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)

Decreased response to vasopressor agents characterizes pregnancy. Endothelium-derived relaxing factors and vasodilating prostaglandins play an important role in the vascular tone during pregnancy. Since inhibition of nitric oxide (NO) biosynthesis induced by NO2-arginine enriched diet produced hypertension we measured in vivo cardiovascular responses to PGF2 alpha, L-arginine (L-arg) and cicletanine (Cic, IPSEN, France) which enhances PGI2 production. From day 13 to day 20 of gestation 4 groups of female Wistar rats were fed NO2-arg (31 mg/kg/d), NO2-arg+Cic (10 mg/kg/d), Cic enriched or control diet (C). Mean arterial pressure (MAP) was measured via a carotid catheter in anesthetized rats. Injection of PGF2 alpha (50 micrograms/kg) in jugular vein significantly increased MAP in the NO2-arg group versus, NO2-arg+Cic, Cic and C group (+23.5 +/- 3.3 vs +15.7 +/- 2.2, +15.8 +/- 2.2 and +17 +/- 1.85 mmHg; p < 0.01). Injection of L-arg (100 mg/kg) or Cic (1 mg/kg) 5 min before PGF2 alpha produced no modification in MAP in C and Cic group. Likewise in NO2-arg group injection of L-arg or Cic produced a diminished pressor response to PGF2 alpha (+23.5 +/- 3.3 vs -17.5 +/- 1.7 mmHg; p < 0.05 and +15.2 +/- 2.4 mmHg; p < 0.01 respectively). In NO2-arg+Cic group, only injection of Cic induced a diminished pressor response to PGF2 alpha which is more important without L-arg (+15.7 +/- 2.2 vs +9.1 +/- 1.3 mmHg; p < 0.001) or with L-arg (+13.6 +/- 1.5 vs +9.1 +/- 1.3 mmHg; p < 0.01). Cicletanine also significantly diminished the proteinuria in the NO2-arg+Cic group versus NO2-arg group (13.9 +/- 4.36 vs 63.4 +/- 21.6 mmHg; p < 0.01). IN CONCLUSION, chronic NO synthesis inhibition enhanced blood pressure and pressor responses to PGF2 alpha during pregnancy in rats. Chronic administration of cicletanine in Wistar pregnant rats decreases the response to vasopressor agents like PGF2 alpha. Moreover acute and chronic administration of cicletanine blunted the pressor effect, which was lower than in normal gestation.
Arch Mal Coeur Vaiss 1995 Aug
PMID:[Chronic and acute effect of cycletanine in NO-dependent hypertensive pregnant rats]. 857 78

The aim of this study was to evaluate the circadian blood pressure variations in subjects with or without microalbuminuria (Urinary Albumin Excretion (UAE) between 30 and 300 mg/24 h. Forty-nine non-insulin dependent diabetic subjects with essential arterial hypertension and without proteinuria (UAE < 300 mg/24 h) were consecutively recruited. Systolic (SBP) and Diastolic Blood Pressure (DBP) have been measured using a SpaceLabs 90207 ambulatory blood pressure monitor, every 15 minutes during daytime (7:00 a.m. to 22:00 p.m.) and every 30 minutes during nighttime (22:00 p.m. 7:00 a.m.). UAE has been measured by nephelometry on three 24 h urine collections. The group with microalbuminuria (n = 16) was not different from the group with normoalbuminuria (n = 33) for age, sex ratio, body mass index, known diabetes duration, proportion of anti-hypertensive treatment, serum creatinine and HbA1c. Daytime blood pressures (SBP/DBP: 144 +/- 15/83 +/- 8 vs 137 +/- 13/84 +/- 9 mmHg) and nighttime DBP (75 +/- 7 vs 74 +/- 9 mmHg) were comparable between both groups. In contrast, the nighttime SBP was higher in subjects with microalbuminuria than in those without (139 +/- 17 vs 129 +/- 17 mmHg; p = 0.016). If dippers are the subjects with a nocturnal blood pressure reduction (SBP and/or DBP) below 4%, there is a relationship between "non dippler" subjects and those with microalbuminuria (Chi-squared test = 5.67; p = 0.017). In conclusion, hypertensive non-insulin dependent diabetic subjects with microalbuminuria have a loss of nocturnal blood pressure decrease.
Arch Mal Coeur Vaiss 1996 Aug
PMID:[Decrease of nocturnal blood pressure in type II diabetic subjects with microalbuminuria]. 894 75

Vascular thrombosis remains severe complication in patients with nephrotic syndrome. Both venous and arterial thrombosis are observed. We report three new cases of arterial thrombosis in patients with nephrotic syndrome. The role of acquired hemostasis disorders, inducing hypercoagulability, is predominant. Extramembranous glomerulonephritis remains the most frequent cause of nephrotic syndrome, complicated by vascular thrombosis. Treatment is based on anticoagulation and corticosteroid therapy. Search for proteinuria should be part of the etiology work-up in all patients with vascular thrombosis of undetermined origin.
J Mal Vasc 1998 Feb
PMID:[Arterial thrombosis in the course of nephrotic syndrome. Report of three cases]. 955 49

Hypertensive pregnant rats with inhibition of NO synthase are frequently considered as model of pre-eclampsia with proteinuria, hypertension and elevated endothelin (ET-1) blood levels. We describe here the cardiovascular in vivo effects of ET-1 in this rat model since ET-1 and NO are both important vasoactive mediators in uteroplacental circulation. From day 13 of gestation 2 groups of Wistar female rats were fed control (C) or nitroarginine enriched diet (0.063%, Treated: T). On gestational day 20 mean arterial pressure (MAP, mmHg) was measured via a carotid catheter in pentobarbital (60 mg/kg) anesthetized rats. After chronic NO synthase inhibition hypertension develops; MAP on day 20: 158 +/- 2.2 in T and 113 +/- 2.2 in C, p < 0.001. ET-1 bolus injection (0.1 nmol/kg) is rapidly followed by a decrease in blood pressure significantly more important in T: -46 +/- 5.1 than in C: -30 +/- 2.2. In vivo depressor effect is blocked by the specific antagonist BQ-788. After inhibition of cycloxygenase with acetylsalicylic acid (27 mumol/kg, 30 min before) the hypotension is not modified. Since NO and PGI2 productions are not expected in our conditions, vasodepressor effect can be explained by an endothelial hyperpolarazing factor (EDHF). In conclusion in vivo ET-1 hypotensive effects in pregnant rats are mediated by ETB receptors and more pronounced in hypertensive NO-deprived animals.
Arch Mal Coeur Vaiss 1998 Aug
PMID:[Hypotensive effect of endothelin-1 in a rat model of pre-eclampsia]. 974 58

A lot of evidence points to the important role of the renin-angiotensin system in the physiopathology of hypertension and the progression of chronic renal failure. In this review, the authors report the data concerning the protective effects of antagonists of angiotensin II AT1 receptors (AT1ra). The AT1 ra have been shown to have beneficial effects in most experimental models of nephropathy in which they have been tested (renal ischaemia, essential or induced hypertension, glomerulonephritis, 5/6 nephrectomy, renal transplantation, induced diabetes, toxic and radiotherapy-induced nephropathy). Clinical trials confirm these beneficial effects. In healthy subjects and hypertensive patients, the AT1 ra have identical effects to those of angiotensin converting enzyme (ACE) inhibitors on renal haemodynamics. In hypertensives, Candesartan and Irbesartan increase renal blood flow and the glomerular filtration rate and decrease the filtration fraction. Two studies have also shown that Candesartan and Irbesartan reduce proteinuria in diabetic patients. Similar results have been reported in essential hypertension with renal failure. These data suggest that AT1 ra have beneficial effects on the progression of experimental kidney disease and on proteinuria in the clinical setting. Of the pharmacological agents available for use in this class, it is essential to propose molecules whose efficacy in antagonising the effects of angiotensin II lasts throughout the 24 hour period. Clinical trials are under way to evaluate the effects of AT1 ra on renal function in man over a long period.
Arch Mal Coeur Vaiss 1999 Jul
PMID:[Are the antagonists of angiotensin II AT1 receptors protectors of the kidney?]. 1044 11

THE RELIEF OF THE RESULTS OF THE HOPE TRIAL WITH RESPECT TO THE INCIDENCE OF CEREBROVASCULAR EVENT UNDER ACE INHIBITOR THERAPY: In 1998, the CAPP trial had raised a serious concern about whether captopril therapy increased the risk of cerebrovascular accidents. When compared with betablocker therapy (+/- diuretics) in 11,000 hypertensives, there was a very worrying number of excess cerebrovascular accidents in the captopril group (+25%) (with no difference in the number of cerebrovascular accidents overall). There were several reasons which led to believe that the captopril was not the causal factor. But a doubt remained. In 1999, the results of the HOPE trial with ramipril, though not primarily for a hypertensive population, provided reassurance beyond the investigators' hopes concerning the value of ACE inhibitors in the prevention of vascular events, including cerebrovascular accidents. THE FRAMINGHAM EXPERIENCE OF LVH AND THE TREATMENT OF HYPERTENSION: The Framingham study reported unique data concerning the effects of antihypertensive therapy on LVH in 10,333 subjects of 45 to 74 years of age followed up for 40 years (1950-1989). As the incidence of antihypertensive therapy increased during the observation period, that of hypertension and LVH decreased in parallel. Although these data were retrospective, they are compatible with a causal relationship between the treatment and regression of LVH. This could explain up to 50% of the decrease in cardiovascular mortality observed in the United States during this period. The Framingham study so reposition, in an epidemiological context, the considerable benefits of antihypertensive therapy and of the regression of the associated LVH. THE SEVERITY OF THE WHO AND IHS RECOMMENDATIONS: Less than 130/85: this is the target value of the blood pressure in adults under antihypertensive therapy according to WHO and IHS. In patients with diabetes or renal failure with proteinuria > 1 g/j, the target is even lower. These recommendations incite physicians to beware of any laxness in the treatment of hypertension. The most recent epidemiological data from France indicates that only a minority of the hypertensive patients under treatment are well controlled and that this advice is probably not superfluous. Moreover, in the decision to treat hypertension (drug therapy or not), these recommendations underline the evaluation of the individual risk of the subject on the basis of associated risk factors, target organ complications and previous history of vascular events.
Arch Mal Coeur Vaiss 2000 Jan
PMID:[The best of arterial hypertension in 1999]. 1072 43

In the aim to determine the importance of renal disease in hypertensives (BP > 160/95 mmHg), we conducted a retrospective study in Burkina Faso, a black african country. 342 adults hypertensive (200 men, 142 women, mean age: 50.6 +/- 13.8 years) hospitalized in the departments of Cardiology or Internal medicine from January 1995 to December 1997 were included. Patients were at their first hospital stay in 273 cases (79.8%). When technical conditions were available, assessments were systematically done. Blood pressure was 183.6 +/- 36.4/113.3 +/- 23.1 mmHg. Total morbidity concerned 316 patients (92.4%). Cardiovascular complications (CVC) have been diagnosed in 236 patients (69%) with a mean age of 51.6 +/- 14 y, neurologic complications (NC) in 85 patients (24.9%, mean age: 55.7 +/- 12) and renal disease (RD) in 123 patients (36%; mean age: 44.7 +/- 14.5 y). Mean age of single RD (n: 27, mean age: 39.5 +/- 12.8 y) was significantly lower than no complicated hypertensives (n: 42, mean age: 48.2 +/- 11.6 y) or single CVC (n: 104, mean age: 55 +/- 12.5) or single NC (n: 34, mean age: 55.1 +/- 11.1) or associated comorbidities (n: 135, mean age: 49.1 +/- 14.5). Patients under 40 years of age have had higher 24 hours proteinuria than other patients (1.05 +/- 1.17 g (n: 51) vs 0.45 +/- 0.68 (n: 170), p < 0.01). Chronic renal failure occurred in youngest patients (n: 72, age: 39.7 +/- 13.4 vs 53.7 +/- 12.3; p < 0.01) with a most high prevalence in rural (31.6%) than urban patients (15.8%; p < 0.01). End stage renal failure concerned 49 patients (mean age: 35.9 +/- 12.7). 27 patients died during hospital stay by renal failure in 17 cases (mean age: 37 +/- 11). CVC in 5 cases (mean age: 68.6 +/- 8) and NC in 5 cases (mean age: 60.2 +/- 9.2). Among survivals, 72 patients (28.9%) were of a bad short-term prognosis and 38 had end stage renal failure. In conclusion, our data suggest that renal disease will be common cause of hypertension and also a selective factor for long term survival of hypertensives in a country where renal replacement therapy is not available.
Arch Mal Coeur Vaiss 2000 Aug
PMID:[Characteristics of renal disease in hypertensive morbidities in adults in Burkina Faso]. 1098 56

Hypertension is almost an inevitable complication of chronic renal failure and it contributes to the acceleration of its progression to terminal renal failure. Cohort studies and large scale clinical trials carried out in the last 10 years have allowed quantification of the respective influences and interactions of hypertension, proteinuria, and metabolic factors on the rate of degradation of renal function. They have conclusively showed a benefit in normalising the blood pressure in diabetic and nondiabetic renal disease especially when the proteinuria is pronounced and when the treatment includes an angiotensin converting enzyme inhibitor. Hypertension is also an increasingly common cause of renal failure, which may become terminal by its consequences associating vascular and ischaemic lesions of the renal parenchyma. Depending on the country studied, 10 to 25% of new dialysis patients are now classified as hypertensive and vascular renal disease. The individual renal risk of essential hypertension is relatively low except in certain groups, such as the coloured population, especially in the USA. The risk of a significant increase in creatinine is doubled by any increase of 20 mmHg of diastolic blood pressure but long-term studies suggest that the effects of increased systolic blood pressure may be even greater.
Arch Mal Coeur Vaiss 2000 Nov
PMID:[Hypertension and renal insufficiency]. 1119 Feb 96

Permanent hypertension is frequently associated with increased glomerular permeability to albumin at an early stage, indicating renal involvement and endothelial dysfunction. The definition of microalbuminuria is an urinary albumin excretion of 30-300 mg/24 hrs, confirmed on two occasions over a 3 month period. It may also be expressed in microgram/min, m/l or mg/mmol of creatinine. Radio-immunological, immunonephelometric methods and Elisa are specific and the most sensitive methods of measurement. There is a large intra-individual variability (25-60%) making it essential to repeat measurements always by the same technique. The prevalence of microalbuminuria is 5-8% in the general population and 6-24% in hypertensive patients. When present, it is a marker of increased cardiovascular risk. Clinical recommendations suggest adaptation of urinary collection according to the context: screening, diagnosis or clinical research. It is always necessary to start by dip-stick detection of proteinuria, haematuria or urinary infection. Clinical research requires repeated measurement of 24 hour microalbuminuria, sometimes divided into two periods of day and night, often associated with ambulatory blood pressure recordings and renal function tests. Studies of the effects of anti-hypertensive drugs on microalbuminuria could provide better evaluation. In conclusion, measurement of microalbuminuria remains a tool of clinical research allowing an assessment of cardiovascular and renal risk of hypertensive patients.
Arch Mal Coeur Vaiss 2000 Nov
PMID:[Microabluminuria in arterial hypertension. Measurement, variables, interpretation, recommendations]. 1119 Apr 59

Non-Invasive coronary investigations are positive in 12 to 52% (average 22%) of type II diabetics, and 11 to 30% (average 17%) of type i diabetics. These statistics vary according to bias of recruitment. Haemodynamic lesions are found at coronary angiography in 35 to 80% of patients who have at least one positive non-invasive investigation. Nine to 12% of diabetics have silent myocardial ischaemia (SMI) confirmed by coronary angiography, compared with 1.3 to 5.3% of non-diabetic controls paired for age and sex. The higher frequency of SMI in diabetics seems to be mostly due to the increased frequency of ischaemic heart disease in diabetics. The importance of cardiac autonomic neuropathy (CAN) in SMI is controversial. The risk factors associated with SMI are those usually associated with coronary artery disease: age, masculine gender, hypercholesterolaemia, hypertriglyceridaemia, hypertension, smoking, a family history of cardiovascular disease, insulin therapy (for type II diabetes), proteinuria, retinopathy, peripheral occlusive arterial disease.... The French recommendations for investigating SMI seem to be contradictory. A single risk score in a given patient could help codify the investigation of SMI in diabetics, but this type of score has not yet been validated.
Arch Mal Coeur Vaiss 2000 Dec
PMID:[Silent ischemic cardiopathy: which diabetics to examine?]. 1129 59


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