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 prevalence of type 2 diabetes continues to show a clear upward trend in Germany. In earlier days it was considered the "harmless diabetes of old age," but has become increasingly recognized as a disease carrying a high risk of vascular sequelae as well as shortening the diabetic's remaining life expectancy if adequate therapy is not initiated. In addition to correcting hyperglycemia, treatment consists in effective management of concomitant risk factors such as hypertension, dyslipidemia, and adiposity resulting from faulty nutrition and lack of exercise. In the large majority of overweight type 2 diabetics, metformin is the oral antidiabetic agent of first choice provided the patient does not exhibit renal insufficiency, which represents the most important contraindication. This recommendation for monotherapy of overweight type 2 diabetics is supported by an endpoint study. In contrast, no equivalent evidence is available on any of the possible options for oral combination therapy.
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PMID:[Oral diabetes treatment. Which substance is indicated at which time?]. 1553 16

Cardiovascular risk is dramatically increased in patients with end-stage renal disease (ESRD). However, even minor dys-functions such as microalbuminuria or a mild increase in serum creatinine (Cr) have a major impact on cardiovascular risk. Increased cardiovascular risk is present in multiple populations, including general populations, patients with moderate risk such as hypertensives, and high-risk patients including patients with heart failure and myocardial necrosis. There are many mechanisms underpinning the increased cardiovascular risk. Regarding atherosclerosis, the kidney can be victim or villain. On the one hand, both kidney disease per se and renal insufficiency can induce vascular damage, thereby increasing cardiovascular risk. Kidney disease without renal insufficiency can cause an increased prevalence in hypertension, dyslipidemia (nephrotic syndrome), sympathetic system hyperactivity, and in renin angiotensin system hyperactivity. A moderate-severe renal insufficiency can induce an increase in many vasculotoxic substances such as ADMA, lipoprotein(a), homocysteine, disturbances in calcium and phosphate metabolism, anemia and left ventricular hypertrophy. A more severe renal insufficiency can induce the ominous malnutrition-inflammation-atherosclerosis (MIA) syndrome. On the other hand, the kidney can be the victim of atherosclerosis. Ischemic nephropathy, caused by atherosclerotic renal artery disease and atheroembolism from abdominal aorta are two examples. Finally, it is important to consider that the kidney, being an organ with a wide vasculature, could be a sophisticated sensor of subclinical cardiovascular damage.
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PMID:[Hypertension, atherosclerosis and kidney]. 1578 9

Dyslipidemia is frequent in patients with renal failure and in transplant recipient patients. This lead to a wide use of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins) in patients with impaired renal function or in patients treated with cyclosporine as post-transplantation immunosuppressive therapy. As a result, it is crucial for those patients' physicians to be aware of how to handle these drugs when renal function is impaired and/or when cyclosporine is co-administered. Most statins have an extensive hepatic elimination and the renal route is usually a minor elimination pathway. However, pharmacokinetic alterations have been described for some of these drugs in patients with renal insufficiency. Cyclosporine is a widely used immunosuppresive therapy in solid organ transplant patients and drug-drug interactions are likely to occur when statins and cyclosporine are administered together. Those interactions may theoretically result in increased statins and/or cyclosporine serum levels with potential muscle and/or renal toxicity. As a result, caution is warranted if concurrent administration is performed. In this review, we synthesized the data from the literature on (1) the pharmacokinetics and dosage adjustment of atorvastatin, fluvastatin, pravastatin, rosuvastatin, and simvastatin in patients with renal failure and (2) the potential drug-drug interactions between these drugs and cyclosporine in transplant recipient patients.
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PMID:Statins' dosage in patients with renal failure and cyclosporine drug-drug interactions in transplant recipient patients. 1586 Mar 77

The vascular endothelium achieved a critical place in the understanding of vascular physiology and pathophysiology, after the discovery of the production of prostacyclin by endothelial cells, followed by the recognition that substances like acetylcholine, assumed to be direct vasodilators, could only trigger dilation in the presence of an intact endothelium. The endothelium-derived relaxing factor (EDRF) behaves as an endogenous nitrovasodilator and causes vasodilatation through stimulation of guanylyl cyclase and cellular accumulation of cyclic GMP. Subsequently, it was demonstrated that the EDRF is nitric oxide (NO), produced through the metabolism of the aminoacid L-arginine by the nitric oxide synthases (NOS). Three isoforms of this enzyme were discovered and cloned: a constitutive neuronal isoform (nNOS); an inducible isoform (iNOS), ubiquitous in cells stimulated by certain cytokines; and an endothelial isoform (eNOS). The importance of the different isoforms is well demonstrated in animal models; more recently, human studies unveiled the importance of these enzymes. The endothelium produces other vasodilators besides NO and prostacyclin; furthermore, it produces several vasoconstrictors. There is a delicate balance between these factors, which can be disturbed: several well known cardiovascular aggressors, like arterial hypertension, diabetes, smoking, dyslipidemia or renal insufficiency, can alter several invasive or non-invasive tests of endothelial function. The fact that an intervention on these factors may reverse endothelial dysfunction as measured by these tests, raises hope that they may be surrogate markers of global cardiovascular risk. If correlation of these tests with clinical outcomes proves to be robust, they may become extensively used in clinical practise.
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PMID:[Vascular endothelium: the history of a recent revolution in angiology]. 1607 83

Studies were carried out in 183 non-dialyzed, 123 hemodialysis, 81 continuous ambulatory peritoneal dialysis and 35 post-transplant patients and in 103 healthy subjects as a reference group. Lipids and apolipoprotein (apo)AI and apoB were determined using Roche kits. An anti-apoB antibody was used to separate apoB-containing apoCIII and apoE-triglyceride-rich lipoprotein (TRL) in the non-high-density lipoprotein (non-HDL) fraction from apoCIIInonB and apoEnonB in the HDL fraction in four groups of patients with chronic renal failure (CRF) and healthy subjects. Multivariate linear regression analysis was used to investigate the relationship between triglyceride (TG) or HDL-cholesterol (HDL-C) concentrations and lipoproteins. Dyslipidemia varied according to the degree of renal insufficiency, the type of dialysis and therapy regime in CRF patients. Lipoprotein disturbances were manifested by increased TG, non-HDL-C and TRL concentrations, and decreased HDL-C and apoAI concentrations, whereas post-renal transplant patients showed normalization of lipid and lipoprotein profiles, except for TG levels and total apoCIII and apoCIIInonB. The present study indicates that CRF patients have disturbed lipoprotein composition, and that hypertriglyceridemia and low HDL-C concentrations in these patients are multifactorial, being secondary to disturbed lipoproteins. The method using anti-apoB antibodies to separate apoB-containing lipoproteins in the non-HDL fraction from non-apoB-containing lipoproteins in HDL can be used in the diagnosis and treatment of patients with progression of renal failure or atherosclerosis. The variability of TG and HDL-C concentrations depends on the variability of TRL and cholesterol-rich lipoprotein concentrations, but the decreases in TG and increases in HDL-C concentrations are caused by apoAI concentration variability. These relationships, however, need to be confirmed in further studies.
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PMID:Disturbed lipoprotein composition in non-dialyzed, hemodialysis, continuous ambulatory peritoneal dialysis and post-transplant patients with chronic renal failure. 1637 88

It has not been established firmly whether dyslipidemia contributes independently to the progression of kidney disease. Lipid and lipoprotein parameters, including levels of total, HDL, and LDL cholesterol; triglycerides; lipoprotein(a); apolipoprotein A-IV; and the apolipoprotein E and A-IV polymorphisms, were assessed in 177 patients who had mostly mild to moderate renal insufficiency and were followed prospectively for up to 7 yr. Progression of kidney disease was defined as doubling of baseline serum creatinine and/or terminal renal failure necessitating renal replacement therapy. In univariate analysis, patients who reached a progression end point (n = 65) were significantly older and had higher serum creatinine and proteinuria as well as lower GFR and hemoglobin levels. In addition, baseline apolipoprotein A-IV and triglyceride concentrations were higher and HDL cholesterol levels were lower. Multivariate Cox regression analysis revealed that baseline GFR (hazard ratio 0.714; 95% confidence interval [CI] 0.627 to 0.814 for an increment of 10 ml/min per 1.73 m(2); P < 0.0001) and serum apolipoprotein A-IV concentrations (hazard ratio 1.062; 95% CI 1.018 to 1.108 for an increment of 1 mg/dl; P = 0.006) were significant predictors of disease progression. Patients with apolipoprotein A-IV levels above the median had a significantly faster progression (P < 0.0001), and their mean follow-up time to a progression end point was 53.7 mo (95% CI 47.6 to 59.8) as compared with 70.0 mo (95% CI 64.6 to 75.4) in patients with apolipoprotein A-IV levels below the median. For the apolipoprotein E polymorphism, only the genotype epsilon2/epsilon4 was associated with an increased risk for progression. In summary, this prospective study in patients with nondiabetic primary kidney disease demonstrated that apolipoprotein A-IV concentration is a novel independent predictor of progression.
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PMID:Apolipoprotein A-IV predicts progression of chronic kidney disease: the mild to moderate kidney disease study. 1638 17

Dyslipidemia and inflammation may promote renal disease via mechanisms of vascular endothelial cell dysfunction in type II diabetes mellitus (DM). Sparse data, however, are available on the relation of lipids and inflammatory biomarkers and glomerular filtration rate (GFR) in type II DM. We performed a cross-sectional study of 732 men with type II DM enrolled in the Health Professionals' Follow-Up Study. Plasma creatinine was used to estimate GFR by the simplified Modification of Diet in Renal Disease (MDRD) equation. In men with a GFR <60 ml/min/1.73 m(2), triglycerides, non-high-density lipoprotein (HDL), apoprotein B, fibrinogen, soluble tumor necrosis factor receptor (sTNFR-2) and vascular cell adhesion molecule-1 (VCAM) were significantly higher when compared to the referent group (GFR> or =90 ml/min/1.73 m(2)). In multivariable logistic regression, those in the highest quartiles of the following biomarkers had increased odds of having a GFR <60 ml/min/1.73 m(2) when compared to those in the lowest quartiles: triglycerides (odds ratio (OR) 3.11; 95% CI, 1.52-6.36), fibrinogen (OR 5.40; 95% CI 2.14-13.65), sTNFR-2 (OR 8.34; 95% CI 3.50-19.88) and VCAM (OR 4.50; 95% CI 1.98-10.23). An inverse association was observed for HDL (OR 0.48; 95% CI 0.24-0.98). We found no association between C-reactive protein and GFR. The results were similar when creatinine clearance by Cockcroft-Gault was used to estimate kidney function. We conclude that several potentially modifiable lipid and inflammatory biomarkers are elevated in the setting of moderately decreased GFR in men with type II DM and may be the link between renal insufficiency and increased risk for cardiovascular events in this population.
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PMID:The association of serum lipids and inflammatory biomarkers with renal function in men with type II diabetes mellitus. 1640 7

Chronic renal disease is accompanied by characteristic abnormalities of lipid metabolism, which appear as a consequence of nephrotic syndrome or renal insufficiency and are reflected in an altered apolipoprotein profile as well as elevated plasma lipid levels. Experimental and clinical studies have suggested a correlation between the progression of renal disease and dyslipidemia. High cholesterol and triglyceride plasma levels have been demonstrated to be independent risk factors for progression of renal disease in humans. The underlying pathophysiologic mechanisms for the relationship between lipid levels and progression of renal disease are not yet fully understood, although there are data that oxidative stress and insulin resistance may mediate the lipid-induced renal damage. In the animal model, lipid-lowering agents seem to ameliorate glomerular damage, preventing glomerulosclerosis and interstitial fibrosis. Although evidence from clinical studies indicates that statin therapy is associated with significant benefit in individuals with established chronic renal failure, whether lipid reduction can slow the renal functional decline awaits a primary renal outcome lipid-lowering therapy study.
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PMID:Lipids and renal disease. 1656 40

Overweight and obesity are associated with increased cardiovascular risk. Some studies have demonstrated that they also can result in renal damage. The aim of this study was to assess the prevalence of renal insufficiency (RI), defined as a GFR <60 ml/min per 1.73 m2, in a cohort of 4585 patients who attended primary care with essential hypertension and a body mass index > or =25 kg/m2. The patients were classified as overweight and obese according to body mass index (25 to 29.9 and > or =30 kg/m2, respectively). Abdominal obesity was defined as a waist circumference > or =88 and 102 cm in women and men, respectively. Both groups had a high prevalence of metabolic syndrome (Adult Treatment Panel III). The prevalence of RI was high in both the overweight group (22.7%; 95% confidence interval [CI] 20.6 to 24.9) and in the obese group (22.8%; 95% CI 21.0 to 24.7). The presence of diabetes increased the risk for RI (odds ratio 1.83; 95% CI 1.55 to 2.16). The prevalence of RI was greater in patients with abdominal obesity (23 versus 17%; P < 0.001). In the presence of abdominal obesity, cardiovascular risk factors and components of the metabolic syndrome also were more prevalent. The higher risk for RI with abdominal obesity persisted even after adjustment for dyslipidemia, elevated blood glucose levels, and other variables that are associated with RI (adjusted odds ratio 1.40; 95% CI 0.84 to 2.33). It was concluded that patients who have hypertension and visceral obesity and attend primary care present a higher prevalence of metabolic syndrome and RI.
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PMID:Prevalence of renal insufficiency in individuals with hypertension and obesity/overweight: the FATH study. 1713 Feb 61

Dyslipidemia is a risk factor for de novo occurrence of renal disease in apparently healthy population, and diabetes, and contributes to progressive decline of renal function in diabetic and nondiabetic kidney disease. Chronic kidney disease and dyslipidemia, frequently occurring together, are independent cardiovascular risk factors. There is a strong association between the level of renal insufficiency and cardiovascular disease. According to available evidence, statin therapy may reduce cardiovascular risk in chronic kidney disease as well as modify its course, especially in patients with moderate impairment of renal function. However, all these findings must be examined in large-scale trials in patients with chronic renal disease and different stages of renal insufficiency. There are several on-going trials aimed at determing the role of statin therapy in this specific population, and confirming its efficacy in reducing cardiovascular risk and halting the progression of chronic kidney disease.
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PMID:[Chronic kidney disease and statins]. 1721 96


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