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 incidence of chronic kidney disease (CKD) in the U.S. continues to increase, and now over 10% of the U.S. population has some form of CKD. Although some patients with CKD will ultimately develop renal failure, most patients with CKD will die of cardiovascular disease before dialysis becomes necessary. Patients with CKD have major proatherogenic lipid abnormalities that are treatable with readily available therapies. The severe derangements seen in lipoprotein metabolism in patients with CKD typically results in high triglycerides and low high-density lipoprotein (HDL) cholesterol. Because of the prevalence of triglyceride disorders in patients with CKD, after treating patients to a low-density lipoprotein goal, non-HDL should be calculated and used as the secondary goal of treatment. A review of the evidence from subgroup analysis of several landmark lipid-lowering trials supports treating dyslipidemia in mild to moderate CKD patients with HMG-CoA reductase inhibitors. The evidence to support treating dyslipidemia in hemodialysis patients, however, has been mixed, with several outcome trials pending. Patients with CKD frequently have mixed dyslipidemia and often require treatment with multiple lipid-lowering drugs. Although statins are the cornerstone of therapy for most patients with CKD, differences in their pharmacokinetic properties give some statins a safety advantage in patients with advanced CKD. Although most other lipid-lowering agents can be used safely with statins in combination therapy in patients with CKD, the fibrates are renally metabolized and require both adjustments in dose and very careful monitoring due to the increased risk of rhabdomyolysis. After reviewing the safety and dose alterations required in managing dyslipidemia in patients with CKD, a practical treatment algorithm is proposed.
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PMID:Managing dyslipidemia in chronic kidney disease. 1989 3

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

The natural history of most chronic kidney diseases (CKD) indicates that glomerular filtration gradually declines over time, progressing to more advanced stages of kidney failure. Since the publication of the first studies by the Modification of Diet in Renal Disease (MDRD) Study Group, numerous factors have been identified that can accelerate this progression. Some are dependent on the etiology, but other are common to all and may accelerate progression of kidney disease: Non-modifiable progression factors for CKD: - Etiology of kidney disease - Degree of initial kidney function - Gender - Age - Ethnicity/Other genetic factors - Birth weight Modifiable progression factors for CKD: - Proteinuria - High blood pressure - Poor glycemic control in diabetes - Smoking - Obesity - Metabolic syndrome/Insulin resistance - Dyslipidemia - Anemia - Metabolic factors (Ca/P, uric acid) - Use of nephrotoxic drugs. Therapeutic intervention on these factors has shown that it reduce the rate of progression of CKD (Strength of Recommendation A).There is no clear evidence that correction of these factors slows CKD (Strength of Recommendation C), although it has been shown to have a beneficial effect on cardiovascular risk at other levels.
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PMID:[Progression factors for chronic kidney disease. Secondary prevention]. 1901 33

Metabolic syndrome (MS) encompasses a series of diseases which, when combined, increase vascular risk more than the sum of their individual risks. Insulin resistance (IR) is one of the basic components of MS. - Abdominal fat distribution is an IR marker and is associated to factors increasing vascular risk such as dyslipidemia, high blood pressure, and hyperglycemia, components of the so-called metabolic syndrome. - IR is related to glomerular sclerosis and renal failure through several mechanisms, Including genetic and environmental factors, and stimulation of the renin-angiotensin-aldosterone system. - IR usually precedes development of DM, and therefore contributes to its early identification. MS increases the risk of chronic complications from DM and is associated to an increased prevalence of cardiovascular disease, particularly coronary heart disease, increasing mortality from this cause. - The presence of MS in DM2 is usually associated to a greater prevalence of microalbuminuria or proteinuria and peripheral polyneuropathy.
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PMID:[Metabolic syndrome and kidney disease]. 1901 36

Accelerated cardiovascular disease (CVD) is a frequent complication of renal disease. Chronic kidney disease (CKD) develops hypertension and dyslipidemia, which in turn can contribute to the progression of renal failure. There is general agreement that endothelin-1 (ET-1), which acts through the two subtypes of receptor ET(A) and ET(B), plays important physiological roles in the regulation of normal cardiovascular function and that excessive ET-1 production is linked to CVD and CKD. Although selective ET(A) or nonselective ET(A)/ET(B) receptor antagonisms have been recognized as a potential strategy for treatment of several cardiovascular disease, it remains unclear which of the antagonisms is suitable for the individuals with CKD because upregulation of the nitric oxide (NO) system via ET(B) receptor is responsible for renal function such as natriuresis, diuresis, and glomerular hemodynamics. Our findings clearly indicate that the blockade of ET receptors, in particular ET(A)-receptor antagonism, not only produces a potential renoprotective effect in CKD but also reduces the risk of CVD. In contrast, pharmacological blockade or genetic deficiency of ET(B) receptor seems to aggravate CKD and CVD in several experimental models of rats. Moreover, preliminary evidence in patients with CKD also suggests that both selective ET(A)- and nonselective ET(A)/ET(B)-receptor blockade decreases blood pressure but that selective ET(A) blockade has additional desirable effects on renal hemodynamics. Thus, at least in CKD, these findings support the notion that ET(B) receptor-mediated actions produce a renoprotective effect and that nonselective ET(A)/ET(B)-receptors blockade seem to offer no advantage over selective ET(A) antagonism, and if anything may potentially reduce the benefits.
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PMID:Drug discovery for overcoming chronic kidney disease (CKD): the endothelin ET B receptor/nitric oxide system functions as a protective factor in CKD. 1915 34

Living donor kidney transplantation (KT) is the treatment of choice for end-stage renal disease patients and exhaustive assessment of the potential live kidney donor leads to successful KT in most occasions. Diabetes mellitus (DM), hypertension and obesity make up contraindications to donation because all of them are associated with postsurgical complications and future development of renal failure and cardiovascular (CV) disorders. However, it is unclear how much risk there is for individuals who donate a kidney and then develop some of these complications, which are grouped under the metabolic syndrome (MS.) Indeed, MS is a cluster of CV risk factors such as obesity, dyslipidemia, hypertension where the insulin resistance is the pathogenic mainstay. MS is an entity very prevalent in the western countries (20-30%) and has been associated with the development of CV disorders, DM and renal disease. Thus, it is crucial to detect MS before living donation in order to avoid these complications in the long-term. Regardless of clinical criteria to diagnosis MS, both oral glucose tolerance test and HbA1c levels may be useful clinical tools for unmasking MS before donation. Moreover, determination of insulin resistance by HOMA could help to achieve this objective. This review will outline the next issues: 1) frequency of MS in the general population (potentially, living kidney donor); 2) the impact of MS on DM, renal function and other CV complications; 3) assessment of living donor to unmask MS before donation; and 4) interventions on risk factors for minimizing MS-related threatening complications in the long-term. In any case, if MS is detected prior to donation, prophylactic and therapeutic measurement should be performed to avoid its progression. By contrast, MS could be considered a contraindication to donation.
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PMID:[Metabolic syndrome and live kidney donor: is this syndrome a contraindication to donation?]. 1924 Jul 68

Cardiovascular disease is a frequent complication of renal failure and is the most common cause of death in patients with chronic kidney disease (CKD). Accelerated atherogenesis has been widely documented in CKD and diabetic nephropathy is the leading cause of renal failure worldwide. Furthermore, CKD promotes hypertension and dyslipidemia, which in turn may contribute to the progression of renal failure. All together, hypertension, dyslipidemia and diabetes are considered major risk factors for the development of endothelial dysfunction and progression of atherosclerosis. Elevated inflammatory mediators and activation of the renin-angiotensin system contribute through enhanced production of reactive oxygen species, to atherogenesis in CKD. Vascular calcification is also important. Calcification of arteries occurs in the intima in association with atherosclerosis, where it may contribute to plaque formation, and in the media, where it causes stiffening. Increased serum levels of calcification promoters, such as hyperphosphatemia, and a decrease in circulating and local inhibitors of calcification, favor vascular calcification. On the other hand, transdifferentiation of vascular smooth muscle cells to osteblast-like cells would be the pivotal event in calcification. Bone morphogenetic protein agonists and antagonists are playing a role in this osteogenic differentiation. Accelerated atherosclerosis and media calcification will then lead to increased prevalence of coronary artery disease, heart failure, stroke, and peripheral arterial disease. Prevention and treatment of cardiovascular disease are major considerations in the management of individuals with CKD.
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PMID:[Vascular damage in chronic kidney disease]. 1930 81

Renal failure in the elderly is currently underestimated and presents a real challenge for the public health system. Kidney function must be routinely assessed by creatinine clearance, estimated with either the Cockcroft and Gault formula or the simplified MDRD formula, which appears especially appropriate for the elderly. Normal kidney aging is related to tissue and functional changes that make older patients very vulnerable to environmental modifications. Numerous factors can accelerate the impairment of rental function during aging. Some of them cannot be modified: sex, genome, and initial kidney disease. Most of them can be managed or treated: hypertension, diabetes mellitus, obesity, smoking, dyslipidemia, proteinuria, and the presence of oxidation and glycation products. Chronic renal failure in the elderly must be managed early with strict treatment targets to avoid the development of end-stage renal disease. Inhibitors of the renin-angiotensin-aldosterone system play an essential role in optimizing nephroprotection: control of hypertension, diabetes complications, and proteinuria. They should be prescribed very carefully in older patients. Age is not a prerequisite for consultations with nephrologists, which should take place early so that nephroprotection can still be useful.
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PMID:[Renal aging: risk factors and nephroprotection]. 1930 36

Extrarenal calcifications, particularly affecting the cardiovascular system, are common observations which can be a source of serious complications in patients with chronic renal disease, especially those on dialysis. In these patients, cardiovascular disease - myocardial infarction, arrhythmia, calcified valvulopathy, stroke, peripheral ischemic arteriopathy, calciphylaxy, etc. - is the leading cause of death (more than 50%). These complications are closely related to the presence of vascular calcifications (VC) which are much more frequent, severe, and progressive than in the general population. Previously, these calcifications were considered to arise via a passive process within the context of comorbid conditions without specific signs of gravity: high blood pressure, atherosclerosis, aging, diabetes, smoking, dyslipidemia, chronic micro-inflammation, hyperhomocysteinemia, disorders of calcium-phosphorus metabolism. It is now established that VC arise via a complex, probably regulated, active process analogous to the processes leading to bone formation and/or remodeling. New insight provided by a large body of work designed to ascertain the mechanisms underlying the onset of VC has enabled the development of new diagnostic and therapeutic approaches. It is now possible to identify factors clearly favoring the formation of VC: TNF-alpha (which stimulates cell necrosis/apoptosis), CRP, oxidized lipids, AGEs, leptin, inorganic phosphate, high calcium-phosphorus product (CaxPO(4)), calcium, 1,25-OH(2)D(3) and Vitamin D(3), PTHrP (via an intracrine pathway), cyclic AMP, TGF-beta, bone morphogenic protein 2 (BMP2) and factors protective against the formation of VC: magnesium, HDL, inorganic pyrophosphate, albumin, ahsg/fetuin A, osteopontin (OPN), osteoprotegerin (OPG), osteonectin (ON), bone morphogenic protein 7 (BMP7), klotho, PTHrP (via a paracrine pathway), matrix gla protein (MGP), PTH (via Msx2) and vitamin K. In conclusion, until recently, neglected disorders of calcium-phosphorus metabolism are currently recognized as the main actors in the process leading to vascular mediacalcosis in patients with chronic kidney failure.
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PMID:[Origin of the mediacalcosis in kidney failure]. 1934 26

Dyslipidemia, often present in patients with metabolic syndrome and chronic kidney disease, contributes to increased cardiovascular risk and progression of renal impairment. In these patients, the probability of death from cardiovascular complications is higher than death consequent to terminal renal failure. Positive neuroprotective effects ofstatins and fibrates are being attributed to hypolipidemic as well as other, lipid-unrelated, properties. Statins are able to slow down the decline in glomerular filtration rate and may decrease proteinuria. Nevertheless, conclusive evidence that statins decrease the incidence of cardiovascular complications in patients with advanced chronic kidney disease is still lacking. Through their effect on albuminuria, fibrates contribute to slowing down ofthe progression of diabetic nephropathy. Controlled trials and clinical practice have shown that monotherapy with statins as well as fibrates is safe. Management of combined dyslipidemia requires, apart from the selection of a suitable statin-fibrate combination, careful monitoring of potential adverse effects and treatment tolerability and compliance. The results of the Czecho-Slovakian pivot study KOLCHRI have demonstrated the efficacy and safety of fenofibrate combined with low dose statin in patients with metabolic syndrome and stage 2-4 chronic kidney disease.
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PMID:[Treatment of dyslipidemia in patients with metabolic syndrome and chronic kidney disease]. 1973 74


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