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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

HMG-CoA reductase inhibitors have been proven effective in decreasing the plasma cholesterol levels in patients affected with various forms of hypercholesterolemia, familial dysbetalipoproteinemia, familial combined hyperlipidemia and in nephrotic and diabetic dyslipidemia. The purpose of this study was to monitor and evaluate the efficiency and safety of the therapy with simvastatin, an HMG-CoA reductase inhibitor, in a group of patients treated by continuous ambulatory peritoneal dialysis (CAPD) with severe hypercholesterolemia. Monitoring of the changes occurring in the various lipids and apolipoproteins in these patients included the measurements of the plasma lipids and apolipoproteins A-I, A-II, B, C-II, A-IV and Lp(a). Lipoproteins were separated by gel filtration, on a Superose 6HR column, before and after 24 weeks of treatment. The patterns were compared to those observed in a group of primary hyperlipidemic patients treated with Lovastatin, a compound of the same class. The drug was well tolerated by the CAPD patients and no adverse reaction was observed. In addition to the decrease of the total and LDL cholesterol, similar to that reported in other groups of patients, we further observed a decrease of the apo E concentration in both the CAPD and the hyperlipidemic patients. This decrease was especially pronounced in the HDLE fraction and could involve an upregulation of the apo B-E and/or apo E receptor. These results should provide information about the mechanism of action of this drug in patients with end-stage renal disease.
Atherosclerosis 1991 Feb
PMID:Effect of simvastatin treatment on the dyslipoproteinemia in CAPD patients. 187 12

Diabetics have an increased risk of cardiovascular morbidity and mortality. Compelling evidence suggests that there is cause-effect relationship between alterations of serum lipids and lipoproteins, and atherosclerosis and coronary heart disease in non diabetic-population. Among insulin dependent diabetics, the prevalence of macrovascular disease is particularly increased in those with established clinical nephropathy and it has been partly attributed to concomitant hypertension and serum lipoprotein abnormalities. However, the effect of diabetic nephropathy and factors associated with it on Coronary Artery Disease (CAD) appears to be conditional. Many Patients in many studies did not have CAD despite a long duration of persistent proteinuria and renal failure There is the possibility that CAD is an outcome of a multistage process, and diabetes related conditions may accelerate progression through certain stage only. In that case, the pattern of appearance of CAD would be determined by the natural history of atherosclerosis rather than by duration of diabetes. The purpose of our study is to analyze retrospectively the incidence of CAD and its association with blood pressure, serum total cholesterol, HDL cholesterol, duration of diabetes, serum triglycerides and HbAlc in a cohort of insulin dependent diabetic patients without nephropathy.
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PMID:"Cardiovascular risk factors in insulin dependent diabetes". 192 85

The nephrotic syndrome comprises proteinuria, oedema, albuminuria, hypoalbuminaemia, and hyperlipidaemia. Some of its manifestations are present throughout the course of progressive renal disease. Hyperlipidaemia is one of the most dramatic of the clinical manifestations of the syndrome, but has not been seen as relevant to the progression of renal disease. Recently, however, increasing interest has been shown in the lipid abnormalities of patients with persistent proteinuria, largely as a result of experimental data which have emphasised the connection between progressive disease and hyperlipidaemia in animal models. This review considers some aspects of the metabolic background against which the pathological changes in animal models of nephrotic syndrome take place. Attention is drawn to analogies between glomerular disease and atherosclerosis. Lack of information on the value of long-term lipid lowering therapy in patients with proteinuria, hyperlipidaemia, and progressive renal disease emphasises the need for long-term studies of lipid-lowering therapy in these individuals. A conceptual framework for understanding the role of lipids is discussed in relation to the underlying disease processes and possible therapeutic approaches in man.
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PMID:Lipids and progressive kidney disease. 204 69

It is proposed that the systemic hyperinsulinemia and hepatic portal hypoinsulinemia that occurs with conventional injectable preparations of insulin currently used in the treatment of patients with diabetes mellitus is largely responsible for the morbidity associated with this disease. Epidemiological evidence and animal experimentation strongly support systemic hyperinsulinemia as a major factor in genesis of atherosclerosis in diabetic patients. In addition, in vitro studies demonstrate a direct effect of insulin on endothelial cell and arterial smooth muscle proliferation. On the other hand, inadequate hepatic delivery of insulin is associated with overproduction of renal vasoregulatory factors leading to glomerular hyperfiltration and ultimately to glomerulosclerosis and its clinical endpoint--end-stage renal disease. In the absence of widespread success of pancreatic and islet-cell transplantation as a means to deliver insulin physiologically into the hepatic portal circulation, methods must be devised and perfected to accomplish such delivery using approaches such as orally administering insulin in intestinal-enzyme protected capsules. Until such methods of delivery are available for safe and widespread use, one should abandon the illusory goal of rigid glucose control in favor of methods that reduce insulin requirement. Along these lines, dietary restriction and aerobic exercise should be the major life style changes advised for diabetic patients. Reduction of glomerular hyperfiltration in diabetic patients can be promoted with the use of low protein diets and/or angiotensin converting enzyme inhibitors.
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PMID:Hypothesis: insulin is responsible for the vascular complications of diabetes. 205 21

The precise pathogenesis of human diabetic kidney disease and the factors responsible for the susceptibility to it remain to be established. However, there is now evidence that renal disease clusters in families and that genetic factors are of central importance in determining liability. A predisposition to arterial hypertension has been suggested as playing a contributory role in the development of kidney disease. Genetically controlled hypertrophic processes may be implicated in the susceptibility to arterial wall damage and glomerular injury in diabetes. This suggestion derives from the observation that the fibroblasts of patients with diabetic nephropathy show a higher Na+/H+ antiport activity and a greater 3H-thymidine incorporation into DNA than fibroblasts of diabetic patients without nephropathy. The first sign of renal damage is the appearance of microalbuminuria and of a small elevation in arterial pressure, changes associated with significant mesangial expansion. Microalbuminuria is associated with abnormalities of lipoprotein profiles possibly as a consequence of insulin-resistance-induced hyperinsulinemia. It could be postulated that the environmental changes brought about by diabetes lead in susceptible individuals to increased systemic and intraglomerular pressure on the one hand and mesangial expansion on the other. These two processes would cause proteinuria and glomerulosclerosis. Lipid abnormalities would further aggravate the renal histological damage and, in combination with hypertension, contribute to the accelerated atherosclerosis typical of patients with diabetic kidney disease. A vicious circle would thus be triggered of reduction in renal function, more hypertension, more proteinuria, more glomerular obsolence, more hyperlipidemia and eventually end-stage renal failure or premature cardiovascular death.
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PMID:Mechanisms of diabetic renal and cardiovascular disease. 207 90

Atherosclerosis is more common and severe in DM. The purpose of this study was to compare the blood lipids profile and the prevalence of different coronary risk factors (CRF) in a mexican population with CHD (coronary heart disease) and DM compared with non DM patients. All had a history of myocardial infarction. Patients with nephropathy or other secondary causes of dyslipidema were excluded. There were two groups of 45 patients, 32 males, 13 females; age was 60 +/- 1 (SEM), body mass index (BMI) 26 +/- 6. Diabetes duration was 10 +/- 1 years. Diabetic individuals referred smoking in 58%, high blood pressure 55%, obesity (IQ greater than 27) 42%. There were no statistical differences with the non DM group. The mean values of total cholesterol, LDL cholesterol and triglycerides were similar in diabetics and non diabetics. HDL cholesterol was significantly lower in diabetic females (p less than 0.01). Hypoalphalipoproteinemia (HDL-C less than or equal to 30 mg/dL) was the most common abnormality in both groups (52% DM vs 38% nonDM) (p less than 0.01) Type IV phenotype was present in 40 vs 29% (NS). Lipid values were not related to BMI, metabolic control or diabetes type of treatment. To conclude, non insulin dependent diabetic patients with CHD have a high prevalence of CRF. Lipid abnormalities, particularly hypoalphalipoproteinemia and hypertriglyceridemia, could be a cause for the increased atherogenic risk, particularly in females.
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PMID:[Diabetes mellitus and ischemic cardiopathy: their relation to changes in plasma lipids and other coronary risk factors]. 209 Nov 76

Today hyperuricaemia and gout are likewise seen in every population of the western industrial world and have been increasing since the fifties. As known from number of studies hyperuricaemia often occurs in connection with hyperlipoproteinaemia, obesity, diabetes mellitus, arterial hypertension and atherosclerosis. Up to now it was not clear whether one disease caused the other. In 1988 Abbot could prove that among men, those afflicted by gout as compared to those without gout experienced a 60% excess of coronary heart disease. Therefore, patients with gout should receive a regular thorough cardiovascular evaluation. Furthermore risk factor levels which predispose to coronary heart disease, arterial hypertension and gout should be reduced. There is a significant positive correlation between the plasma uric acid levels and the prevalence of attacks of gouty arthritis and nephrolithiasis. It is possible to avoid gouty arthritis, tophi and nephrolithiasis with a consequent diet and medical treatment. Unfortunately, many patients interrupt therapy during intervals free of pain. The consequence is that even today the complications of hyperuricaemia cause days of inability to work and to earn one's living, despite of modern therapy. Hyperuricaemia not sufficiently treated reduces the quality of life through attacks of gout, chronic gout and nephrolithiasis as well as life expectancy caused by nephropathy, arterial hypertension and atherosclerosis. This is of special importance because of the frequency of gout and hyperuricaemia in our population. An early diagnosis, a consistent therapy and a thorough monitoring could stop an increase of this disease and prolong life expectancy for those who have gout and the other attendant diseases.
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PMID:[Hyperuricemia--does modern therapy improve life expectancy?]. 227 73

The present study has indicated that significant shifts in plasma, urinary, and tissue taurine and in non-taurine dialyzable amines occur in the STZ-induced diabetic rat, especially in the kidney. Taurine administration at relatively low dosage ameliorated only kidney taurine concentration. Anticipated alterations in plasma glucose and creatinine were observed but neither of these changes was affected by taurine administration. Similarly, urinary output of creatinine, glucose, and NAG increased significantly among diabetic rats, but none of these were detectably influenced by taurine. Increases in plasma triglycerides observed in STZ-induced diabetes appear to be attenuated by taurine administration, and although cholesterol concentrations were lower in taurine-treated rats, the differences were not statistically significant. These findings should encourage further studies of these effects in rats as a useful model for several complications of human diabetes including atherosclerosis, retinopathy, and nephropathy.
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PMID:Supplemental taurine in diabetic rats: effects on plasma glucose and triglycerides. 231 Jun 8

The incidence of second wave of platelet aggregation induced by a small dose of ADP (1 mumol/l) was compared with plasma levels of beta-thromboglobulin in 81 normal individuals, 34 patients with acute myocardial infarction, 11 patients with acute cerebrovascular disease and 26 patients with renal disease. Platelet hyperaggregability was observed in 7% of normal individuals. Plasma levels of beta-thromboglobulin were higher in normal individuals over 60 years of age (48 vs. 32 micrograms/l). In contrast, hyperaggregability was observed in 79% of patients with acute myocardial infarction and in 64% of those with acute cerebrovascular disease. Median plasma levels of beta-thromboglobulin were also significantly elevated in patients with acute myocardial infarction (82 micrograms/ml) or acute cerebrovascular disease (99 micrograms/l). Levels of beta-thromboglobulin in plasma were significantly higher in those patients who demonstrated hyperaggregability. In patients with renal disease only 12% had signs of hyperaggregability. Nevertheless their plasma levels of beta-thromboglobulin were elevated (76 micrograms/l) and correlated with the serum creatinine values. These investigations indicate that patients with acute myocardial infarction or stroke have hyperreactive platelets and evidence of increased platelet inactivation in the circulation. However, evaluation of increased levels of beta-thromboglobulin requires consideration of renal function.
Atherosclerosis 1985 Jun
PMID:Relationship between platelet aggregation and plasma beta-thromboglobulin levels in arterio-vascular and renal diseases. 240 89

In the last few years, remarkable advances have been made in the understanding of lipoprotein metabolism in the pathogenesis of renal disease in animal models and in vitro cell culture. Central to this work is the problem of the progression of renal disease in humans. This review recapitulates the theory (Lancet 1982; II: 1309-1312) that the progression of disease depends in part on the damage inflicted on the glomerulus by lipoproteins. The glomerular environment of high or low pressure, basement membrane damage, and destruction or damage of the mesangial and epithelial cells permits the filtration of protein, the consequence of which is hyperlipidemia. Whatever the therapeutic measures employed, if proteinuria persists, hyperlipidemia will follow. This suggest that lipoprotein toxicity may contribute to the final common path of renal damage in progressive renal disease. "Lipoprotein toxicity" in arteries is called atherosclerosis, but this term ignores the complexity of the glomerulus and the possible tubular damage that might be caused by filtered lipoprotein. It is clear there is insufficient knowledge of the metabolism of the damaged kidney to confidently attribute the pathology of progression of disease to any single process.
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PMID:Glomerular structures and lipids in progressive renal disease. 248 39


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