients with CKD, particularly in stages 4-5; indication for treatment in this situation should therefore be individualised because of its greater risk of bleeding. - Adequate good blood pressure control should previously be achieved to minimise the risk of haemorrhagic stroke (Strength of Recommendation C).
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PMID:[Arterial hypertension and dyslipidemia in patients with chronic kidney disease (CKD). Anti-platelet aggregation. Goal oriented treatment]. 1901 37

Hitherto unknown efficacy of the peel extracts of Mangifera indica (MI), Cucumis melo (CM) and Citrullus vulgaris (CV) fruits in ameliorating the diet-induced alterations in dyslipidemia, thyroid dysfunction and diabetes mellitus have been investigated in rats. In one study, out of 4 different doses (50-300 mg/kg), 200 mg/kg of MI and 100 mg/kg for other two peel extracts could inhibit lipidperoxidation (LPO) maximally in liver. In the second experiment rats were maintained on pre-standardized atherogenic diet CCT (supplemented with 4% cholesterol, 1% cholic acid and 0.5% 2-thiouracil) to induce dyslipidemia, hypothyroidism and diabetes mellitus and the effects of the test peel extracts (200 mg/kg of MI and 100 mg/kg for CM and CV for 10 consecutive days) were studied by examining the changes in tissue LPO (in heart, liver and kidney), concentrations of serum lipids, thyroid hormones, insulin and glucose. Rats, treated simultaneously with either of the peel extracts reversed the CCT-diet induced increase in the levels of tissue LPO, serum lipids, glucose, creatinine kinase-MB and decrease in the levels of thyroid hormones and insulin indicating their potential to ameliorate the diet induced alterations in serum lipids, thyroid dysfunctions and hyperglycemia/diabetes mellitus. A phytochemical analysis indicated the presence of a high amount of polyphenols and ascorbic acid in the test peel extracts suggesting that the beneficial effects could be the result of the rich content of polyphenols and ascorbic acid in the studied peels.
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PMID:Possible amelioration of atherogenic diet induced dyslipidemia, hypothyroidism and hyperglycemia by the peel extracts of Mangifera indica, Cucumis melo and Citrullus vulgaris fruits in rats. 1927 33


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