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)

The antihypertensive effect of enalapril maleate, a new converting enzyme inhibitor, was evaluated in a multiclinic, double-blind, randomized study in patients with mild to moderate essential hypertension. The analyses were done in two ways, with patients who violated the entry criteria of the protocol excluded, and according to the intention to treat principle. Enalapril in dosages of 10 to 40 mg daily administered alone or concomitantly with hydrochlorothiazide was compared to propranolol (80 to 240 mg daily) alone or concomitantly with the diuretic. The study showed that enalapril significantly lowered both systolic and diastolic blood pressure. At each timepoint measured in the course of 26 weeks of therapy, the patients in the enalapril group consistently had greater decreases in blood pressure than patients in the propranolol group although not always significantly. The enalapril treatment group had a decrease in the mean arterial blood pressure of 22.2 mmHg compared to the propranolol group of 17.9 mmHg at the end of the study. These results were similarly independent of the way the data were analyzed. Fewer patients in the enalapril group required the addition of hydrochlorothiazide to maintain optimal control of blood pressure. Enalapril was found to be safe and well tolerated over the long-term of 48 weeks. Side effects such as leukopenia and taste perversions believed to be sulfhydryl-related were not encountered. The occurrence of rash and proteinuria was rare. Thiazide-induced hypokalemia, hyperuricemia and hyperglycemia appeared to be attenuated by enalapril. The favorable efficacy and side-effect profile provide the basis for enalapril to be a drug of choice when initiating antihypertensive therapy.
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PMID:Long-term enalapril--a new converting enzyme inhibitor--in the treatment of mild to moderate essential hypertension, results of a worldwide multiclinic study. Comparing two ways of analyzing data. 300 72

Angiotensin-converting enzyme (ACE) inhibitors are a new class of drugs, whose main indications are the treatment of hypertension and of heart failure. Data obtained with captopril, the first orally active ACE inhibitor, affords an understanding of the rationale of their therapeutic use based on the knowledge of their mechanisms of action, efficacy, contraindications and precautions, dosage and frequency of administration, side-effects, interactions and advantages. ACE inhibitors appear to exert their haemodynamic effect mainly by inhibiting the renin-angiotensin-aldosterone system, but also by modulating sympathetic nervous system activity and by increasing prostaglandin synthesis. Therefore they act both on vasoconstrictor and volume factors, since they cause vasodilation (the main effect) and mild natriuresis without affecting the heart rate and contractility and, probably, favourably influencing renal, coronary and cerebral circulation. So far it appears that ACE inhibitors can be usefully employed in the treatment of heart failure, in which they reduce both pre- and after-load, and mainly of hypertension. In the past captopril has been used to treat only severe and or resistant hypertension and some secondary forms, like renal parenchymal and renovascular hypertension, but now it seems that captopril is useful also to treat mild to moderate essential hypertension. Their efficacy in reducing blood pressure is similar to that of thiazide diuretics and of beta-blockers, the two drugs now considered of first choice and they exert their hypotensive action without the development of pseudotolerance or tolerance. ACE inhibitors seem, at the moment, contraindicated in pregnancy and in hyperkalaemic syndromes and must be used with caution in patients with collagen disease (mainly associated with renal failure), with severe bilateral renal artery stenosis (and with severe artery stenosis of a solitary kidney) and with severe sodium depletion. It is now established that captopril has a flat dose response curve and that it must be given (twice daily) at a dose not exceeding 150 mg/day. The same pharmacological approach must be used with future ACE inhibitors in order to establish the right posology and the frequency of administration. In this respect enalapril seems to be a promising ACE inhibitor with a prolonged action (at least 24 hours). The exact posology of ACE inhibitors might be crucial, since it has been shown that the side-effects of captopril (skin rashes, fever, taste disturbances, proteinuria and neutropenia) are dose dependent.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Angiotensin-converting enzyme inhibitors in hypertension: a review. 300 82

The long-term antihypertensive response to captopril (25-50 mg/day) and 75g oral glucose tolerance (75g oGTT) following a 6-10 month period of captopril administration was evaluated in 20 patients with essential hypertension without persistent proteinuria. Eleven of these 20 patients exhibited impaired glucose tolerance (IGT), while the remaining nine patients had normal glucose tolerance (NGT). All patients tolerated long-term captopril therapy with no untoward effects. Six months' administration of captopril significantly decreased blood pressure in patients with NGT from 171 +/- 12/105 +/- 5 mm Hg (mean +/- SE) to 146 +/- 7/88 +/- 4 mm Hg. Also in patients with IGT, long-term captopril therapy decreased blood pressure from 165 +/- 3/97 +/- 2 to 143 +/- 5/86 +/- 2 mm Hg. No patient with NGT developed diabetes mellitus. Neither fasting nor post-glucose-load venous blood glucose deteriorated in any of the patients during the therapy. There were no significant changes in the insulinogenic index (delta IRI/delta BG at 30 minutes after glucose load) in both the patients with NGT and IGT. In patients with IGT, the concentration of glycosylated hemoglobin (Hb A1 and Hb A1c slightly but significantly decreased from 8.1 +/- 0.3 to 7.7 +/- 0.4% (P less than 0.05) and from 5.9 +/- 0.3 to 5.5 +/- 0.3% (P less than 0.01) after 6.2 +/- 1.4 months' captopril therapy. These results suggest that in addition to its antihypertensive effects, long-term captopril therapy does not compromise glucose metabolism in hypertensive patients.
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PMID:Long-term captopril therapy with no effect on glucose metabolism in patients with essential hypertension. 304 27

Numerous trials have shown the efficacy of ACE-inhibitors in moderate and severe essential hypertension. Their use must be regarded as very promising. They lower peripheral vascular resistance without influencing cardiac index and heart rate. Additionally, they maintain serum potassium and do not effect plasma lipids or provoke diabetes mellitus or gout. In 20-30% of hypertensive patients ACE-inhibitors have to be combined with diuretics and/or calcium antagonists. The addition of beta-blockers is useful in patients with resting tachycardia. In mild hypertension the use of ACE-inhibitors as first-line drugs is indicated in patients with adverse reactions to beta-blockers or diuretics. In bilateral renovascular hypertension, ACE-inhibitors may induce a strong blood pressure fall; in bilateral stenosis they contribute to a deterioration of renal function with reversible renal insufficiency. In renoparenchymal hypertension, ACE-inhibitors may attenuate the progression of renal insufficiency; in addition, proteinuria is lowered. In systolic hypertension in the elderly, one must be aware of a marked first-dose hypotensive effect. ACE-inhibitors decrease exaggerated exercise-induced elevation of blood pressure and heart rate and therefore lower myocardial oxygen consumption. In patients with hypertension and diabetes mellitus, antihypertensive treatment should be initiated for blood pressure levels above 140/90 mmHg, to attenuate the progression of vascular damage in the kidney. In patients with severe left ventricular hypertrophy, ACE-inhibitors reduce left ventricular mass within three months by about 30%. In hypertension and coronary heart disease, recent studies report benefits of ACE-inhibitors on coronary circulation. Presently available ACE-inhibitors and those in preparation do not differ in pharmacodynamic, but in pharmacokinetic properties, concerning the beginning and duration of blood pressure lowering. A hypotensive first-dose effect can be observed in diuretic pretreated patients, in severe (malignant) and renovascular hypertension. ACE-inhibitors should not be used during pregnancy or in patients with autoimmune diseases or those undergoing treatment with immunosuppressive drugs, due to the side effects of neutropenia and proteinuria, which are more often seen under these conditions. Results from long-term studies on the influence of ACE-inhibitor treatment on cardiovascular risk in mild hypertension have not been available until now. In the decision to treat mild hypertension with ACE-inhibitors as first-line drug therapy, the costs of therapy in comparison to cheaper antihypertensives must be taken into account.
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PMID:[The value of angiotensin-converting enzyme inhibitors in the treatment of hypertension]. 306 60

Within hypertensive populations, the risk of future cardiovascular complications and of death varies substantially according to the risk factor profile of the hypertensive subject. In primary hypertension, significant renal insufficiency is rarely observed, whereas proteinuria can be observed at various frequencies according to the method of analysis and severity of hypertension. The incidence of clinically apparent proteinuria varies between 4 and 16% in different hypertensive patient series. One prospective observational, epidemiological study has clearly shown that proteinuria is an important, independent predictor of both mortality and cardiovascular morbidity in an untreated population. Two large studies of hypertensive populations treated for 4 and 10 years, respectively, have shown that clinically apparent proteinuria remains as an independent predictor of death and cardiovascular morbidity in treated patients. A third long term study suggests that 'microalbuminuria' (i.e. subclinical urinary albumin excretion), if present at start of therapy, also has an important prognostic meaning during long term follow-up. However, it is not yet known whether a reduction and normalisation of the urinary excretion of albumin during long term treatment will also be associated with an improved prognosis.
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PMID:Proteinuria as a prognostic factor during long term hypertensive care. 306 85

Captopril is an orally active inhibitor of angiotensin-converting enzyme (ACE) and has been widely studied in the treatment of patients with mild to moderate essential hypertension, severe hypertension not responsive to conventional diuretic/beta-adrenoceptor blocker/vasodilator regimens, and patients with chronic congestive heart failure refractory to treatment with a diuretic and digitalis. In patients with mild or moderate essential hypertension, titrated low doses of captopril used alone or in conjunction with a diuretic are similar in efficacy to usual doses of hydrochlorothiazide, chlorthalidone, or beta-adrenoceptor blocking drugs, as well as to the other ACE inhibitors. In addition, captopril improved well-being to a greater extent than methyldopa or propranolol in a study designed specifically to determine the effect of treatment on the quality of life of patients with mild or moderate essential hypertension. The earlier demonstrated efficacy of captopril, used with a diuretic and often also with a beta-adrenoceptor blocking drug, in the treatment of severe hypertension refractory to conventional 'triple therapy' has been confirmed in more recent trials which illustrate the generally marked antihypertensive effect of captopril-containing regimens in such patients. Results of initial trials in patients with scleroderma are promising, with control of hypertension and stabilization of renal function in these patients when treated at an early stage of the disease. Several comparative and long term trials of captopril in patients with chronic congestive heart failure refractory to treatment with a diuretic/digitalis regimen clearly demonstrate that initial haemodynamic improvement is maintained and correlates with clinical benefit. A tendency for overall clinical response to captopril to be better than the response to prazosin, hydralazine, nisoldipine or enalapril has been reported. Results of a multicentre comparison with digoxin and placebo indicate that captopril is a suitable alternative to digoxin in patients with mild to moderate heart failure who are receiving maintenance diuretic therapy. The tolerability of captopril has now been studied in many thousands of patients involved in formalized trials and the early impression of poor tolerability can no longer be justified. The use of generally lower dosages of captopril in patients with normal or slightly impaired renal function has resulted in a generally low incidence of rash (0.5 to 4%), dysgeusia (0.1 to 3%), proteinuria (0.5%), neutropenia (0.3% during first 3 months) and symptomatic hypotension (0.1 to 3%). Cough is an infrequent but troublesome effect resulting from ACE inhibition.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Captopril. An update of its pharmacodynamic and pharmacokinetic properties, and therapeutic use in hypertension and congestive heart failure. 306 99

The relation between hypertension and diabetic nephropathy is complex. Nephropathy is probably involved in the elevated blood pressure found in diabetic patients. In maturity onset diabetes, patients may also have hypertension which is associated with obesity or essential hypertension. It has been suggested that in both types of diabetes, hypertension enhances the development of diabetic nephropathy. Moreover, an aggressive antihypertensive treatment seems able to reduce rate of decline in kidney function in insulin-dependent diabetic patients with patent nephropathy. In this work, creatinine clearance and microalbuminuria in 20 diabetic patients (mostly with maturity-onset-diabetes) with known moderate and effectively treated hypertension were therefore measured and the results were compared with those for 18 normotensive diabetic patients and 22 controls. Duration of diabetes was from one to 26 years (mean: 11 years) and duration of hypertension was from one to 35 years (mean: 10 years). Patients and controls had normal serum creatinine and proteinuria below 0.1 g/l. Microalbuminuria was measured by immunonephelometric assay using specific antiserum (sensitivity = 1.5 mg/l; intra and interassay coefficients: 6.5% and 8% respectively). The highest value was observed in hypertensive diabetic patients with retinopathy (group 1). But hypertensive patients without retinopathy (group 2) and normotensive patients also had significantly increased microalbuminuria. In group 1, microalbuminuria was significantly higher than in group 2. The creatinine clearance was reduced in groups 1 and 2 versus normotensive diabetics, but hypertensive patients were older.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Microalbuminuria in diabetics with moderate hypertension]. 309 93

Heavy proteinuria in patients with essential hypertension raises the question of underlying primary renal disease. While malignant hypertension may be associated with proteinuria in the nephrotic range, it is generally held that protein excretion in benign nephrosclerosis is almost invariably less than 0.5-1.0 g/24 h. We report 18 patients with biopsy-proven hypertensive nephropathy and heavy proteinuria, of which only 6 had malignant hypertension. In the remaining 12 patients with benign nephrosclerosis, protein excretion reached up to 6.5 g/24 h, and nephrotic range proteinuria was present in 3 patients. All patients with heavy proteinuria suffered from long-standing moderate or severe, poorly controlled hypertension and were azotemic. We suggest that hypertensive nephrosclerosis be included in the differential diagnosis of massive proteinuria accompanying azotemia in poorly controlled hypertensives.
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PMID:Marked proteinuria in hypertensive nephrosclerosis. 316 Feb 40

Spontaneous (not experimentally induced) systemic hypertension was detected in 5 male dogs that were examined because of apparent blindness caused by intraocular hemorrhage and/or retinal detachment. Secondary causes of hypertension, including renal, adrenal, and thyroid disease, were investigated. Four of the dogs had glomerulonephropathy, renal insufficiency, and proteinuria. Four dogs had compensatory cardiac hypertrophy. Hypertension in 4 of 5 dogs was associated with glomerulosclerosis with chronic renal insufficiency, bilateral adrenocortical hyperplasia, adrenocortical adenoma with renal amyloidosis, and immune-mediated glomerulonephritis with chronic renal insufficiency, respectively. The fifth dog was determined to have essential hypertension. The dogs were treated for their primary diseases. Sodium restriction alone was inadequate to reduce blood pressure; 4 of the dogs also required antihypertensive medications.
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PMID:Spontaneous systemic hypertension in dogs: five cases (1981-1983). 317 Mar 25

In 51 patients with pregnancy hypertension (H) and 51 normotensive gravid women (N), matched for age of gestation, plasma prolactin was measured at 8.30 am (PRL1) and 9.30 am (PRL2) in basal conditions and after 10 minutes of upright posture (PRL3). While in N there was a fall from PRL1 to PRL2 which was nonsignificant, in H there was a significant fall from PRL1 to PRL2. With upright posture there was a further decrease in prolactin in N and a significant increase in H. With multiple regression analysis, systolic and diastolic blood pressure did not show any independent relations with PRL1, PRL2 and PRL3, while serum proteins and proteinuria showed a significant relation with PRL1, as did serum proteins, serum potassium and serum urate with PRL2 and serum urate with PRL3. As has been suggested in primary hypertension, a certain increase in peripheral sympathetic tone, dependent on a decreased central dopaminergic activity, may be present in patients who develop pregnancy hypertension compared to normotensive pregnant controls and may be involved in the pathogenesis of pregnancy hypertension.
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PMID:Role of prolactin in pregnancy hypertension. 330 30


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