Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is clearly recognized that patients with NIDDM have an increased risk for CHD. Recent data indicate that persons with glucose concentrations in the nondiabetic range also may be at higher risk for CHD. These associations may not represent cause and effect, however. Emerging data suggest that hyperglycemia and CHD may both arise from hyperinsulinemia/insulin resistance. In support of this hypothesis are studies showing that NIDDM and CHD have many risk factors in common, including age, elevated blood pressure, dyslipidemia, adiposity, and a central pattern of fat distribution. Moreover, these risk factors are frequent concomitants of hyperinsulinemia, itself a risk factor for CHD and perhaps for NIDDM. Although the duration of NIDDM has been infrequently related to risk of CHD, the authors hypothesize that duration of hyperinsulinemia/insulin resistance would be a more sensitive marker for risk of CHD. The relation of IDDM to CHD is a different situation. The etiological process leading to IDDM, namely the destruction of beta-cells in genetically predisposed persons, is not related to cardiovascular risk. However, IDDM patients still have an excess of CVD, the risk factors for which may vary according to the location of the diseases (e.g., LEAD vs. CHD). There is a strong relationship between proteinuria and CVD, which has led to a general theory of vascular complications in IDDM based on defective heparan sulfate metabolism (Steno hypothesis). Recent evidence challenges parts of this hypothesis, and the possibility is raised that a higher case-fatality rate in a subgroup of patients with both renal and CVD explains part of the renal connection, as does the general worsening of CVD risk factors.
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PMID:Diabetes mellitus and macrovascular complications. An epidemiological perspective. 139 12

A review of the putative risk factors associated with the development of coronary heart disease in diabetes is presented. Emphasis is given to the effect of nephropathy (persistent proteinuria) and hypertension on cardiovascular mortality in IDDM. Risk factors associated with CHD in NIDDM are also reviewed. Finally, possible reasons to explain the increased incidence of CHD associated with proteinuria in IDDM patients, including lipoprotein abnormalities, increased fibrinogen levels, increased platelet adhesiveness, and altered hemostatic variables, are discussed.
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PMID:Risk factors for coronary heart disease in diabetes mellitus. 152 26

The effects of long-term (10 years) management at a special out-patient hypertension clinic with respect to dropout rate, side effects, blood pressure (BP) control, target organ involvement, prognostic factors and cardiovascular morbidity have been studied in 686 middle-aged male hypertensives. The impact of antihypertensive treatment, as one ingredient of multiple risk factor intervention, on mortality and morbidity in an urban, male population have been analysed. The hypertensive patients were derived from a random sample of men, aged 47-54 years at entry, constituting the intervention group (n = 7,455) of a multifactorial primary prevention trail. The whole population sample was studied regarding the effect of treatment on morbidity. The 10-year drop-out rate (declined follow-up/unknown reasons) was low (5%) being highest during the first year. The frequency of severe adverse drug effects was low (3% per year) after the initial period when treatment was started. An acceptable BP reduction was achieved in the majority of patients, but in many cases first after a few years' treatment and requiring combination drug therapy. Two-thirds of the patients achieved the goal BP (i.e. less than 160/95 mm Hg). These results are attributed to the organisation of the clinic and emphasise the need for frequent check-ups during the early phase of treatment and an easy accessibility to nurses and physicians. Except for a significant regression of ST- and T-wave changes on the conventional ECG during the first treatment year signs of heart (conventional ECG, chest X-ray) and kidney (albuminuria, serum creatinine) involvement remained unchanged or increased slightly during follow-up. Angina pectoris (AP), intermittent claudication (IC) and congestive heart failure (CHF) were common complications. The prevalence increased steadily with an average annual incidence of 1.3% (AP), 0.6% (IC) and 0.6% (CHF). ECG signs indicating subclinical heart disease were risk factor for AP and CHF. Smoking was an independent risk factor for any one of these cardiovascular disorders. The 10-year incidence of total mortality was 11.1%, and of CHD and stroke morbidity 12.2% and 4.1%, respectively. Independent risk factors (entry variables) for CHD were diastolic BP, smoking, serum cholesterol, AP and proteinuria. A previous stroke, smoking and proteinuria were independently associated with stroke morbidity. Hence, the risk factor pattern was similar to that known to operate in the general population.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Hypertension in middle-aged men. Management, morbidity and prognostic factors during long-term hypertensive care. 386 85

The main complications of hypertension, i.e. coronary heart disease, ischaemic strokes and peripheral vascular disease (PVD), are usually related to thrombosis. Increasing evidence also suggests that hypertension fulfils the components of Virchow's triad, thus conferring a prothrombotic or hypercoagulable state, as evident by abnormalities of haemostasis, platelets and endothelial function. It therefore seems plausible that use of antithrombotic therapy may help prevent these thrombosis-related complications of hypertension. Indeed, hypertensive patients with an estimated 10-year CHD risk > or = 15% will have their cardiovascular risk reduced by 25% using antihypertensive treatment, but the addition of aspirin further reduces major cardiovascular events by 15%. Recent guidelines recommend the use of aspirin 75 mg daily for hypertensive patients who have no contraindication to aspirin, in one of the following categories: (i) secondary prevention - cardiovascular complications (myocardial infarction, angina, non-haemorrhagic stroke, peripheral vascular disease or atherosclerotic renovascular disease); and (ii) primary prevention - those with blood pressure controlled to < 150/90 mmHg and one of: (a) age > or = 50 years and target organ damage (e.g. LVH, renal impairment, or proteinuria); (b) a 10-year CHD risk > or = 15%; or (c) type II diabetes mellitus. However, some of the risks of aspirin administration, namely increased incidence of major bleeding events, may possibly outweigh the benefits, especially in low-risk individuals.
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PMID:Should patients with hypertension receive antithrombotic therapy? 1128 41

Atherosclerosis and coronary artery disease (CAD) are now the commonest sequelae of hypertension and all clinical manifestations of CAD occur in excess in persons with elevated blood pressure. Risk increases in relation to the extent of blood pressure elevation whether this is in the systolic or diastolic component, at any age and in either sex. Even isolated systolic hypertension increases cardiovascular risk. Elevated pressures are often accompanied by lipid abnormalities, hyperglycemia, elevated fibrinogen, obesity, and ECG abnormalities, all of which augment the risk. These risk factors associated with hypertension influence the coronary risk potential more than the nature of the blood pressure elevation. Although blood pressure makes an independent contribution to CAD, the risk at any level of pressure is markedly influenced by the cardiovascular risk profile. In mild to moderate hypertension in particular, the risk of CHD is concentrated in those who have impaired glucose tolerance, increased total/HDL ratio, ECG abnormalities, and smoke cigarettes. One or more of these associated risk factors also predisposes to other cardiovascular sequelae of hypertension, including stroke, peripheral vascular disease, and cardiac failure. The presence of organ involvement indicated by proteinuria, evidence of impaired ventricular function, or left ventricular hypertrophy greatly escalates the risk and usually indicates a compromised coronary circulation. Most myocardial infarctions and sudden deaths occur prior to the appearance of such evidence. Hypertensive risk assessment requires consideration of the multivariate risk profile because of the interdependence of the risk factors. The nature and urgency of treatment is better determined from such a risk profile than from the blood pressure parameters alone. Optimal preventive management of hypertension requires more than normalization of the blood pressure if coronary sequelae are to be avoided.
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PMID:Influence of multiple risk factors on the hazard of hypertension. 1152 37

Mercury, cadmium, and other heavy metals have a high affinity for sulfhydryl (-SH) groups, inactivating numerous enzymatic reactions, amino acids, and sulfur-containing antioxidants (NAC, ALA, GSH), with subsequent decreased oxidant defense and increased oxidative stress. Both bind to metallothionein and substitute for zinc, copper, and other trace metals reducing the effectiveness of metalloenzymes. Mercury induces mitochondrial dysfunction with reduction in ATP, depletion of glutathione, and increased lipid peroxidation; increased oxidative stress is common. Selenium antagonizes mercury toxicity. The overall vascular effects of mercury include oxidative stress, inflammation, thrombosis, vascular smooth muscle dysfunction, endothelial dysfunction, dyslipidemia, immune dysfunction, and mitochondrial dysfunction. The clinical consequences of mercury toxicity include hypertension, CHD, MI, increased carotid IMT and obstruction, CVA, generalized atherosclerosis, and renal dysfunction with proteinuria. Pathological, biochemical, and functional medicine correlations are significant and logical. Mercury diminishes the protective effect of fish and omega-3 fatty acids. Mercury, cadmium, and other heavy metals inactivate COMT, which increases serum and urinary epinephrine, norepinephrine, and dopamine. This effect will increase blood pressure and may be a clinical clue to heavy metal toxicity. Cadmium concentrates in the kidney, particularly inducing proteinuria and renal dysfunction; it is associated with hypertension, but less so with CHD. Renal cadmium reduces CYP4A11 and PPARs, which may be related to hypertension, sodium retention, glucose intolerance, dyslipidemia, and zinc deficiency. Dietary calcium may mitigate some of the toxicity of cadmium. Heavy metal toxicity, especially mercury and cadmium, should be evaluated in any patient with hypertension, CHD, or other vascular disease. Specific testing for acute and chronic toxicity and total body burden using hair, toenail, urine, serum, etc. with baseline and provoked evaluation should be done.
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PMID:The role of mercury and cadmium heavy metals in vascular disease, hypertension, coronary heart disease, and myocardial infarction. 1740 90

The objective of this study was to determine the frequency of Metabolic Syndrome (MetS) in patients with SLE and to analyze the association of MetS with traditional risk factors for CHD and lupus characteristics. In this cross-sectional study the frequency of MetS was determined according to the National Cholesterol Education Program Adult Treatment Panel III in patients with SLE. The association of MetS with the traditional risk factors for CHD not included in the syndrome definition, and with lupus characteristics was examined. The mean age (sd) of the 162 females patients was 38.8(11.2) years. The frequency of MetS was 32.1%. Abdominal obesity and hypertension were the two most common components of the syndrome (86.5% each) followed by low levels of HDL-cholesterol (84.6%), hypertriglyceridemia (69.2%) and hyperglycemia (15.4%). MetS was significantly associated with older age, family history of CHD, obesity, postmenopausal status, LDL-c > or =100mg/dl, and higher Framingham risk score. Lupus characteristics associated with MetS were history of nephrotic proteinuria during follow-up and current cyclophosphamide use, higher modified SLEDAI-2k, higher damage index score (SLICC/ACR), and older age at lupus diagnosis. In the logistic regression analysis, obesity, LDL-c > or =100mg/dl, older age at lupus diagnosis, higher damage index and nephrotic proteinuria were independently associated with MetS. We conclude that MetS diagnosis was frequent in patients with lupus. The syndrome was associated not only with traditional risk factors for CHD, confirming the clustering of those risk factors, but also with lupus characteristics. Some of those factors, especially LDL-c > or =100mg/dl and age at lupus diagnosis, have been associated with atherosclerosis in lupus patients. Lupus (2010) 19, 803-809.
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PMID:Metabolic syndrome in patients with systemic lupus erythematosus: association with traditional risk factors for coronary heart disease and lupus characteristics. 2011 59

The aim of this work was to study the incidence of chronic renal disease (CRD) in 100 patients with systemic scleroderma (SS) who underwent general clinical and laboratory examination; glomerular filtration rate (GFR) was calculated. Statistica 8.0 and Excel 2007 programs were used to treat the results. 88% of the patients with SS had CRD, 80% showed lowered GFR and 81% suffered hypostenuria and/or proteinuria. GFR correlated with the presence of cardiac lesions and pulmonary hypertension, Valentini activity index, renal vessel resistance, concomitant renal pathology, arterial hypertension and/or CHD. Also, reduced GFR associated with myocardiofibrosis, atrioventricular valve incompetence, age and concomitant diseases (AH, DM, CRD, renal and urinary tract pathology).
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PMID:[Chronic renal disease in patients with systemic scleroderma: the prevalence and associated factors]. 2441 65

Donnai-Barrow syndrome (DBS; MIM 222448) is characterized by typical craniofacial anomalies (major hypertelorism with bulging eyes), high grade myopia, deafness and low molecular weight proteinuria. The disorder results from mutations in the low density lipoprotein receptor-related protein 2 gene LRP2 that maps to chromosome 2q31.1. LRP2 encodes megalin, a multi-ligand endocytic receptor. Herein, we describe the clinical presentation of 4 patients from 2 unrelated Saudi families. Two novel LRP2 mutations, a homozygous nonsense mutation (c.4968C>G; p.Tyr1656*) and a missense mutation (c.12062G>A; p.Cys4021Tyr), were detected in the first and second family respectively. Interestingly, intrafamilial phenotypic variability was observed in one family, while DBS features were atypical in the second family. Differential diagnosis of DBS includes several syndromes associating hypertelorism with high grade myopia, and several syndromal forms of CDH, which are briefly summarized in this study.
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PMID:Variable expression pattern in Donnai-Barrow syndrome: Report of two novel LRP2 mutations and review of the literature. 2568 1