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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:[Vascular calcification and phosphate metabolism]. 1577 97

Chronic renal disease is generally appreciated as a major and rapidly growing health problem. In the United States alone, as many as 19.5 million people may have markers of early renal disease, and more than 660,000 people are expected to require renal replacement therapy by the year 2010. By contrast, the presence and pathological role of renal disease in patients with cardiovascular disease are somewhat underrecognized. Evidence now shows that even minor impairments in renal function, as indicated by measures including glomerular filtration rate and microalbuminuria, are common in cardiovascular disease states and predictive of cardiovascular events. Indeed, microalbuminuria may be a marker of systemic vascular disease rather than kidney dysfunction alone. In patients with hypertension, diabetes, metabolic syndrome, acute coronary syndromes, and stroke, markers of renal disease have proved to be at least as predictive of morbidity and mortality as conventional risk factors. Yet, chart reviews in a variety of clinical settings reflect poor recognition and management of renal disease in at-risk patients. Models for renal protection are based on the control of risk factors, particularly blood pressure, that are associated with renal and cardiovascular outcomes. Screening protocols for markers of renal disease should recognize the potential inaccuracy of serum creatinine concentrations and the preferability of glomerular filtration rate estimates that take age and gender into account. Pilot programs for screening high-risk populations have shown efficacy in detecting renal disease.
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PMID:Renal disease in cardiovascular disorders: an underrecognized problem. 1578 15

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.
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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.
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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.
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PMID:Dimethylthetin treatment causes diffuse alveolar lung damage: a pilot study in a sheep model of Continuous Ambulatory Peritoneal Dialysis (CAPD). 1717 48

Diabetes mellitus is one of the most common non-communicable diseases, and is the fifth leading cause of death in most of the developed countries. It can affect nearly every organ and system in the body and may result in blindness, end stage renal disease, lower extremity amputation and increase risk of stroke, ischaemic heart diseases and peripheral vascular disease. Hyperglycemia in diabetes causes non-enzymatic glycation of free amino groups of proteins (of lysine residues) and leads to their structural and functional changes, resulting in complications of the diabetes. Glycation of proteins starts with formation of Shiff's base, followed by intermolecular rearrangement and conversion into Amadori products. When large amounts of Amadori products are formed, they undergo cross linkage to form a heterogeneous group of protein-bound moieties, termed as advanced glycated end products (AGEs). Rate of these reactions are quite slow and only proteins with large amounts of lysine residues undergo glycation with significant amounts of AGEs. The formation of AGEs is a irreversible process, causing structural and functional changes in protein leading to various complications in diabetes like nephropathy, retinopathy, neuropathy and angiopathy. The present review discusses about role of glycation in various complications of diabetes.
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PMID:Non-enzymatic glycation of proteins: a cause for complications in diabetes. 1728 97

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.
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PMID:Hyperhomocysteinemia and polymorphisms of the methylenetetrahydrofolate gene in hemodialysis and peritoneal dialysis patients. 1796 40

Diabetes as the dominant cause of ESRD is also the major cause of renal anaemia. However, most patients with diabetic kidney disease will succumb to co-morbid vascular disease or heart failure before developing severe renal impairment. In these patients, anaemia is also common finding, with a 2-3 times greater prevalence and earlier onset than in patients with renal impairment from other causes. We have recently shown that at least one in five outpatients with type 1 or type 2 diabetes in tertiary referral clinics have anaemia, in whom it constitutes a significant additional burden. Impaired renal erythropoietin release in response to declining haemoglobin levels appears to be the major contributor to anaemia in diabetes. This may be due to the predominance of damage to cells and vascular architecture of the renal tubulointerstitium associated with diabetic nephropathy that may be apparent, like albuminuria, before demonstrable changes in renal function. In addition, systemic inflammation, autonomic neuropathy and reduce red cell survival may also compound anaemia in diabetes. While anaemia may be considered a marker of diabetic kidney disease, reduced haemoglobin levels, even within the normal range, identify diabetic patients with an increased risk of hospitalisation and mortality. Anaemia may also be significant in determining the outcome of heart failure and hypoxia-induced organ damage in patients with diabetes. Upcoming studies will determine whether correction of anaemia in diabetes will lead to improved outcomes in these patients.
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PMID:Anaemia in diabetes: an emerging complication of microvascular disease. 1822 May 87

To ensure our patients are receiving an adequate dose in every dialysis session there must be a target to achieve this in the short or medium term. The incorporation during the last years of the ionic dialysance (ID) in the monitors, has provided monitoring of the dialysis dose in real time and in every dialysis session. Lowrie y cols., recommend monitoring the dose with Kt, recommending at least 40 L in women and 45 L in men or individualizing the dose according to the body surface area. The target of this study was to monitor the dose with Kt in every dialysis session for 3 months, and to compare it with the monthly blood test. 51 patients (58% of our hemodialysis unit), 32 men and 19 women, 60.7+/-14 years old, in the hemodialysis programme for 37.7+/-52 months, were dialysed with a monitor with IC. The etiology of their chronic renal failure was: 3 tubulo-interstitial nephropathy, 9 glomerulonephritis, 12 vascular disease, 7 polycystic kidney disease, 7 diabetic nephropathy and 13 unknown. 1,606 sessions were analysed during a 3 month period. Every patient was treated with the usual parameters of dialysis with 2.1 m2 cellulose diacetate (33.3%), 1.9 m2 polisulfone (33.3%) or 1.8 m2 helixone, dialysis time of 263+/-32 minutes, blood flow of 405+/-66, with dialysate flow of 712+/-138 and body weight of 66.7+/-14 kg. Initial ID, final ID and Kt were measured in each session. URR and Kt/V were obtained by means of a monthly blood test. The initial ID was 232+/-41 ml/min, the final ID was 197+/-44 ml/min, the mean of Kt determinations was 56.6+/-14 L, the mean of Kt/V was 1.98+/-0.5 and the mean of URR was 79.2+/-7%. Although all patients were treated with a minimum recommended dose of Kt/V and URR when we used the Kt according to gender, we observed that 31% of patients do not get the minimum dose prescribed (48.1+/-2.4 L), 34.4% of the men and 26.3% of the women. If we use the Kt individualized for the body surface area, we observe that 43.1% of the patients do not get the minimum dose prescribed with 4.6+/-3.4 L less than the dose prescribed. We conclude that the monitoring of dialysis dose with the Kt provides a better discrimination detecting that between 30 and 40% of the patients perhaps do not get an adequate dose for their gender or body surface area.
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PMID:[Kt as control and follow-up of the dose at a hemodialysis unit]. 1833 26

Paraoxonase is a high-density lipoprotein-associated enzyme and has been shown to reduce the susceptibility to low-density lipoprotein peroxidation. This study aimed to investigate the activity of serum paraoxonase in uremic patients on hemodialysis (HD) and in the predialysis period, and to evaluate the correlations of vascular disease with paraoxonase activity. Thirty patients with chronic renal failure (CRF) undergoing HD (group 1), 30 patients with CRF under conservative treatment (group 2), and 30 healthy controls (group 3) were included. Basal, salt-stimulated, and arylesterase activity were tested by UV spectrophotometry. Serum lipid parameters were determined. B-Mode Doppler ultrasound was used to assess common carotid intima-media thickness (IMT). Basal paraoxonase, salt-stimulated, and arylesterase activity showed no significant difference between group 1 and group 2. However, it was significantly lower in group 1 and in group 2 than controls. Carotid IMT was significantly higher in group 1 than group 2 and both were significantly higher than controls. Basal paraoxonase-1 (PON1), salt-stimulated PON1, and arylesterase activity correlate with BUN, but only basal PON1 and salt-stimulated PON1 correlate with serum albumin. Linear regression showed that the most significant determinant of carotid IMT was PON1 arylesterase activity in group 1 and arylesterase activity and basal PON1 activity in group 2. Patients with CRF, whether under HD or conservative treatment, have reduced basal and stimulated paraoxonase activities, and this could be an important factor causing increased vascular disease in those patients. Modifying this factor can be of great value to protect against this common complication.
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PMID:Paraoxonase-1 (PON1) activity as a risk factor for atherosclerosis in chronic renal failure patients. 1909 Aug 70


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