Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The frequencies of 10 diseases in a cadmium (and zinc) contaminated region in The Netherlands were analysed by comparing hospital admissions with those of a non-contaminated region and with national values. No significant differences were found for diseases which are commonly associated with increased cadmium uptake such as renal insufficiency, nephrolithiasis, hypertension, cancer, immaturity of the new-born. For the contaminated region a significantly higher frequency was only found for atherosclerosis; this was relatively strong for men aged > 40 yrs. However, no higher death frequency for atherosclerosis was observed. The results are discussed in relation to limitations in the evaluation techniques used. The absence of major health risks in the contaminated area is obvious, but the possible influence of long term-low level cadmium uptake on atherosclerosis requires more attention.
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PMID:Prolonged low-level cadmium intake and atherosclerosis. 825 93

To study the influence of cardiovascular damage on plasma endothelin in chronic renal failure, we have measured the plasma concentration of this peptide in 32 uremic patients (7 undialyzed uremics, 8 CAPD patients and 16 hemodialysis patients) and in 9 healthy subjects. Sixteen patients had severe cardiovascular damage while the other 16 had no cardiovascular involvement. Endothelin was markedly raised (p < 0.01) in the uremic group as a whole (13.9 +/- 2.6 pmol/l) in comparison with the group of healthy subjects (8.6 +/- 1.6 pmol/l). Hemodialysis patients displayed endothelin levels much higher (p < 0.01) than CAPD patients and undialyzed uremics. Endothelin was directely related with BUN (r = 0.37) and with serum creatinine (r = 0.52) in dialysis patients. Similar correlations were also found in undialyzed uremics. Plasma endothelin was almost identical in patients with severe cardiovascular damage (15.5 +/- 1.6 pmol/l) and in those without cardiovascular involvement (15.9 +/- 2.6 pmol/l). There was no relationship between arterial pressure and plasma endothelin. Residual renal function is an important determinant of circulating endothelin even at very advanced stages of renal insufficiency. It appears unlikely that atherosclerosis plays a major role in the pathogenesis of high plasma concentration of this peptide in uremic patients.
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PMID:Influence of cardiovascular damage and residual renal function on plasma endothelin in chronic renal failure. 844 66

We evaluated two patients with systemic cholesterol embolization (SCE) associated with the development of pleural effusions. These two patients had evidence of atherosclerosis and presented with livedo reticularis, renal insufficiency, and gangrenous cutaneous changes as manifestations of their SCE. In both cases, closed pleural biopsies demonstrated acute inflammation of the parietal pleura. Our experience with these individuals and a review of the medical literature suggest that pleural injury from atheromatous embolization may occur. Physicians caring for patients with SCE should be aware of the possible association of pleural reactions with this process.
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PMID:Pleural effusion in patients with systemic cholesterol embolization. 844 70

Plasma lipid peroxidation in noninsulin dependent diabetes mellitus (DM) patients were evaluated in DM patients undergoing hemodialysis (HD) by means of a chemiluminescence-HPLC for the specific determination of phosphatidylcholine hydroperoxide (PCOOH). Thirty-three uremic patients with DM nephropathy, undergoing 12 hours HD a week using polymethylmethacrylate membrane, were studied. Of them 22 DM patients on HD were divided into 2 age and sex matched groups treated and conventional group in order to clarify therapeutic effect of 500 mg alfa-tocopherol and 600 mg probucol daily. Fifty DM patients without end-stage renal disease (ESRD) who were age-, period of diabetes-, and sex-matched, were selected as positive control of the subjects. Plasma PCOOH levels were significantly elevated in both DM patients, while the plasma PCOOH in normal controls were 227.0 +/- 68.7 pmol/ml. Plasma PCOOH levels of DM patients undergoing HD were significantly higher than that of patients without ESRD (1,330.8 +/- 642.7 pmol/ml vs. 756.6 +/- 431.9 pmol/ml, p < 0.025). Partial correlation coefficient of plasma PCOOH level demonstrated PCOOH and period of HD in DM patients were highly significantly positively correlated (p < 0.01), although single session of HD was not found to produce significantly increased lipid-peroxidation. Plasma PCOOH roughly remained within similar levels as base lines by medication with anti-oxidant compared to that of conventional group. From these results we conclude that HD intensifies lipid peroxidation and such accumulation of hydroperoxide could account for accelerated progress of atherosclerosis in DM patients with renal insufficiency. It is worthwhile to try an administration of free radical scavenger in order to reduce PCOOH and slow down the progression of atherosclerotic vascular disease.
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PMID:Accumulation of phosphatydilcholine-hydroperoxide in dialysis patients with diabetic nephropathy. 860 60

Understanding the pathophysiology, diagnosis, and management of renovascular hypertension (RVH) is of paramount importance due to the severity of hypertension (HT) and renal insufficiency (RI). Moreover, adequate treatment by surgery and/or endovascular intervention can improve HT and revert RI. The comprehension of the pathophysiology of RVH had its origin on the experiments of Goldblatt which led to the recognition of the renin dependent, volume dependent, and mixed types. A continuum seems to exist, from an acute phase, supported by the endocrine renin angiotensin aldosterone system, evolving towards a chronic phase sustained by the local renin angiotensin system. The involved vasoconstrictor and mitogenic mechanisms may contribute to the arterial remodeling. The most common forms of pathology, i.e. atherosclerosis, fibromuscular dysplasia (FD), and Takayasu's arteritis, and their natural history, are described. The prevalence of RVH, ranging from 0.2% to more than 25%, depending on the clinical situation, is evidenced. Clinical symptoms and signs and the most important diagnostic tests are pointed out: functional tests (captopril test, postcaptopril renography, scintigraphy, and renin determinations) and anatomical tests (intravenous digital angiography and intrarterial angiography). New imaging techniques are also referred. A diagnostic work-up based on the index of clinical suspicion is described. The therapeutic goal is the resolution of the two main problems of RVH: hypertension and ischemic nephropathy. Revascularization is becoming mandatory either by percutaneous transluminal angioplasty mostly for FD and atheromatous non-ostial stenoses, or by surgery, which is preferred for patients with ostial or peripheral stenoses, aneuryms, occlusions and concomitant aortic disease. A better knowledge of RVH allows, not only diagnosis and treatment of one of the most frequent types of secondary hypertension, but also the control of the resulting ischemic nephropathy.
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PMID:[Renovascular arterial hypertension. From physiopathology to therapy]. 870 4

Patients with renal disease have an increased cardiovascular mortality. Hyperlipidemia, a hallmark of renal disease, is recognized as a principal cause of atherosclerosis. However, it is difficult to prove a pathogenetic role of renal dyslipidemia per se in this increased cardiovascular risk since multiple risk factors are often present in patients with progressive renal insufficiency, e.g. hypertension, diabetes and hypercoagulability. However, evidence is accumulating demonstrating detrimental effects of hyperlipidemia during both initiation and progression of the atherosclerotic process. The present review discusses this evidence in patients with renal disease, and the possible implications for treatment.
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PMID:Mechanisms of cardiovascular injury in renal disease. 871 68

Renal artery stenosis may be caused by either atherosclerosis or fibromuscular dysplasia, and is responsible for hypertension or renal failure. Universal screening of all hypertensive patients is not recommended because of the relatively low prevalence of the disease. A selective approach is needed. The detection of renal artery stenosis requires noninvasive tests with a high predictive value (Doppler ultrasonography, intravenous angiography, spiral CT angiography, captopril renography) in patients in whom hypertension is severe, refractory to therapy, or associated with progressive renal insufficiency. Yet, after such screening, arteriography remains the gold standard of detecting and quantifying renal artery stenosis.
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PMID:[Screening of renal artery stenosis: which patients, by what methods?]. 876 15

Long-term outcome was studied in 233 patients who had undergone renal artery revascularization (51 with balloon angioplasty, 182 with surgery) between 1976 and 1992. Patients (excluding renal transplants) were treated for renal vascular hypertension without or with renal insufficiency (serum creatinine > 1.6 mg/dl. All patients still alive (n = 188) were contacted to determine current blood pressure, medications, serum creatinine, and subsequent significant medical events. In patients who had died the cause of death was determined and renal function status at the time of death noted from medical records. Some follow-up information was obtained on all 233 patients; follow-up serum creatinine data were obtained in 193 (82.8%) patients. Some 24 patients (10.3%) became dialysis-dependent. Using a multiple logistic regression analysis only, preoperative creatinine maintained significance (P < 0.001) for increased dialysis risk. There was no statistically significant association of dialysis for type of revascularization (percutaneous transluminal angioplasty, autogenous artery, saphenous vein, endarterectomy or synthetic material), simultaneous or previous aortic or other vascular surgery (carotid endarterectomy, femoropopliteal bypass, etc.), pathology (atherosclerosis or fibromuscular dysplasia), number of renal arteries stenosed or treated, length of follow-up, age, coronary artery disease, congestive heart failure, stroke, chronic lung disease or type II diabetes. It is concluded that, in patients with renal artery stenosis, the timing of renal artery revascularization relative to the level of renal function is the most important determinant for long-term renal salvage.
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PMID:Late renal function in patients undergoing renal revascularization for control of hypertension and/or renal preservation. 890 17

A 69-year-old diabetic woman with diffuse atherosclerosis presented with acute renal failure due to contrast nephropathy and severe metformin-induced lactic acidosis. There was a discrepancy between the patient's elevated serum creatinine level, indicative of severe renal insufficiency, and her very low blood urea nitrogen content. It is postulated that the patient's extremely severe acidosis interfered with her hepatic urea generation, contributing to this unusual biochemical abnormality.
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PMID:Metformin-induced lactic acidosis associated with acute renal failure. 895 64

We have established a mouse model for human LCAT deficiency by performing targeted disruption of the LCAT gene in mouse embryonic stem cells. Homozygous LCAT-deficient mice were healthy at birth and fertile. Compared with age-matched wild-type littermates, the LCAT activity in heterozygous and homozygous knockout mice was reduced by 30 and 99%, respectively. LCAT deficiency resulted in significant reductions in the plasma concentrations of total cholesterol, HDL cholesterol, and apoA-I in both LCAT -/- mice (25, 7, and 12%; p < 0. 001 of normal) and LCAT +/- mice (65 and 59%; p < 0.001 and 81%; not significant, p = 0.17 of normal). In addition, plasma triglycerides were significantly higher (212% of normal; p < 0.01) in male homozygous knockout mice compared with wild-type animals but remained normal in female knockout LCAT mice. Analyses of plasma lipoproteins by fast protein liquid chromatography and two-dimensional gel electrophoresis demonstrated the presence of heterogenous prebeta-migrating HDL, as well as triglyceride-enriched very low density lipoprotein. After 3 weeks on a high-fat high-cholesterol diet, LCAT -/- mice had significantly lower plasma concentrations of total cholesterol, reflecting reduced levels of both proatherogenic apoB-containing lipoproteins as well as HDL, compared with controls. Thus, we demonstrate for the first time that the absence of LCAT attenuates the rise of apoB-containing lipoproteins in response to dietary cholesterol. No evidence of corneal opacities or renal insufficiency was detected in 4-month-old homozygous knockout mice. The availability of a homozygous animal model for human LCAT deficiency states will permit further evaluation of the role that LCAT plays in atherosclerosis as well as the feasibility of performing gene transfer in human LCAT deficiency states.
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PMID:Targeted disruption of the mouse lecithin:cholesterol acyltransferase (LCAT) gene. Generation of a new animal model for human LCAT deficiency. 905 54


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