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)

Both dietary protein restriction and angiotensin converting enzyme inhibitors (CEI) reduce proteinuria in experimental renal disease. To determine whether the effects of dietary protein on albuminuria (UalbV) in nephrotic rats are modified by CEI, we measured UalbV and glomerular filtration rate (GFR) in rats with passive Heymann nephritis fed 40 (HP) or 8.5% (LP) protein diets. Half of each group received enalapril beginning 2 days after injection of antibody. Enalapril prevented the greater UalbV and fractional clearance of albumin (FCalb) observed in HP (HP + enalapril, 136 +/- 44 mg/day and 0.88 +/- 0.54 X 10(-2), vs. HP, 368 +/- 60 mg/day and 4.40 +/- 2.90 X 10(-2), P less than 0.05 and P less than 0.05, respectively) but did not alter GFR significantly. Enalapril did not alter UalbV or FCalb in LP. To determine if CEI would reduce UalbV in rats after proteinuria was already present, rats fed 21% protein were studied 1 wk after the onset of proteinuria. Enalapril decreased UalbV (423 +/- 35 to 169 +/- 18 mg/day, P less than 0.001) and FCalb (3.19 +/- 0.36 X 10(-2) to 0.71 +/- 0.11 X 10(-2), P less than 0.001) after 3 days. Thus CEI reduced albuminuria in nephrotic rats fed high- or normal-protein diets without modifying GFR or serum albumin. This effect may be due to changes in glomerular hemodynamics or permselectivity.
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PMID:Modulation of albuminuria by dietary protein and converting enzyme inhibition. 282 30

The effects of the angiotensin converting enzyme (ACE) inhibitor enalapril on the proteinuria and degree of focal glomerular sclerosis hyalinosis (FSH) in chronic puromycin aminonucleoside nephropathy (PAN) were examined. Chronic PAN was induced in male Sprague-Dawley rats by seven subcutaneous injections of puromycin aminonucleoside (20 mg/kg) over 10 weeks (Groups I and II). Group II rats also received enalapril 10 mg/kg/day in the drinking water throughout the study (12 weeks). Group III rats served as age-matched controls. Proteinuria was similar in Groups I and II (35.5 +/- 9.7 versus 29.1 +/- 4.1 mg protein/mg creatinine, mean +/- SEM, P greater than 0.05). Serum creatinine remained unchanged in Group I, but rose from 0.7 +/- 0.04 to 1.2 +/- 0.1 mg/dl (mean +/- SEM, P less than 0.05) in Group II. FSH was 13.8% in Group I, 12.9% in Group II (P greater than 0.05), and 0.6% in Group III. There was no significant difference in glomerular lipid content and in immunofluorescence for rat albumin, fibrinogen, IgM, IgG, and C3 between Groups I and II. ACE activity was inhibited by 94% in serum, 83% in lungs, and 92% in kidneys; and blood pressure response to. Angiotensin I challenge was decreased by 50% in rats similarly treated with enalapril versus controls. In summary, proteinuria and glomerular sclerosis in this model are not affected by ACE inhibition.
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PMID:Failure of angiotensin converting enzyme inhibition to affect the course of chronic puromycin aminonucleoside nephropathy. 282 16

In view of the pharmacological and chemical reasons for using ACE-inhibitors to treat diabetic hypertension, a group of 40 outpatients were treated with Enalapril. The sample consisted of 20 outpatients, 6 males, 14 females aged 48-76 (mean age 63.75), 18 of whom had type II and 2 type I diabetes and 11 under treatment by diet and hypoglycaemic drugs or insulin. All these patients presented slight or moderate essential arterial hypertension (diastolic pressure less than 115 mmHg). For about one year 17 of the patients were given 20 mg/die Enalapril and the remaining three 10 mg/die in a single morning dose. In 16 cases no other treatment was given. In 4 a non-potassium conserving diuretic was also given. Check-ups before six months into and at the end of treatment showed: a statistically significant reduction in systolic (p less than 0.05) and diastolic (p less than 0.01) pressure. In contrast no significant change was noted in heart beat, glycaemia before or after meals, body weight, glycosylated haemoglobin or any other blood chemical parameter considered. In one case only there was a slight increase in proteinuria that was however present at the start of treatment. As far as side effects are concerned there was one case of cardiac palmus during treatment and one case of coughing that regressed totally when treatment was suspended but nothing else of significance. It should be noted that the antidiabetic treatment remained unchanged throughout the period considered in most cases and at most was subjected to minimal qualitative and quantitative adjustments.
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PMID:[Prolonged treatment of hypertension in diabetic patients with enalapril. 1-year follow-up]. 282 79

Oral inhibitors of angiotensin converting enzyme (ACE) now have an established place in the treatment of hypertension and heart failure. Captopril, the first of these agents, was initially used in high doses and was associated with adverse effects including proteinuria, skin rash and taste disturbance. We report 11 patients who developed side effects during captopril therapy (proteinuria two, rash four, taste disturbance four and taste disturbance with rash one) who were subsequently treated with enalapril, a second generation angiotensin converting enzyme inhibitor. Proteinuria did not recur in either patient, skin rash resolved in all five cases and taste disturbance resolved in four of five during enalapril therapy. We conclude that the side effects of proteinuria, skin rash and taste disturbance are consequences of captopril idiosyncrasy rather than inhibition of the angiotensin converting enzyme. The reported incidence of these side effects with the current recommended dosage of captopril is low.
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PMID:Lack of cross sensitivity between captopril and enalapril. 284 55

A collective, multicentre (Ljubljana, Split, Zagreb) comparison of the antihypertensive effects between two angiotensin converting enzyme inhibitors (ACEI) captopril and enalapril was made in 69 hypertensives of both sexes, having a diastolic blood pressure (DBP), following two weeks on a placebo, of between 110 and 130 mm Hg (14.7 and 17.3 kPa). There were 35 patients on enalapril (20-40 mg), and 34 on captopril (50-100 mg). Both drugs under study decreased significantly the mean DBP already after the first week of ACEI treatment (p less than 0.001). By the end of the trial (9th week) captopril had decreased the DBP in the supine position from the initial 180.3 +/- 15.3/117.7 +/- 6.4 mm Hg to 151.6 +/- 11.1/96.8 +/- 7.2 mm Hg. Enalapril had lowered the DBP more efficiently: from 182.7 +/- 16.7/118.7 +/- 7.7 to 145.6 +/- 12.8/92.2 +/- 6.4 mm Hg (p less than 0.05). The average reduction in mean DBP was 16.9% on captopril, and 20.9% on enalapril. Low dose ACEI monotherapy (i.e. 50 mg and 20 mg) achieved DBP normalization in 11.8% on captopril and in 26.4% on enalapril (p less than 0.01). There were no significant heart rate changes. The laboratory results did not change appreciably and there were no relevant side-effects, although particular attention was paid to the expected adverse reactions, such as cough, ageusia or proteinuria. It is concluded that the ACEIs under study showed comparable effectiveness within the used dose range, enalapril being more potent, longer acting, and possibly safer.
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PMID:Enalapril versus captopril: a double-blind multicentre comparison in essential hypertension. 284 Dec 51

Angiotensin II is the main regulator of both glomerular haemodynamics and glomerular capillary permeability. An alteration in the function of intrarenal angiotensin II seems to be the cause of diabetic glomerulopathy in animals and humans. In order to investigate the renal effects of the angiotensin converting enzyme (ACE) inhibitor enalapril (5 mg once a day), 24 normotensive diabetic patients with persistent proteinuria, after a 3-month run-in period, were randomly allocated to receive the active drug (12 patients) or the corresponding placebo, for the 6 months. Effective renal plasma flow, glomerular filtration rate, renal vascular resistance and filtration fraction were measured at the end of the run-in and the treatment periods. Blood pressure, heart rate, urinary albumin excretion, plasma renin activity and aldosterone, blood glucose, serum fructosamine and body weight were checked monthly during the run-in and every 2 months during the treatment period. Enalapril decreased urinary albumin excretion in the normotensive diabetic patients without any changes in systemic blood pressure or glomerular haemodynamics. These results indicate that ACE inhibition interferes with the glomerular capillary permeability induced by angiotensin II.
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PMID:Angiotensin converting enzyme inhibition with a low dose of enalapril in normotensive diabetics with persistent proteinuria. 285 53

The MRL/1 and New Zealand black-New Zealand white cross (NZB x W) mice spontaneously develop a disease similar to systemic lupus erythematosus in man. The effect of antihypertensive treatment on MRL/1 and NZB x W mice was studied with respect to survival, blood pressure, proteinuria, haematuria and renal histopathology. The treatment consisted of angiotensin converting enzyme (ACE) inhibitors (captopril and enalapril) and bretylium, a sympathetic blocker. Tail systolic blood pressure was measured with a strain gauge technique. All antihypertensive drugs caused a reduction in blood pressure in both strains. In MRL/1 bretylium and both ACE inhibitors improved renal histopathology, but only captopril prolonged survival, and it decreased proteinuria and haematuria. In NZB x W captopril decreased proteinuria but did not influence survival or renal histopathology. Bretylium was without any effect on these parameters. At the doses used captopril improves survival in MRL/1 mice and decreases proteinuria and haematuria in both MRL/1 and NZB x W mice. Since bretylium and enalapril lack this property despite a similar blood pressure reduction, it seems to be a drug-specific action.
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PMID:Effect of captopril on murine systemic lupus erythematosus disease. 285 67

Systemic hypertension does not always reflect concomitant glomerular hypertension. At similar levels of systemic hypertension, glomerular injury occurs only in kidneys that lack protective preglomerular vasoconstriction, which results in glomerular hypertension. indeed, glomerular hypertension and glomerular injury do not develop in rats with spontaneous hypertension that have effective preglomerular vasoconstriction. In the experiments reported herein, the normal adaptive response (afferent arteriolar dilation) to a reduction of one and five-sixths of the renal mass in rats with spontaneous hypertension was examined to ascertain whether that response would expose the remaining nephrons to the injurious effects of high perfusion pressure. In addition, the efficacies of two different antihypertensive regimens were compared. Rats with spontaneous hypertension received either no therapy, or a combination of hydralazine, reserpine, and hydrochlorothiazide, or the angiotensin converting enzyme inhibitor enalapril. Three weeks after ablation of one and five-sixths of the renal mass, blood pressure, glomerular filtration rate, urinary protein excretion, and histologic injury scores for mesangial expansion and glomerulosclerosis were determined. Untreated rats with hypertension had severe glomerulosclerosis and mesangial expansion. Both antihypertensive regimens normalized systemic blood pressure and reduced glomerulosclerosis. However, enalapril was more effective than the combination of hydralazine, reserpine, and hydrochlorothiazide in reducing the exaggerated glomerular filtration rate (0.52 +/- 0.40 versus 0.82 +/- 0.10 ml per minute; p less than 0.05), the injury score for mesangial expansion (79 versus 103; p less than 0.05), and the degree of proteinuria (32 +/- 4 versus 42 +/- 3 mg per 24 hours; p less than 0.05). Persistence of hyperfiltration accompanied by increased mesangial expansion, may lead to progression of glomerular damage despite "adequate" control of systemic hypertension, as observed in rats treated with a combination of hydralazine, reserpine, and hydrochlorothiazide.
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PMID:Therapeutic implications of hypertension-induced glomerular injury. Comparison of enalapril and a combination of hydralazine, reserpine, and hydrochlorothiazide in an experimental model. 299 45

Micropuncture and morphologic studies were performed in six groups of male Munich-Wistar rats after removal of the right kidney and segmental infarction of two-thirds of the left kidney. Groups 1 and 4 received no specific therapy. Groups 2 and 5 were treated with the angiotensin I-converting enzyme inhibitor, enalapril, 50 mg/liter, in the drinking water. Groups 3 and 6 were treated with reserpine (5 mg/liter), hydralazine (80 mg/liter), and hydrochlorothiazide (25 mg/liter). All rats were fed standard chow. Groups 1-3 underwent micropuncture study 4 wk after renal ablation. Untreated group 1 rats exhibited systemic hypertension and elevation of the single nephron glomerular filtration rate (SNGFR) due to high average values for the mean glomerular transcapillary hydraulic pressure gradient (delta P) and glomerular plasma flow rate (QA). In group 2 rats, treatment with enalapril prevented systemic hypertension and maintained delta P at near-normal levels without significant reduction in SNGFR and QA. In contrast, triple drug therapy normalized systemic hypertension, but failed to lower delta P in group 3 rats. Groups 4-6 were followed for 12 wk after renal ablation. Untreated group 4 rats demonstrated continuous systemic hypertension, progressive proteinuria, and glomerular structural lesions, including mesangial expansion and frequent areas of segmental sclerosis. In group 5 rats, treatment with enalapril maintained systemic blood pressure at normal levels over the 12-wk period and dramatically limited the development of proteinuria and glomerular lesions. Despite equivalent systemic blood pressure control in group 6 rats, failure of triple drug therapy to control glomerular hypertension was associated with progressive proteinuria and glomerular lesions comparable to those seen in untreated group 4 rats. Thus, unless glomerular capillary hypertension is corrected, control of systemic blood pressure is insufficient to prevent progressive renal injury in rats with reduced renal mass.
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PMID:Therapeutic advantage of converting enzyme inhibitors in arresting progressive renal disease associated with systemic hypertension in the rat. 301 63

The safety profiles of the angiotensin converting enzyme inhibitors, captopril and enalapril, are the focus of this review. Adverse effects are reviewed as those associated with sulfhydryl compounds and as those considered class-specific adverse effects of angiotensin converting enzyme inhibitors. Specifically discussed are the incidences of the adverse effects of rash, taste disturbance, neutropenia, and proteinuria, which are characteristic of compounds containing sulfhydryl moieties, such as captopril. It is concluded from the review of these safety data that enalapril is well tolerated, has few class-specific adverse effects, and may offer a potential advantage over captopril by having fewer sulfhydryl-related adverse effects.
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PMID:Safety profiles of the angiotensin converting enzyme inhibitors captopril and enalapril. 302 84


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