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)

30 hypertensive patients were treated in outpatients conditions for a 6 month period with captopril "Pharmachem". The patients were classified in accordance with the degree of the arterial hypertension into three groups: light hypertension--II patients, moderate hypertension 13 patients and severe hypertension--6 patients. Captopril was applied the first two weeks in a dose of 25 mg 3 times daily. When there was no effect the dose was increased every two weeks with 25 mg daily up to a 150 mg daily dose. A very good result was achieved in 11 patients (36.7%) and in 15 patients (50%) the result was considered good. In 4 patients the arterial pressure fell to normal after the addition of chlorthalidone. The following side effects were observed: decrease of the leucocyte number in reference ranges, insignificant increase of the uric acid in reference ranges, proteinuria below 1 gr/24 h. Captopril "Pharmachem" applied alone or in combination with a diuretic is a very efficient drug for the treatment of all stages of arterial hypertension.
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PMID:[Captopril from Pharmachem in the treatment of arterial hypertension]. 267 94

We studied the long-term effect of an angiotensin converting enzyme (ACE) inhibitor, captopril, on the progression of chronic renal failure and on the rate of urinary protein excretion. When compared with standard triple therapy, captopril slowed the progression of renal failure. Captopril was also able to reduce the proteinuria of non-diabetic glomerular origin. This reduction was not dependent on the presence or absence of arterial hypertension but was limited by the presence of low serum albumin levels, and only occurred in patients with proteinuria in excess of 3 g/24 h.
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PMID:Effects of angiotensin converting enzyme inhibitors on the progression of renal failure and proteinuria in humans. 269 57

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

The authors studied clinical and biological data occurring in 165 patients observed during 23 years and afflicted with polyarteritis nodosa. Hypertension was present in 52 patients (31.5%) and seven of them suffered from malignant hypertension (4%). Mean age of patients (6 male, 1 female), with malignant hypertension was 38 +/- years old. Mean follow up was 49 +/- 28 months including 26 +/- 21 months after discontinuation of treatment of polyarteritis nodosa. Malignant hypertension occurred during the first year of evolution of polyarteritis nodosa. Renal insufficiency was present in 5 of 7 patients. Proteinuria was greater than 1 gr/d in 4 cases. Renal arteriography was performed in 6 patients and showed in every case renal ischemia and microaneurysms in five. In 4 patients measurements of plasma renin activity and of aldosterone were obtained. A stimulation of those hormones was demonstrated. Some symptoms of polyarteritis nodosa were present with a high incidence in case of malignant hypertension: digestive signs (6/7), orchitis (3/6). HBs antigen was present in 6 cases and hepatitis in 5. Captopril was effective in every case, alone or associated with other treatments. Follow up of hypertension went from 8 months to 4 years. At present time 6 patients are alive and one is lost of follow up. A treatment is necessary in 6 of 7 patients. Creatininemia is greater than 300 micromol/l in 4 patients. A successful kidney transplantation was performed in one case. Our study shows a close relation between malignant hypertension observed in polyarteritis nodosa, vascular nephropathy, digestive and urologic signs. Hepatitis B virus could be responsible of those manifestations.
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PMID:[Malignant arterial hypertension in periarteritis nodosa. Incidence, clinicobiologic parameters and prognosis based on a series of 165 cases]. 287 20

The chemistry, pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosage of enalapril maleate, a nonsulfhydryl angiotensin-converting enzyme (ACE) inhibitor, are reviewed. Enalapril is rapidly converted by ester hydrolysis to enalaprilat, a potent ACE inhibitor; enalapril itself is only a weak ACE inhibitor. Enalapril lowers peripheral vascular resistance without causing an increase in heart rate. In patients with congestive heart failure, enalapril has beneficial hemodynamic effects based on reduction of both cardiac preload and afterload. Approximately 60% of a dose of enalapril is absorbed after oral administration. Excretion of enalaprilat is primarily renal. Accumulation of enalaprilat occurs in patients with creatinine clearances less than 30 mL/min. Enalapril 10-40 mg per day orally has shown efficacy comparable to that of captopril in treating patients with mild, moderate, and severe hypertension, hypertension caused by renal-artery stenosis, and in congestive heart failure resistant to digitalis and diuretics. When given alone for hypertension, enalapril has efficacy comparable to that of thiazide diuretics and beta blockers. Side effects observed with enalapril have generally been minor. Captopril-associated side effects such as skin rash, loss of taste, and proteinuria have been observed in a small number of patients receiving enalapril to date; neutropenia less than 300/mm3 has been noted with captopril but not enalapril. The incidence of these side effects has been noted to be greatly decreased in patients on low doses of captopril. Enalapril appears to be similar in efficacy to captopril for treating hypertension and congestive heart failure. Whether enalapril is safer than low-dose captopril in patients at high risk for captopril-associated side effects will require further investigation.
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PMID:Enalapril, a nonsulfhydryl angiotensin-converting enzyme inhibitor. 298 41

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

MRL lpr/lpr (MRL/l) mice exhibit a disease similar to systemic lupus erythematosus (SLE) in humans. To investigate the influence of antihypertensive treatment on this disease, four groups of MRL/l mice were treated with the angiotensin-converting enzyme inhibitor captopril (n = 25), with the sympathetic blocker bretylium (n = 15), and with cyclophosphamide (n = 10). Thirty-five mice did not receive any treatment and served as controls. Survival rate, blood pressure, incidence of proteinuria and hematuria, renal pathology, lymphoid hyperplasia and dermatitis were studied. The survival at the age of 36 weeks was significantly improved by captopril as compared to controls (60 vs. 25%, p = 0.035). The cyclophosphamide group showed no mortality at that time and the bretylium group did not differ from the control group. Captopril and bretylium reduced systolic blood pressure significantly while cyclophosphamide was without effect. Captopril and cyclophosphamide diminished significantly the glomerular damage with less proliferative changes and a decreased incidence of proteinuria. The bretylium-treated animals also exhibited an improved renal pathology index but they did not differ from the controls with respect to proteinuria and hematuria. Lymphoid hyperplasia and dermatitis were decreased only by captopril and cyclophosphamide. It is concluded that captopril improves survival in SLE disease of MRL/l mice, counteracting lymphoid hyperplasia, renal disease, dermatitis and decreasing arterial blood pressure.
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PMID:Beneficial effect of captopril on systemic lupus erythematosus-like disease in MRL lpr/lpr mice. 328 May 1

Oral treatment of female NZB/NZW F1 hybrid mice with captopril prevented the development of proteinuria and prolonged survival in mice demonstrating slight (trace to 1+) proteinuria. Captopril treatment also markedly reduced the incidence and magnitude of proteinuria and prevented death in mice showing significant (3+ or greater) proteinuria. Histopathological studies of the kidneys of treated mice further demonstrated improvements in the renal lesions of autoimmune mice. The mechanisms whereby captopril treatment influences the course of disease in NZB/NZW mice are not known.
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PMID:Effect of captopril treatment on proteinuria in NZB/NZW F1 hybrid mice. 328 64

The progression of adriamycin-induced nephrotic syndrome in rats was studied over a 3-month period. The effect of an angiotensin-converting enzyme inhibitor, captopril, on this model of renal disease, was also studied. Two weeks following a single iv injection of adriamycin, rats were divided into two treatment groups: one received a daily po dose of captopril and the other received a placebo. Measurements of renal function were performed at 4, 8, and 11 weeks following the initiation of therapy. Necropsies and light microscopic evaluation of the kidneys were performed at the end of the treatment period. Functional and morphologic alterations in both groups of rats were compared to each other and to normal age/weight-matched control rats studied over the same time period. At 13 weeks following the administration of adriamycin, both treatment groups had significant renal dysfunction when compared to normal controls. In addition to severe proteinuria, rats receiving adriamycin exhibited polyuria, polydipsia, increased plasma urea nitrogen and plasma creatinine, and decreased endogenous creatinine clearance. They had severe generalized kidney lesions characterized by tubular dilation and atrophy, cast formation, interstitial fibrosis and lymphocytic infiltration, and focal, global glomerulosclerosis. The histopathologic ranking of the kidneys was correlated with some antemortem laboratory parameters but not with the degree of proteinuria. Captopril had no ameliorating effects on the progression of renal disease. Certain findings indicate that captopril may actually have promoted the deterioration of renal function. We conclude that adriamycin-induced nephrotic syndrome in the rat is a progressive disease resulting in generalized renal dysfunction, and that captopril, at the dose given in this experiment, is unable to slow the progression of the disease.
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PMID:The progression of adriamycin-induced nephrotic syndrome in rats and the effect of captopril. 351 65

The effect of captopril, an angiotensin converting enzyme inhibitor, on the progression of chronic puromycin aminonucleoside (PAN) nephrosis was examined. Rats were injected with 15 mg/100 gm body weight PAN and 5 mg/100 gm body weight, on weeks - 1 and 5, respectively. A third group was injected with an equivalent volume of 0.9% saline, intraperitoneally (Group III) on week - 1 and 5. Beginning week 0, group I received 50 mg/kg captopril daily in the drinking water for 12 weeks. Group II received no treatment. Captopril failed to attenuate the peak level of proteinuria induced by the first injection of PAN or to alter the rate of decline of proteinuria when begun 1 week after the PAN injection. However, captopril did blunt the increase in urinary protein excretion following the second injection of PAN (p less than 0.05). Group II became hypertensive compared to Group I on week 8 and 12 and Group III on week 12 (p less than 0.05). Group I and II could not be distinguished on the basis of renal histologic rank (p = 0.80). We conclude that captopril affords some protection against the development of PAN-induced proteinuria, but it does not accelerate the recovery phase when glomerular permselectivity is being regained.
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PMID:Effect of captopril on chronic puromycin aminonucleoside nephrosis in rats. 353 53


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