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)

Electron beam CT (EBCT) has been used to measure coronary artery calcification score (CACS). We have been studied CACS on chronic dialysis patients and examined the relationship between CACS and laboratory variables, incidence of ischemic heart disease, and survival. High CACS is often observed in patients with high serum phosphate, high calcium phosphate product, and dyslipidemia. Several factors for calcification both stimulating and suppressing have been playing a role in chronic dialysis patients. CACS is a surrogate marker of adequate control of uremia.
Clin Calcium 2004 Jun
PMID:[Evaluation and related factors in coronary artery calcification in chronic dialysis patients]. 1557 62

Magnesium plays essential roles in fundamental cellular reaction and physiological regulation of vascularture, nervous system, and organs. Accumulating findings have revealed that magnesium deficiency relates cardiovascular risk factors including elevated blood pressure, insulin resistance, dyslipidemia, platelet aggregation, and inflammatory reaction, and leads to atherosclerosis.
Clin Calcium 2005 Feb
PMID:[Magnesium, cardiovascular risk factors and atherosclerosis]. 1569 60

This article describes the relationship between CVD and CKD, the current state of knowledge regarding medical interventions, and underscores the importance of attending to both CVD and kidney disease aspects in each individual. The burden of cardiac disease in CKD patients is high with severe LVH, dilated cardiomyopathy and coronary artery disease occurring frequently. This predisposes to congestive heart failure, angina, myocardial infarction, and death. Multiple risk factors for cardiac disease exist and include hypertension, diabetes, smoking, anemia, abnormal calcium and phosphate metabolism, inflammation, and LVH. The efficacy of risk factor intervention has not been established in these populations, although there is good evidence for good blood pressure control, partial correction of anemia, treatment of dyslipidemia, cessation of tobacco use, correction of divalent abnormalities, and aspirin us. Appropriate use of ACE inhibitors, beta-blockers, and statins should be encouraged.
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PMID:Multiple risk factor intervention in chronic kidney disease: management of cardiac disease in chronic kidney disease patients. 1575 65

It is important for prevention of vascular complications in diabetics to control blood glucose, blood pressure, and dyslipidemia, and to stop smoking. Recently, it has been reported that the HMG-CoA reductase inhibitor has angiogenetic effects independent of lipid lowering effect. Moreover, gene therapy using VEGF and HGF has shown dramatic effects for peripheral arterial disease. Endothelial progenitor cells injection is also expected for treatment of ischemic heart disease.
Clin Calcium 2003 Sep
PMID:[Division of endocrinology and metabolism, strategy for treatment of diabetic vascular complications for physicians]. 1577 99

Vascular calcifications are more frequent in dialysis patients than in the general population or in patients with cardiovascular disease (CVD) and normal renal function. The reasons for this high incidence are multiple; they include traditional factors such as hypertension, diabetes, dyslipidemia, and specific factors such as sodium overload, hyperomocysteinemia, chronic inflammation and oxidative stress, as well as mineral metabolism disturbances. Specifically, hyperphosphatemia and the elevated calcium (Ca) x phosphate product have been associated with an increased risk for the development of vascular calcification and death. Treatment with Ca salts can induce hypercalcemia, increased Ca x phosphate product and Ca overload. Sevelamer substitution for Ca salts has been documented to attenuate the progression of coronary artery and aortic calcification. A possible mechanism explaining this observation could be ongoing Ca loading related to oral Ca ingestion. Treatment with Ca salts could induce Ca overload, particularly in patients dialyzed against a high dialysate Ca (>1.5 mmol/L) solution, which is known to determine a positive dialysis balance. Conversely, an overall negative Ca balance can result from low Ca dialysate use (1.25 mmol/L) when the patients do not receive Ca supplements or vitamin D metabolites. Maintaining normal Ca and phosphate balances remains a primary goal in the management of dialysis patients. Control of hyperphopshataemia should be achieved either using Ca and aluminum-free phosphate binders, such as sevelamer, or Ca salts, alone or in combination, provided that a daily oral elemental Ca intake of 1.5 g is not exceeded.
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PMID:[Control of calcium and phosphate metabolism and prevention of vascular calcifications in uremic patients]. 1578 2

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

Vitamin D3 is modified by vitamin D3-25-hydroxylase in the liver, and 25-hydroxyvitamin D3-1alpha-hydroxylase in the kidney, to form the active metabolite, 1,25-dihydroxyvitamin D3. Chronic kidney disease (CKD) is characterized by reduced synthesis of 1,25-dibydroxyvitamin D3, inadequate renal phosphate clearance and calcium imbalance, secondary hyperparathyroidism (SHPT) and bone disease. CKD patients encounter a much higher risk of cardiovascular disease (CVD) than the general public. The cardiovascular risk factors for CKD patients include conventional factors such as age, gender, hypertension, diabetes, dyslipidemia and smoking, and non-conventional factors, such as anemia, uremia, reduced vascular compliance, inflammation and various hormonal factors. Several vitamin D analogs are currently available for the treatment of SHPT, and recent clinical data show that these analogs provide survival benefit for CKD patients in the order of paricalcitol > calcitriol > no vitamin D analog, independent of parathyroid hormone and calcium. Moreover, the survival benefit seems to be associated with cardiovascular causes. The observations made from these clinical studies raised intriguing questions about the involvement of the vitamin D receptor locus (VDR) in the cardiovascular system. This review discusses recent data regarding the role of vitamin D and its analogs in the CVD associated with CKD.
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PMID:Cardiovascular disease in chronic kidney failure: is there a role for vitamin D analogs? 1581

Recent evidences from epidemiological and intervention trials suggest that a higher calcium intake is associated with a lower body weight and a reduction in total and central body fat. The potential role of calcium intake in the regulation of body adiposity has been explained by the intracellular calcium, which is able to promote adipocyte fat accumulation by exerting a coordinate regulation stimulating lipogenesis and suppressing lipolysis. Moreover, the intracellular calcium has been implicated on the etiopathogenesis of hypertension, insulin resistance and dyslipidemia, appearing as a potential common substrate in the metabolic syndrome. Dietary modulation of intracellular calcium through calciotropic hormones opens an exciting possibility to prevent and tackle obesity and its associated complications by increasing the calcium intake. However, available evidences are mostly indirect and further studies specifically designed for this purpose are needed.
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PMID:[Role of calcium intake in obesity]. 1582 85

One of the factors involved in accelerated atherosclerosis in hemodialysis patients is dyslipidemia. In this study we considered factors involved in intensification of dyslipidemia in hemodialysis patients. This study was done on 36 maintenance hemodialysis patients. Serum lipoprotein (a), Triglyceride, Cholesterol, HDL-C,LDL-C and also serum Intact parathormone(iPTH), Calcium, Phosphorus, Magnesium were measured. In statistical analysis there was not any correlation between serum lipids and iPTH. There was not correlation between serum calcium with serum lipids (p > 0.05). There was not correlation between CaxP product with serum lipids (p > 0.05). There was a positive correlation between serum Magnesium and Lipoprotein(a) (P < 0.05) and also positive correlation between serum magnesium with triglyceride level (P < 0.05) was seen too. Magnesium doesn't increase the lipoprotein synthesis. It may involve in the regulation of some enzymes responsible for lipoprotein synthesis. Correlation of serum magnesium with serum triglycerides can be due to changes in hepatic triglyceride metabolism. Lipoprotein(a) is a non traditional factor of premature atherosclerosis, its association with serum magnesium needs more attention in hemodialysis patients.
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PMID:Correlation of serum magnesium with dyslipidemia in maintenance hemodialysis patients. 1584 6

Metabolic syndrome has recently been identified to be involved in the development of multiple diseases, such as type 2 diabetes (or glucose intolerance), dyslipidemia and hypertension. Its principal features are obesity and insulin resistance. Bone metabolism is a complex process that is regulated by complicated local and systemic factors. Recent investigations demonstrate an involvement of sympathetic nervous system and glucose and lipid metabolism in bone metabolism. Obesity and insulin resistance may favor bone dynamics, whereas diabetes and dyslipidemia may not. More importantly, various drugs for these disorders have been reported to have beneficial effects on bone health. On clinical situation to manage metabolic syndrome, physicians may want to evaluate outcome of their practice for bone metabolism.
Clin Calcium 2005 May
PMID:[Bone metabolism in metabolic syndrome and its treatment]. 1587 41


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