Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Despite significant progress in renal replacement therapy, the mortality from cardiovascular disease (CVD) in patients with chronic renal failure (CRF) is many times higher than in the general population. The traditional risk factors are frequently present in CRF patients. However, based upon conventional risk factor analysis, these factors do not fully explain the extraordinary increase in morbidity and mortality in CVD among patients with CRF. Accumulating evidence suggests that CRF is associated with impaired endothelial cell function. In recent years, the role of endothelial dysfunction (ED) and excessive oxidative stress (OS) in the development of CVD has been highlighted. ED is an early feature of vascular disease in different diseases such diabetes, hypertension, hypercholesterolemia, and coronary heart disease. The precise mechanism which induces ED is not clear. Several factors however, including OS-related accumulation of uremic toxins, hypertension and shear stress, dyslipidemia with cytotoxic lipoprotein species such as small, dense low-density lipoprotein (LDL) particles, competitive inhibition of endothelial nitric oxide (NO) by increased production by asymmetrical dimethylarginine (ADMA) are pathogenic. In addition, it is known that excessive OS causes ED. An overproduction of reactive oxygen species (ROS) may injure the endothelial cell membrane, inactivate NO, and cause oxidation of an essential cofactor of nitric oxide synthase (NOS). Recent studies have demonstrated that an impaired endothelium-dependent vasodilation and OS are closely related to each other in patients with CRF.
 ...
PMID:Endothelium-dependent vasodilation and oxidative stress in chronic renal failure: impact on cardiovascular disease. 1269 8

Exposure to organic solvents has been suggested to cause or exacerbate renal disease, but methodologic concerns regarding previous studies preclude firm conclusions. We examined the role of organic solvents in a population-based case-control study of early-stage chronic renal failure (CRF). All native Swedish residents aged 18 to 74 yr, living in Sweden between May 1996 and May 1998, formed the source population. Incident cases of CRF in a pre-uremic stage (n = 926) and control subjects (n = 998), randomly selected from the study base, underwent personal interviews that included a detailed occupational history. Expert rating by a certified occupational hygienist was used to assess organic solvent exposure intensity and duration. Relative risks were estimated by odds ratios (OR) in logistic regression models, with adjustment for potentially important covariates. The overall risk for CRF among subjects ever exposed to organic solvents was virtually identical to that among never-exposed (OR, 1.01; 95% confidence interval [CI], 0.81 to 1.25). No dose-response relationships were observed for lifetime cumulative solvent exposure, average dose, or exposure frequency or duration. The absence of association pertained to all subgroups of CRF: glomerulonephritis (OR, 0.96; 95% CI, 0.68 to 1.34), diabetic nephropathy (OR, 1.02; 95% CI, 0.74 to 1.41), renal vascular disease (OR, 1.16; 95% CI, 0.76 to 1.75), and other renal CRF (OR, 0.92; 95% CI, 0.66 to 1.27). The results from a nationwide, population-based study do not support the hypothesis of an adverse effect of organic solvents on CRF development, in general. Detrimental effects from subclasses of solvents or on specific renal diseases cannot be ruled out.
 ...
PMID:Absence of association between organic solvent exposure and risk of chronic renal failure: a nationwide population-based case-control study. 1469 71

Patients with end-stage renal disease have a high mortality, with the majority of deaths due to vascular disease. The prevalence of vascular risk factors and vascular disease in predialysis chronic renal failure (CRF) is poorly characterized. The aim of the present study was to determine the prevalence of vascular risk factors and clinically overt vascular disease in an Australian cohort of patients with predialysis CRF. We performed a retrospective chart review of outpatients with CRF and noted demographic data, the cause of renal failure, the presence or otherwise of vascular risk factors and vascular disease and calculated glomerular filtration rate. The prevalence of overt vascular disease and modifiable vascular risk factors was calculated. One hundred and eighty patients completed the study. Eighty-nine per cent of patients had hypertension, 68% had dyslipidaemia, 32% were diabetic and 38% were previous smokers. The subgroup with diabetic nephropathy had significantly more risk factors (P < 0.001) than other groups. Twenty-seven per cent of the group had cardiovascular disease, 22% had cerebrovascular disease, 23% had peripheral vascular disease and 9% had renal artery stenosis. Patients with ischaemic nephropathy had significantly more vascular disease than other groups (P < 0.001). Patients with overt vascular disease were older, had a higher number of risk factors and a higher calcium phosphate product than those without vascular disease. In conclusion, the present study suggests a high prevalence of vascular risk factors and vascular disease in predialysis CRF. Early detection provides an opportunity for early intervention and may help reduce the development of vascular disease, and the associated mortality, once these patients progress to dialysis.
 ...
PMID:Prevalence of vascular risk factors and vascular disease in predialysis chronic renal failure. 1501 97

Patients with chronic kidney disease (CKD) have a substantially increased risk of cardiovascular disease (CVD) compared with the general population. The high prevalence of established traditional risk factors for atherosclerosis (diabetes, hypertension, dyslipidemia) in these patients undoubtedly contributes to the accelerated rate of vascular disease. In addition, several hypotheses have emerged to explain the high prevalence of CVD in patients with chronic renal failure. Growing evidence has been gathered over the last 15 years regarding the role of uremia-related risk factors such as inflammation and oxidant stress in the pathogenesis of atherosclerosis in subjects with renal failure. This paper will review current knowledge regarding the potential role of these non-traditional or uremia-related risk factors for atherosclerosis with special emphasis on prevalence, cardiac risk, and management in patients with CKD.
 ...
PMID:[Vascular risk factors and renal failure]. 1558 63

Hypoalbuminemia is the result of the combined effects of inflammation and inadequate protein and caloric intake in patients with chronic disease such as chronic renal failure. Inflammation and malnutrition both reduce albumin concentration by decreasing its rate of synthesis, while inflammation alone is associated with a greater fractional catabolic rate (FCR) and, when extreme, increased transfer of albumin out of the vascular compartment. A vicious cascade of events ensues in which inflammation induces anorexia and reduces the effective use of dietary protein and energy intake and augments catabolism of the key somatic protein, albumin. Hypoalbuminemia is a powerful predictor of mortality in patients with chronic renal failure, and the major cause of death in this population is due to cardiovascular events. Inflammation is associated with vascular disease and likely causes injury to the vascular endothelium, and hypoalbuminemia as two separate expressions of the inflammatory process. Albumin has a myriad of important physiologic effects that are essential for normal health. However, simply administering albumin to critically ill patients with hypoalbuminemia has not been shown to improve survival or reduce morbidity. Thus the inference from these clinical studies suggests that the cause of hypoalbuminemia, rather than low albumin levels specifically, is responsible for morbidity and mortality.
 ...
PMID:Serum albumin: relationship to inflammation and nutrition. 1566 May 73

Vascular calcification is often encountered in the development of atherosclerotic intimal lesions. In chronic renal failure patients, vascular calcification contributes to both the morbidity and mortality. Although the molecular mechanisms regulating vascular calcification remain obscure, recent studies suggest that vascular calcification may be an actively regulated process in which vascular cells may acquire osteoblast-like functions. Several clinical studies indicate that a high serum phosphate level is highly correlated with the extent of vascular calcification and vascular disease. In vitro studies demonstrated that inorganic phosphate regulates the expression of bone matrix proteins, and that calcification is regulated by inorganic phosphate through a sodium dependent phosphate transport system. These findings suggest that inorganic phosphate may play an important role in the development of vascular calcification.
 ...
PMID:[Vascular calcification and phosphate metabolism]. 1577 97

Glycation adducts formed in the later stages of protein glycation reactions, advanced glycation endproducts (AGEs), are a class of uraemic toxin. Protein glycation was viewed originally as a post-translational modification that accumulated mostly on extracellular proteins. We now know that AGE residues are also formed on short-lived cellular and extracellular proteins. Cellular proteolysis forms AGE free adducts from these proteins, which are released into plasma for urinary excretion. AGE free adducts are also absorbed from food. AGE free adducts are the major molecular form by which AGEs are excreted in urine. They normally have high renal clearance, but this declines markedly in chronic renal failure patients, leading to profound increases in plasma AGE free adducts. Accumulation of plasma AGE free adducts is increased further in end stage renal disease patients on peritoneal dialysis and haemodialysis by increased AGE formation. The impact of AGEs absorbed from food is probably most marked for undialysed patients with mild uraemia. The toxicity of AGEs has been associated with resistance of the extracellular matrix to proteolysis and AGE receptor-mediated responses. AGE free adducts may also contribute to vascular disease in uraemia. They represent an important new age for glycation research in nephrology.
 ...
PMID:Glycation free adduct accumulation in renal disease: the new AGE. 1613 53

Ischemic nephropathy is an independent pathway towards end-stage renal disease. Its prevalence is estimated to be significant and increasing among populations with vascular disease, hypertension, and chronic renal failure. Angiography remains the gold standard for evaluation of ischemic nephropathy; however, selection by clinical criteria and noninvasive screening with ultrasound are recommended for most patients. Surgical revascularization of ischemic kidneys can halt or reverse deterioration of renal function and is preferable to medical treatment. Direct comparison of angioplasty and stent placement with surgery is needed.
 ...
PMID:Ischemic nephropathy. 1703 55

Total plasma homocysteine (Hcy) concentration correlates with risk of vascular disease. Over 80% of chronic renal failure patients have elevated plasma Hcy and a 10-20 times higher incidence of vascular disease. Glycine betaine lowers plasma Hcy through methylation catalysed by betaine-homocysteine methyltransferase (BHMT). Dimethylthetin (DMT), a synthetic glycine betaine analogue, is a more effective BHMT substrate. DMT is therefore a potential therapeutic agent for reducing plasma Hcy in humans and may be particularly useful in renal failure patients receiving dialysis because of chronic betaine depletion as a result of treatment. We aimed to determine whether the addition of DMT to dialysis fluid lowered plasma Hcy concentrations in a Continuous Ambulatory Peritoneal Dialysis sheep model using animals that were either in acute renal failure (n=3) or had normal renal function (n=1). Sub-acute exposure to DMT was toxic to all four animals, which died with total lung consolidation and collapse and Diffuse Alveolar Damage within 48 h of beginning treatment. Adverse side effects were observed after 4-8 doses. DMT was not detected in pre-dialysis plasma samples and the final concentration at death was 0.5-7.8 mmol/L, depending on the number of doses each animal was exposed to. Abnormalities were not observed in animals supplied standard dialysis fluid, or fluid with added glycine betaine. Toxicity associated with DMT treatment raises concerns for its use in further studies. However, sub-acute administration of DMT to sheep may provide a useful model of acute alveolar damage.
 ...
PMID:Dimethylthetin treatment causes diffuse alveolar lung damage: a pilot study in a sheep model of Continuous Ambulatory Peritoneal Dialysis (CAPD). 1717 48

Hyperhomocysteinemia has been documented in chronic renal failure (CRF). Premature as well as progressive occlusive vascular disease is common. Mutations or polymorphisms in the gene of the enzyme methylenetetrahydrofolate reductase (MTHFR), as C677T, A1298C and G1793A, are associated with hyperhomocysteinemia and possibly with elevated risk for vascular diseases. This study was conducted on 89 individuals with renal failure on dialysis to determine the allelic and genotypic frequencies of the mutations in the MTHFR gene and hyperhomocysteinemia. Blood samples were colleted for determination of homocysteine and DNA. The C677T, A1298C and G1793A mutations were detected. This study confirmed the high prevalence of hyperhomocysteinemia in patients on dialysis, which was diagnosed in 76 patients (85.39%) and high incidence of the C677T and A1298C mutation, 42 (47.19%) and 29 (32.58%) patients, respectively. Five patients (5.62%) presented the G1793A mutation and hyperhomocysteinemia. The authors concluded that there was no influence of the polymorphisms on homocysteine levels in these patients.
 ...
PMID:Hyperhomocysteinemia and polymorphisms of the methylenetetrahydrofolate gene in hemodialysis and peritoneal dialysis patients. 1796 40


<< Previous 1 2 3 4 5 6 7 8 9 Next >>