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)

In many reports, the prevalence of target organ damage in renovascular hypertension (RVH) appears to be higher than in essential hypertension (EH). Since in most studies the renal artery stenosis is part of a diffuse atherosclerotic disease, it is not known whether these complications are due to RVH itself or to the vascular disease. We have undertaken a case control study of 92 patients divided into two groups (46 in each), one with RVH and the other with EH and abdominal aortic aneurysm, with a comparable degree of diffuse atherosclerotic vascular disease. The vascular state of the extracranial carotid arteries and abdominal and inferior limb districts was investigated with angiography and sonography. The prevalence of left ventricular hypertrophy (LVH) and ischemic heart disease (IHD) were assessed by electrocardiography. Serum creatinine and urinary protein excretion were employed in the renal evaluation. While the analysis of the results confirmed an even diffusion of atherosclerotic vascular disease between the two groups, a significant difference was found in the prevalence of heart and renal damage. LVH was present in 32.6% of RVH patients versus 10.8% in EH (P = .02). Serum creatinine > 1.4 mg/dL was found in 50% of RVH and in 23.9% of EH, (P = .01). The prevalence of proteinuria in RVH was also higher although not reaching the statistical significance. The results suggest that, in patients with comparable degrees of atherosclerotic vascular disease, RVH is responsible for the higher prevalence of target organ damage in this condition compared to those with EH.
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PMID:Comparison of target organ damage in renovascular and essential hypertension. 893 30

A 46-year-old man was admitted to our clinic because of acute heart failure. Six years before admission he was pointed out cardiomegary and hematuria. One year later, he was diagnosed as having jugular foramen syndrome. On admission, he had a fever and dyspnea. Pansystolic blowing murmur was audible at the apex. The chest ratio on his chest X-ray was 52.5%. An electrocardiogram showed left ventricular hypertrophy. An echocardiogram showed marked dilatation and severe dysfunction of left ventricle. Radionuclide scanning with technetium 99 m pyrophosphate identified inflammatory change in the apex. Myocardial biopsy showed fibrotic degeneration and IgG deposits in myocardium. Blood examination showed anemia, lymphopenia. positive anti-nuclear antibody (1000 times, shaggy pattern), positive anti ds-DNA antibody and hypocomplementemia. Furthermore, proteinuria was pointed out. Renal biopsy showed focal segmental glomerulonephritis with active necrotizing lesion (type III nephritis). Lupus myocarditis and nephritis was diagnosed. After prednisolone (80 mg/day) was administered. left ventricular function and hypocomplementemia improved. The ACE inhibitor was also used for proteinuria. In spite of a little amount of blood transfusion, he showed hepatic hemosiderosis. We suspect that the cause of hemosiderosis was related chronic inflammation of active lupus. It was treated with Erythropoietin.
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PMID:[A case of lupus myocarditis and nephritis with transient foramen jugular syndrome]. 939 74

Between 1988 and 1992, 565 type 2 diabetic patients were examined for nephropathy and diabetes-associated diseases during hospital treatment. Stages of nephropathy were defined as no clinical sign of nephropathy (N = 280), microalbuminuria (N = 38), overt proteinuria (N = 105), impaired renal function (N = 55), and chronic dialysis therapy (N = 87). In dialyzed patients, HbA1c averaged 6.8%, and, in the other groups, HbA1c was between 7.6% and 8.3% (normal range, 3.8%-6.1%). Cataract was not associated with the severity of nephropathy. Stroke was most common in the stage of renal insufficiency (34%). The following complications, as found in medical history or as current event, showed a significant association with the stage of nephropathy and occurred most frequently in dialysis patients (percentage is displayed for patients with nephropathy in comparison to diabetic dialysis patients): hypertension (53%-89%), left ventricular hypertrophy (39%-81%), myocardial infarction (14%-36%), peripheral vascular disease (27%-77%), foot lesions (7%-75%), minor or major amputations (3%-23%), proliferative retinopathy (6%-46%), blindness (2.9%-16.1%), and internal carotid artery stenosis (15%-36%). In this preselected cohort of diabetic patients, a high morbidity was found already without nephropathy that increased several-fold in the course of the development of nephropathy. Our data identify patients with diabetic nephropathy as a high-risk group for excess morbidity.
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PMID:Morbidity in 565 type 2 diabetic patients according to stage of nephropathy. 955 88

Although angiotensin-converting enzyme (ACE) plays an important role in blood pressure regulation, no relationship between the insertion/deletion (I/D) polymorphism of the ACE gene and essential hypertension has been observed. However, as the pathogenesis and genetic background of essential hypertension are heterogeneous, we investigated whether the ACE gene is a marker of subgroups of patients with essential hypertension. A group of 178 patients with essential hypertension (90 men/88 women; 53 +/- 13 years of age, mean age +/- SD ) and 101 normotensive control subjects (54 men/47 women; 51 +/- 14 years of age, mean age +/- SD ) were included in the study. The allele frequencies of the two groups were similar. There were no differences in age, blood pressure, retinopathy grade, presence of proteinuria, or resting plasma renin activity (PRA) among the hypertensive patients with the II, ID, and DD genotypes. However, the age of onset of hypertension of patients with the DD genotype was lower (p < 20.05) and their left ventricular mass index was higher (p < 2 0.05) than those in patients with the non-DD genotype. These data suggest that the I/D polymorphism of the ACE gene is associated with an early onset of hypertension and left ventricular hypertrophy in Japanese patients with essential hypertension.
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PMID:DD genotype of the angiotensin I-converting enzyme gene is a risk factor for early onset of essential hypertension in Japanese patients. 962 82

We examined the relationship between left ventricular hypertrophy (LVH) and renal and retinal damage in 174 untreated patients with essential hypertension. As an index of renal and retinal damage, we examined proteinuria and retinal vascular change. LVH was diagnosed according to left ventricular mass obtained from echocardiography. Of the hypertensive patients, 111 patients (64%) had LVH. The incidences of proteinuria and advanced retinal vascular change were higher in patients with LVH than in those without LVH. In a multiple regression model, there was a significant positive correlation between left ventricular mass and proteinuria, as well as diastolic blood pressure, sex, age and body mass index. In conclusion, proteinuria is related to elevated left ventricular mass in patients with essential hypertension.
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PMID:Relationship between left ventricular hypertrophy and renal and retinal damage in untreated patients with essential hypertension. 971 82

Essential hypertension is a major Public Health issue. Although the number of treated hypertensive patients has increased, only 25% of treated patients have their blood pressure levels under control. The benefit of treating hypertension has been proven, but cardiovascular morbidity and mortality rates remain high. The ideal antihypertensive drug should not only normalize blood pressure levels, but also reduce the associated cardiovascular morbidity and mortality rates. The role of angiotensin II in systemic hypertension and its complications has been recently redefined. The potent trophic effects of angiotensin II on blood vessels and on cardiac cells have been well demonstrated, especially the role of angiotensin II in left ventricular hypertrophy, vascular hypertrophy, endothelial dysfunction, and congestive heart failure. Of all ongoing mortality and morbidity trials in systemic hypertension, VALUE (Valsartan Antihypertensive Long-term Use Evaluation) is the only one comparing an angiotensin II antagonist (valsartan) with a third-generation calcium channel blocker (amlodipine). The main hypothesis of the VALUE trial is that, for an equivalent decrease in blood pressure, valsartan will be more effective than amlodipine in decreasing cardiac mortality and morbidity. VALUE is a prospective, multinational, multicentre, double-blind, randomized, active-controlled, 2-arm parallel group comparison with a response-dependent dose titration scheme. VALUE involves 14,400 patients in over 30 countries, who will be followed for 4 years or until 1450 patients experience a primary endpoint. The population to be included in VALUE consists of hypertensive men and women, aged 50 years or older, and at a relatively high risk of sustaining a cardiovascular event. The high risk profile is defined taking into account age, gender, and a list of cardiovascular risk factors and disease factors. Risk factors are cigarette smoking, hypercholesterolaemia, diabetes mellitus, uncomplicated left ventricular hypertrophy, proteinuria, and high serum creatinine. Disease factors include documented history of myocardial infarction, peripheral vascular disease, stroke or transient ischaemic attack, or the presence of left ventricular hypertrophy with strain on the ECG. A unique feature of VALUE is the assessment of the predictive power of this cardiovascular risk factor scale in a large population of treated hypertensive patients. The trial started on 10 September 1997.
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PMID:The Valsartan Antihypertensive Long-term Use Evaluation (VALUE) trial of cardiovascular events in hypertension. Rationale and design. 975 88

Although a number of risk factors for cardiovascular morbidity and mortality have been identified in young and middle-aged adults, their prevalence and importance are less known in the elderly. Elderly people have a risk profile different from that of younger subjects, but representative data on risk factors for cardiovascular disease in the elderly are difficult to find in the literature. Some typical 'major' risk factors, like blood pressure (BP), total cholesterol or left ventricular hypertrophy, do not have a clear predictive role for cardiovascular mortality in the elderly, especially in the extreme ages, while risk indicators usually labelled as 'minor' (serum uric acid, ventilatory function or proteinuria), do have a strong predictive value in these individuals. This must be taken into account when evaluating the cumulative risk of the elderly, in order to avoid overtreatment of subjects with mildly elevated BP or cholesterol.
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PMID:Cardiovascular risk factors in the elderly. 978 83

Inhibition of cytochrome P-450 (CYP450) enzymes with cobalt chloride (CoCl2) prevented hypertension, organ hypertrophy, and renal injury induced by DOCA and salt (1% NaCl) in uninephrectomized (UNx) rats. Systolic blood pressure (SBP) rose to 193 +/- 6 mmHg by day 21 from control levels of 150 +/- 7 mmHg in response to DOCA-salt treatment, a rise that was prevented by CoCl2 (24 mg. kg-1. 24 h-1). The effects of DOCA-salt treatment, which increased protein excretion to 88.3 +/- 6.9 mg/24 h on day 21 from 9.0 +/- 1.1 mg/24 h on day 3, were prevented by CoCl2. CoCl2 also attenuated the renal and left ventricular hypertrophy and the increase in media-to-lumen ratio in hypertensive rats. DOCA-salt treatment increased excretion of endothelin (ET)-1 from 81 +/- 17 to 277 +/- 104 pg. 100 g body wt-1. 24 h-1 associated with a fourfold increase in 20-hydroxyeicosatetraenoic acid (20-HETE) excretion from 3.0 +/- 1.1 to 12.2 +/- 1.9 ng. 100 g body wt-1. 24 h-1 (days 3 vs. 21). CoCl2 blunted these increases by 58 and 72%, respectively. In aortic rings pulsed with [3H]thymidine, ET-1 increased its incorporation. Dibromododec-11-enoic acid, an inhibitor of 20-HETE synthesis, attenuated ET-1-induced increases in [3H]thymidine incorporation. We distinguished effects of CoCl2 acting via CO generation vs. suppression of CYP450-arachidonic acid metabolism by treating UNx-salt-DOCA rats with 1-aminobenzotriazole (ABT), which suppresses CYP450 enzyme activity, and compared these results to those produced by CoCl2. ABT reduced hypertension, as did CoCl2. Unlike CoCl2, ABT did not prevent organ hypertrophy and proteinuria, suggesting that these effects were partially related to CO formation. Blockade of the ETA receptor with BMS-182874 reduced SBP, organ hypertrophy, and proteinuria, indicating the importance of ET-initiated abnormalities to the progression of lesions in UNx-salt-DOCA.
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PMID:Endothelin-1 and CYP450 arachidonate metabolites interact to promote tissue injury in DOCA-salt hypertension. 1007 Jan 37

Angiotensin II antagonists block the actions of angiotensin II by occupying the AT1 receptors. With this blockade there is no bradykinin increase, the angiotensin II synthetized by the cardiac chymase is also blocked, and the AT2 receptor is stimulated (antiproliferative effect). In animal experiments, losartan reverses left ventricular hypertrophy, inhibits myocardial fibrosis and diabetic glomerulosclerosis and significantly protects from vascular cerebral diseases. In humans, the efficacy of the angiotensin II antagonists and that of other antihypertensives is similar and is potentiated by the addition of a thiazide. They are very well tolerated and no important adverse reactions are reported. Losartan decreases insulin resistance, has a very favourable hemodynamic and neurohormonal profile in patients with cardiac insuficiency, reverses proteinuria and has a uricosuric effect. Angiotensin II antagonists are a step forward towards the ideal antihypertensive drugs.
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PMID:[Therapy of arterial hypertension with angiotensin receptor blockers]. 1037 49

Plasma albumin leaks into urine as a result of glomerular hypertension and basement membrane injury, while urinary type IV collagen derives from mesangial matrix and glomerular basement membrane. The purpose of this study was to elucidate the pathophysiological significance of these urinary microproteins as an indicator of cardiovascular organ injuries in hypertension. In health-checkup participants without diabetes, proteinuria, or microhematuria, and who were not being treated for hypertension or any other disease at the time of enrollment, urinary albumin and type IV collagen were measured and their relations to organ injuries and cardiovascular risk factors were evaluated. Of 1,079 subjects (40- to 65-year-old; 256 men and 823 women) enrolled in the study, 120 (11.1%) had untreated hypertension exceeding 140/90 mmHg. Urinary albumin was positively correlated with both age (r=0.16, p<0.001) and systolic blood pressure (r=0.27, p<0.001). Urinary type IV collagen was not only positively correlated with age (r=0.12, p<0.001) and diastolic blood pressure (r=0.14, p<0.001) but also negatively correlated with blood hemoglobin (r=-0.12, p<0.001). Urinary albumin, but not type IV collagen, had a significant relation to electrocardiographic signs of left ventricular hypertrophy (p=0.012) and retinal arteriosclerosis on fundoscopy (p <0.001). Thus both albumin and type IV collagen would seem to have increased in association with age and hypertension in this cohort. It is suggested that urinary albumin is an indicator not only of renal injury, but also possibly of development of cardiac hypertrophy and arteriosclerotic changes. Urinary type IV collagen, on the other hand, may be associated with renal tissue injuries that affect erythrokinetics.
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PMID:Urinary excretions of albumin and type IV collagen in normotensive and hypertensive subjects. 1101


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