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)

Abnormalities in circulating lipoprotein concentrations are a characteristic finding in patients undergoing dialytic therapy. A substantial number of these patients display type IV hyperlipoproteinemia. Certain data suggest that secondary hyperparathyroidism may induce disturbances in lipid metabolism. To evaluate the effects of pulse calcitriol therapy on the lipid profile in these patients, we undertook a prospective study in 12 patients on stable bicarbonate hemodialysis. Lipid parameters comprising cholesterol and the low- as well as the high-density lipoprotein subfractions, triglycerides, apolipoproteins A and B, serum parathyroid hormones (iPTH), alkaline phosphatase, calcium, phosphorus, hematocrit, and blood urea were obtained prior to commencement of pulse calcitriol therapy and again 8-10 weeks later. Calcitriol therapy was associated with a decrease in serum iPTH levels (701 +/- 103.9 vs. 220.3 +/- 50.5 pmol/l; p < 0.001). Significant increases in high-density lipoprotein cholesterol (32.8 +/- 2.7 vs. 38.8 +/- 2.3 mmol/l; p < 0.05) and apolipoprotein A-I (107.8 +/- 6.1 vs. 121.8 +/- 5.8 g/l; p < 0.05) were noted during the course of the study. Moreover, serum iPTH correlated inversely with high-density lipoprotein cholesterol and apolipoprotein A-I. There were no changes in other lipid parameters except for low-density lipoprotein cholesterol which showed a tendency to increase. We conclude that in short-term study, pulse oral calcitriol therapy is associated with an improvement in the lipid profile in patients with secondary hyperparathyroidism. However, it remains to be established whether ameliorating the uremic dyslipidemia results in any long-term clinical benefits.
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PMID:Effects of treatment of secondary hyperparathyroidism on the lipid profile in patients on hemodialysis. 951 59

The less rigorous attention to the management of the complications of chronic renal insufficiency (CRI) and its comorbid conditions has potentially tragic consequences. In fact, with early recognition and intervention, many of the complications of CRI and its comorbid conditions can be ameliorated or prevented. We review here the most prevalent, troublesome, and potentially preventable complications and comorbidities of CRI with a view toward developing high-quality, cost-effective strategies for delivering early interventional care. Complications of CRI include malnutrition, anemia, disorders of divalent ion metabolism and osteodystrophy, metabolic acidosis, and dyslipidemia. Important comorbid conditions of CRI are hypertension, diabetes mellitus, and cardiovascular disease. Clinical intuition suggests that early intervention will avert morbidity related to the hypoalbuminemia and other nutritional disorders of CRI, the metabolic acidosis, and the dyslipidemias, but prospective data are lacking at present. Correction of anemia, usually with recombinant human erythropoietin, may be key to the prevention of cardiac disease and other comorbidities of CRI. Incipient disorders of bone and mineral metabolism are managed prospectively using such measures as protein restriction to reduce phosphorus intake, phosphate binders, calcium supplementation, and vitamin D analogues. Hypertension, whatever its original etiology, is clearly an important risk factor for the progression of kidney failure and for the development of diffuse vascular disease; appropriate and aggressive treatment is essential. In patients with diabetic nephropathy, the principles of both primary and secondary prevention have been validated in several large trials of glycemic and blood pressure control. The seeds of these insidious, challenging, and costly comorbid conditions are sown very early in CRI, at a time when they are-in theory-most amenable to intervention. We therefore must be as proactive as possible in the timely implementation of relatively simple therapies that have the potential to prevent some of these adverse outcomes of CRI.
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PMID:Complications of chronic renal insufficiency: beyond cardiovascular disease. 1111 56

Arteriosclerosis, atherosclerosis and vascular calcification are causally related to the high morbidity and mortality of patients with chronic renal failure. Oxidative stress and carbonyl stress of uremia, dialysis procedure and/or intravenous iron therapy result in AGE (advanced glycation end-product), ALE (advanced lipoxidation end-product) and AOPP (advanced oxidation protein product) formation, favouring together with elevated CRP (C-reactive protein) levels the development of cardiovascular and cerebrovascular complications. Enhanced plasma levels of homocysteine and ADMA (asymmetric dimethylarginine) contribute to this process. In addition, in chronic renal insufficiency hyperphosphatemia and an enhanced calcium x phosphorus ion product are associated with the morbidity and mortality of the patients, particularly in the presence of fetuin deficiency. Phosphorus, AGEs and AOPPs, beside other factors, catalyze the conversion of vascular smooth muscle cells to osteoblast--like cells (particularly in the presence of monocytes/macrophages), resulting in bone matrix protein formation. Other risk factors, such as age, male sex, smoking, hypertension, diabetes, chronic inflammation, insulin resistance or dyslipidemia (enhanced non-HDL-cholesterol) also contribute to the atherosclerotic risk profile of the patient with chronic renal insufficiency. While there is growing understanding of the mechanisms involved in arteriosclerosis, atherosclerosis and vascular calcification in uremia, we are still missing effective therapeutic maneuvers for reduction of excess mortality in uremic patients.
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PMID:[Atherosclerosis and uremia: signifance of non-traditional risk factors]. 1277 74

Hyperphosphatemia and dyslipidemia are common clinically significant conditions in end-stage renal disease (ESRD). Hyperphosphatemia management is essential; however, use of calcium-based phosphate binder has been associated with elevated risk of cardiac calcification in ESRD, increasing risks for cardiovascular disease and death. An alternative to calcium-based phosphate binders is sevelamer hydrochloride, a calcium-free, metal-free, nonabsorbed polymer that binds phosphate effectively. We conducted a meta-analysis on the effects of sevelamer hydrochloride on parameters of mineral metabolism (serum phosphorous, calcium, Ca x P, and iPTH) and the lipid profile (total, LDL, HDL, and non-HDL cholesterol, and triglycerides) in dialysis patients. After application of inclusion/exclusion criteria, 17 core studies were statistically analyzed to determine the sevelamer treatment effect on the study parameters as demonstrated by simple, n-weighted, and inverse variance-weighted mean changes. Analysis of inverse variance-weighted mean changes indicated that sevelamer treatment was associated with a 2.14 mg/dL drop in serum phosphorus (P <.001), no significant overall effect on calcium (0.09 mg/dL, P =.364), significant decline in Ca x P product (15.91 mg(2)/dL(2), P <.001), 35.99 pg/mL reduction in iPTH (P =.026), significant reduction in total cholesterol (30.58 mg/dL, P <.001), 31.38 mg/dL drop in LDL cholesterol (P <.001), significant increase in HDL cholesterol (4.09 mg/dL, P =.008), and a significant reduction in triglycerides (22.04 mg/dL, P x.001). This meta-analysis suggests that sevelamer offers a dual therapeutic benefit in dialysis patients-a population at high risk for cardiovascular disease-by improving phosphorus control and the lipid profile, without altering serum calcium.
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PMID:Meta-analysis of the effect of sevelamer on phosphorus, calcium, PTH, and serum lipids in dialysis patients. 1287 74

Cardiovascular (CV) disease is one of the major causes of mortality in patients with renal diseases, with an increased odds ratio of mortality with risk factors as diverse as blood pressure (high or low), cholesterol level (high or low), left ventricular hypertrophy, vascular stiffness, chronic inflammation, and hyperhomocysteinemia. Mainly cross-sectional studies of renal patients showed excess CV calcification (CVC) compared with the general population, but a clear link between calcification and subsequent mortality is tenuous to date. Several factors have been incriminated to explain the increase in CVC in this particular population. Increased duration of dialysis therapy, dyslipidemia, altered calcium-phosphorus metabolism, and chronic inflammation have all been associated with increased CVC. However, with the shortage of large, observational, population-based, prospective studies tracking these potential risk factors and the pathogenesis of CVC in renal patients not yet sufficiently understood, it is difficult with the present state of knowledge to make robust recommendations about care strategies. The purpose of this review is to examine the 10 available studies of renal patients that have used modern CVC imaging and quantification techniques for clues to likely targets for future interventional studies.
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PMID:Cardiac calcification in renal patients: what we do and don't know. 1475 88

Cardiovascular disease (CVD) is one of the major causes of mortality in patients with renal diseases, with increased odds ratio of mortality with risk factors as diverse as cholesterol, vascular stiffness, chronic inflammation and hyperhomocysteinemia. Several factors have been incriminated to explain the increase in coronary vascular calcification (CVC) in this particular population. Increased duration of dialysis, dyslipidemia, altered calcium-phosphorus metabolism, and chronic inflammation have all been associated with increased CVC. We present here four case reports illustrating the differences in the pathophysiology, therapy and prognosis of calcific coronary heart disease seen in uremic patients.
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PMID:Inflammation and coronary calcification in renal patients--factors that may explain increased cardiovascular risk, and poorer results of coronary interventions? 1515 Dec 68

The reduction of cardiovascular disease risk in kidney failure involves treatment of modifiable risk factors and provision of proven interventions to patients with established disease. Volume status management is key to blood pressure control. Statins are the agents of choice for the treatment of dyslipidemia. Target hemoglobin levels should be achieved using intravenous iron and erythropoietic agents. Combinations of calcium and noncalcium-containing phosphorus binders and vitamin D and its analogues should be used to attain target parathyroid hormone, phosphorus, and calcium phosphorus product levels. beta Blockers and aspirin are recommended in patients with ischemic heart disease and angiotensin-converting enzyme inhibitors (or angiotensin II receptor blockers), and beta blockers are recommended in patients with heart failure with reduced ejection fraction. In patients who require revascularization, studies suggest a survival benefit of coronary artery bypass graft surgery over percutaneous transluminal coronary angioplasty and coronary artery stenting.
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PMID:Treating the Patient with Kidney Failure to Reduce Cardiovascular Disease Risk. 1521 21

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

Chronic kidney disease (CKD) is a permanent, progressive loss of kidney function characterized by a decline in glomerular filtration rate (GFR). Early identification of CKD risk factors provides an opportunity to prevent or delay the progression of kidney disease and decrease morbidity and mortality. There is increasing evidence to suggest that the adverse outcomes of CKD can be delayed or prevented by early detection and treatment. Current literature suggests that a low-protein, low-phosphorus diet may retard the progression of kidney disease. Other modifiable risk factors affecting CKD include proteinuria, hypertension, hyperglycemia, dyslipidemia, bone disease, anemia, and obesity. This discussion will review the current clinical nutrition guidelines for managing adult patients with CKD.
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PMID:Integrating clinical nutrition practice guidelines in chronic kidney disease. 1620 58

We have shown that renal injury and chronic kidney disease (CKD) directly inhibit skeletal anabolism, and that stimulation of bone formation decreases the serum phosphate. Most recently, these observations were rediscovered in low-density lipoprotein receptor null mice fed high-fat/cholesterol diets, a model of the metabolic syndrome (hypertension, obesity, dyslipidemia, and insulin resistance). We had demonstrated that these mice have vascular calcification (VC) of both the intimal atherosclerotic type and medial type. We have shown that VC is worsened by CKD and ameliorated by bone morphogenetic protein -7 (BMP-7). The finding that high-fat-fed low-density lipoprotein receptor null animals without CKD have hyperphosphatemia led us to examine the skeletons of these mice. We found significant reductions in bone formation rates, associated with increased VC and superimposing CKD results in the adynamic bone disorder (ABD), while VC was worsened and hyperphosphatemia persisted. A pathological link between abnormal bone mineralization and VC through the serum phosphorus was demonstrated by the partial effectiveness of directly reducing the serum phosphate by a phosphate binder that had no skeletal action. BMP-7 treatment corrected the ABD and corrected hyperphosphatemia, compatible with BMP-7-driven stimulation of skeletal phosphate deposition reducing plasma phosphate and thereby removing a major stimulus to VC. Thus, in the metabolic syndrome with CKD, a reduction in bone-forming potential of osteogenic cells leads to ABD producing hyperphosphatemia and VC, processes ameliorated by the skeletal anabolic agent BMP-7, in part through increased bone formation and skeletal deposition of phosphate, and in part through direct actions on vascular smooth muscle cells. We have demonstrated that the processes leading to vascular calcification begin with even mild levels of renal injury before demonstrable hyperphosphatemia, and they are preventable and treatable. Therefore, early intervention in CKD is warranted and may affect mortality of the disease.
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PMID:Connections between vascular calcification and progression of chronic kidney disease: therapeutic alternatives. 1633 68


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