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)

Renal disease is often associated with an increased risk of vascular events. Moreover, an accelerated form of atherosclerosis commonly occurs in these patients. The reasons for these associations are not clearly defined but include the widespread presence of several established risk factors (eg, dyslipidemia, hypertension, and diabetes). Other predictors of atherosclerotic disease may also be abnormally elevated (eg, homocysteine, fibrinogen, and lipoprotein a). In addition, there is evidence that impaired renal function per se predicts vascular risk. Despite this high-risk background, the potential benefit of treatment with statins has not been widely investigated in these patients. The present review considers the evidence (experimental and clinical) that statins exert beneficial effects in patients with different types of renal disease. This includes improved renal function, decreased microalbuminuria, and a fall in blood pressure. Statins may also improve renal allograft survival. The potential mechanisms mediating these effects are considered. The interactions between statins and several risk factors that may be present in patients with impaired renal function are also considered. There is an urgent need to define the role of statins in these high-risk patients. Which is the statin of choice? This question is relevant because impaired renal function can interfere with statin pharmacokinetics. Furthermore, other drugs administered to these patients may cause serious interactions with statins.
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PMID:Statins and renal function. 1236 55

Diabetes mellitus increases the risk for hypertension and associated cardiovascular diseases, including coronary, cerebrovascular, renal and peripheral vascular disease. The risk for developing cardiovascular disease is increased when both diabetes and hypertension co-exist; in fact, over 11 million Americans have both diabetes and hypertension. These numbers will continue to climb, internationally, since the leading associated risk for diabetes development, obesity, has reached epidemic proportions, globally. Moreover, the frequent association of diabetes with dyslipidemia, as well as coagulation, endothelial, and metabolic abnormalities also aggravates the underlying vascular disease process in patients who possess these comorbid conditions. The renin-angiotensin-aldosterone system (RAS) and arginine vasopressin (AVP) are overactivated in both hypertension and diabetes. Drugs that inhibit this system, such as ACE inhibitors and more recently angiotensin receptor antagonists (ARBs), have proven beneficial effects on the micro- and macrovascular complications of diabetes, especially the kidney. The BRILLIANT study showed that lisinopril reduces microalbuminuria better than CCB therapy. Numerous other long-term studies confirm this association with ACE inhibitors including the HOPE trial. Furthermore, the European Controlled trial of Lisinopril in Insulin-dependent Diabetes (EUCLID) study, showed that lisinopril slowed the progression of renal disease, even in individuals with mild albuminuria. In fact, there are now five appropriately powered randomized placebo-controlled trials to show that both ACE inhibitors and ARBs slow progression of diabetic nephropathy in people with type 2 diabetes. These effects were shown to be better than conventional blood pressure lowering therapy, including dihydropyridine CCBs. In patients with microalbuminuria, ACE inhibitors and ARBs reduce the progression of microalbuminuria to proteinuria and provide a risk reduction of between 38 and 60% for progression to proteinuria. This is important since microalbuminuria is known to be associated with increased vascular permeability and decreased responsiveness to vasodilatory stimuli. Recently, increased AVP levels have been lined to microalbuminuria and hyperfiltration in diabetes. The microvascular and macrovascular benefits of ACE inhibition, ARBs and possible role of AVP antagonists in diabetic patients will be discussed, as will be recommendations for its clinical use.
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PMID:Treatment of the diabetic patient: focus on cardiovascular and renal risk reduction. 1243 44

Patients with end-stage renal disease (ESRD) are at extreme cardiovascular risk. At least half of all patients starting dialysis therapy have overt cardiovascular disease (CVD). In addition, recent studies suggest annual incidence rates for new-onset cardiac failure, peripheral vascular disease, ischemic heart disease (IHD), and stroke of approximately 7%, 7%, 5%, and 1%, respectively. High-level exposure to traditional risk factors, such as smoking and dyslipidemia, hemodynamic overload factors, such as anemia and hypertension, and a myriad of metabolic factors related to uremia are all likely to play a role. There has been explosive growth in observational studies and a heartening, if less dramatic, increase in risk factor intervention trials, suggesting that risk factor modification can lead to meaningful benefit.
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PMID:Clinical epidemiology of cardiac disease in dialysis patients: left ventricular hypertrophy, ischemic heart disease, and cardiac failure. 1264 74

The medical, social, and financial burdens posed by end-stage renal disease (ESRD) are many and growing rapidly. People generally reach ESRD as a result of chronic progressive kidney disease. Advancing kidney disease is associated with several treatable complications, which if poorly managed reduce the length and quality of life. In addition, there are strong links between chronic kidney disease (CKD) and cardiovascular disease (CVD). Many people with less advanced CKD will die or suffer complications of CVD before reaching ESRD. Efficacious interventions, such as lowering blood pressure and treating dyslipidemia, can substantially reduce the progression of both kidney and cardiovascular disease. Careful management of these complex and interrelated diseases and risk factors requires detailed longitudinal and focused care which does not seem to be optimally delivered by health service practitioners organized in traditional ways. A disease management approach offers promise in this setting, but requires further study of clinical and economic impact.
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PMID:Applying multiple interventions in chronic kidney disease. 1264 81

Kidney transplantation is preferred over dialysis for management of end-stage renal disease complicating type I or type 2 diabetes, for those who are eligible. Simultaneous pancreas-kidney (SPK) or pancreas after kidney transplantation (PAK) is an important alternative to kidney transplantation alone for type I diabetes patients if the patient is able to withstand the additional risks of these procedures, because of the benefits of glucose control on other diabetic complications. Pancreas transplantation alone (PTA) is most useful for the treatment of debilitating, frequent hypoglycemia complicating type I diabetes, if renal function is adequate. One-year pancreas graft survival is best after SPK (82%) but has significantly improved after both PAK (74%) and PTA (76%). The I-year kidney graft and patient survival rates after SPK are similar to kidney transplantation alone. Pancreas transplantation normalizes glucose beyond what can be achieved with insulin therapy and has been shown to decrease progression of or improve most, if not all, diabetic end-organ complications using current immunosuppression regimens. However, the diabetologist and endocrinologist should remain involved in the care of the pancreas or kidney transplant recipient for treatment of vascular disease risk factors such as dyslipidemia, surveillance of other diabetic complications including foot ulcers, surveillance and treatment of bone loss, and management of hyperglycemia if it recurs.
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PMID:Pancreas and kidney transplantation. 1264 96

Transplantation is the preferred organ replacement therapy for most patients with end-stage renal disease. Despite impressive improvements over recent years in the treatment of acute rejection, approximately half of all grafts will loose function within 10 years after transplantation. Chronic renal transplant dysfunction, also known as transplant atherosclerosis, is a leading cause of late allograft loss. To date, no specific treatment for chronic renal transplant dysfunction is available. Although its precise pathophysiology remains unknown, it is believed that it involves a multifactorial process of alloantigen-dependent and alloantigen-independent risk factors. Obesity, posttransplant diabetes mellitus, dyslipidemia, hypertension, and proteinuria have all been identified as alloantigen-independent risk factors. Notably, these recipient-related risk factors are well-known risk factors for cardiovascular disease, which cluster within the insulin resistance syndrome in the general population. Insulin resistance is considered the central pathophysiologic feature of this syndrome. It is therefore tempting to speculate that it is insulin resistance that underlies the recipient-related risk factors for chronic renal transplant dysfunction. Recognition of insulin resistance as a central feature underlying many, if not all, recipient-related risk factors would not only improve our understanding of the pathophysiology of chronic renal transplant dysfunction, but also stimulate development of new treatment and prevention strategies.
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PMID:Insulin resistance as putative cause of chronic renal transplant dysfunction. 1266 73

Despite a rapid improvement in dialysis technology during the last 20 years, the mortality rate is still very high in patients with end-stage renal disease (ESRD), and the death rate is comparable with that of many cancer patients with metastases. The main cause of mortality in ESRD is cardiovascular disease (CVD), and cardiac mortality for dialysis patients aged 45 years or younger is more than 100-fold greater than in the general population. The high cardiovascular mortality rate suggests that ESRD patients are subjected to a process of accelerated atherogenesis. Because factors proven to contribute to atherosclerosis in the general population, such as dyslipidemia, smoking, diabetes mellitus, and hypertension are highly prevalent in ESRD patients, it is reasonable to assume that such risk factors also apply to these patients. However, as it has been shown that the high cardiovascular risk in ESRD is incompletely accounted for by traditional risk factors, it may be speculated that nontraditional risk factors, seemingly more difficult to reconcile, also contribute. Among several putative nontraditional risk factors, chronic inflammation has attracted a lot of interest recently because it seems to be associated to both increased vascular oxidative stress and endothelial dysfunction, both of which are important predictors of cardiovascular events in nonrenal patient groups.
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PMID:Interactions between inflammation, oxidative stress, and endothelial dysfunction in end-stage renal disease. 1267 39

Cardiovascular mortality is markedly increased in patients with end-stage renal disease (ESRD), particularly those receiving dialysis. Coronary artery disease is the most important cause of death in these patients. As in the general population, older age, male gender, and the postmenopausal state in women are cardiovascular risk factors in patients with ESRD. However, hypertension, diabetes mellitus, and dyslipidemia, known to promote cardiovascular disease in the general population, are particularly likely to do so in patients with ESRD because of their high prevalence in this population. In addition, nontraditional cardiovascular risk factors, such as hyperhomocystinemia, inflammation, elevated calcium x phosphate product, endothelial dysfunction, and oxidant stress, occur frequently in patients with ESRD. Vigorous treatment of modifiable cardiovascular risk factors has reduced cardiovascular risk in patients without ESRD. The extent to which such risk factor modification would alter cardiovascular risk in ESRD remains uncertain.
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PMID:Risk factors for coronary artery disease in patients with renal failure. 1269 26

To elucidate the relationships between obesity, glycemic control, dyslipidemia, hypertension, microvascular complications, and insulin resistance assessed using an euglycemic hyperinsulinemic clamp technique, we studied 54 hospitalized type 2 diabetic subjects (DM) and 10 age- and sex-matched normotensive, nonobese control subjects (C). Glucose infusion rate (GIR) derived from the clamp study was used as an index of insulin resistance. Body mass index (BMI), the prevalence of hypertension, HbA1c and serum nonesterified fatty acids (NEFA) were significantly higher, and serum high-density-lipoprotein (HDL)-cholesterol was significantly lower in DM than in C (p < 0.05 or less). The median GIR level was significantly lower inDM than in C (p = 0.038). The difference in GIR between the two groups wasstill statistically significant even after adjustment for BMI, mean BP, HbA1c, NEFA, and HDL-cholesterol. However, after simultaneous adjustment for these factors, there was no difference in GIR between the two groups. Body mass index, mean BP, HbA1c, and NEFA showed negative correlations, and serum HDL-cholesterol showed a positive correlation with GIR, but neither age nor duration of diabetes correlated with GIR. When GIR values in DM were divided according to the degree of neuropathy, retinopathy, and nephropathy, and compared to those in C, GIR levels tended to be decreased with increasing severity of each microvascular complication, but there was no difference in median GIR levels among the diabetic subgroups. Relationships between the GIR levels and confounding factors such as age, sex, BMI, mean BP, HbA1c, serum NEFA, and serum HDL-cholesterol, were examined simultaneously with a multiple regression analysis. This analysis revealed that HbA1c and serum NEFA may affect the GIR level. Furthermore, together with these two factors, the relationships between the GIR levels and the severity of each microvascular complication were explored with the same analysis. This model clearly demonstrated that both the decreased CVR-R and pronounced orthostatic fall in systolic BP were independent factors for the decreased GIR. These findings suggest that marked autonomic dysfunction, rather than other confounding factors, is related to increased insulin resistance in DM.
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PMID:Insulin resistant state in type 2 diabetes is related to advanced autonomic neuropathy. 1271 78

Patients with end-stage renal disease (ESRD) treated with dialysis have a dramatically elevated rate of cardiovascular disease (CVD) compared to the general population. Lipid-lowering therapy with 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors ("statins") has been shown to markedly reduce cardiovascular risk in patients without renal failure, but their effect has not been fully studied in the dialysis population. In this article we will first discuss the known benefits of statin therapy in the general population and summarize the current guidelines for such therapy. We will then examine the evidence linking dyslipidemia and cardiac disease in the dialysis population and discuss possible pathophysiologic mechanisms by which statins could prevent cardiac disease in these patients. We will also review prior clinical studies of the effects of statins in patients on dialysis, with particular attention to the safety and efficacy of these drugs in this population. Finally, we will review how statins are currently being used in the care of dialysis patients and suggest whether an expanded utilization of these drugs could help reduce the enormously high rates of cardiac disease in this patient population.
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PMID:Are HMG-CoA reductase inhibitors underutilized in dialysis patients? 1275 74


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