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)

We investigated the effect of captopril, an orally active angiotensin converting enzyme inhibitor, on urinary protein excretion in puromycin aminonucleoside nephrotic rats. The administration of captopril (10 mg/100 g body weight) decreased proteinuria on days 10-14 following the administration of puromycin aminonucleoside (73.0 versus 125.0 mg, p less than 0.01), without affecting glomerular filtration rate. The beneficial effect of captopril was not abolished by the continuous intravenous infusion of angiotensin II (10 micrograms/kg/h for 9 days) or subcutaneous injections of aprotinin (50,000 KIU/day for 3 days). Indomethacin, in moderate (5 mg/kg/day for 3 days) or high (10 mg/kg/day) doses, abolished the captopril attenuation in urinary protein excretion. The salutory effect of captopril was characterized by a reduction in the fractional excretion of protein without compromising the glomerular filtration rate. No difference in renal ultrastructure was noted in captopril-treated versus control animals. Captopril was ineffective in reducing urinary protein excretion in rats with adriamycin-induced glomerulopathy. We conclude that captopril acts to reduce proteinuria in renal disease states arising from depletion of the glomerular basement membrane polyanion. The mechanism of action is postulated to be an alteration in renal hemodynamics, namely increased blood flow and a decrease in the ultrafiltration coefficient, that are the consequence of increased intrarenal prostaglandin production.
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PMID:The effect of captopril on urinary protein excretion in puromycin aminonucleoside nephrosis in rats. 389 1

We investigated whether captopril, an angiotensin-converting-enzyme inhibitor, would reduce proteinuria in patients with advanced diabetic nephropathy. Captopril (37.5 mg given in divided doses three times daily) was administered to 10 azotemic diabetics with heavy proteinuria. Urinary protein decreased promptly within two weeks (from 10.6 +/- 2.2 to 6.1 +/- 1.4 g per day [mean +/- S.E.M.]; P less than 0.01). The decrease in proteinuria did not coincide with a fall in systemic blood pressure or in the blood glucose concentration. Serum creatinine and potassium values did not change in any of the patients except one. We suggest that captopril caused a decrease in intrarenal hypertension, which contributed to the reduction of urinary protein excretion. The therapeutic value of this intervention remains to be established.
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PMID:Effect of captopril on heavy proteinuria in azotemic diabetics. 390 98

A controlled study was conducted in hypertensive patients to investigate whether captopril can be substituted for the various other antihypertensive drugs (not including diuretics) to reduce side effects and improve the quality of life. Captopril in a twice daily dose of 25-50 mg, was substituted and titrated in 54 patients. Fifty-two patients, matched by age and sex, comprised the control group, and were treated with a variety of agents. During a follow-up of 9 months, 44 of the patients receiving captopril (81%) achieved the goal of supine blood pressure less than 90 mmHg. Captopril was discontinued in two patients due to side effects. Mild proteinuria was observed in two patients. A significant reduction in scores or rates of side effects (numbness, blurred vision, insomnia, vivid dreams, cold extremities, sleepiness, sexual dysfunction and fatigue) and improvement in quality of life (general feeling, mood and concentration) was observed in the study group compared with the control group. Captopril alone in a twice daily dose of 25-50 mg, or in co-treatment with thiazide, provided sustained blood pressure control with minimal side effects and improvement in quality of life compared with the treatment of hypertension with beta-blockers, vasodilators or methyldopa.
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PMID:Captopril as a replacement for multiple therapy in hypertension: a controlled study. 391 Jul 75

The patients with severe and 10 with accelerated or malignant hypertension were treated with the angiotensin-converting enzyme inhibitor captopril. Captopril acutely reduced blood pressure in all patients except two who had suppressed plasma renin activity. Four patients with encephalopathy showed immediate improvement after the first dose. Two patients could be withdrawn from nitroprusside infusion upon administration of captopril. Nineteen of 20 patients have remained on captopril for 12-32 months. Blood pressure is controlled in 18 and improved in two. Eleven required addition of diuretic and one addition of clonidine. The maximal antihypertensive effect of captopril with or without diuretics was evident after 3 months of continuous therapy and was associated with elevated plasma renin levels, normal aldosterone excretion and preservation of renal function. Captopril was well-tolerated, but produced occasional rash, loss of taste and proteinuria. We conclude that captopril, alone or in combination with other drugs, is effective in both the acute and long-term management of severe and malignant hypertension.
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PMID:Acute and chronic treatment of severe and malignant hypertension with the oral angiotensin-converting enzyme inhibitor captopril. 616 12

Eleven patients with severe, treatment-resistant essential or renovascular hypertension were treated with captopril after withdrawal of various multiple drug regimes. If supine diastolic blood pressure remained greater than 90 mm Hg on a maximum daily dose of 450 mg captopril, a diuretic and then a beta-adrenoceptor blocker were added. Patient-volunteered complaints were carefully noted. Mean (+/- SE) systolic and diastolic blood pressures fell from 225 +/- 6.8/131 +/- 4.4 mm Hg on various multiple drug regimes to 182 +/- 9.0/105 +/- 5.0 mm Hg on a regime including captopril. The reported and observed incidence of adverse effects were as follows: maculopapular rash (one patient); urticaria and pruritus (three patients); loss of taste (one patient); tachycardia (four patients); increased frequency of trivial infections (three patients); severe myalgia (one patient); and deterioration in renal function (one patient). However, these patients were able to continue captopril after either temporary withdrawal or dose reduction. Captopril was discontinued permanently in five patients, in two because of poor blood pressure control, in one who developed persistent severe urticaria, and in one because of marked proteinuria. In the fifth patient intractable diarrhoea occurred. Captopril lowers blood pressure very effectively in patients with severe hypertension refractory to other agents. Adverse effects are common but acceptable in this situation where prognosis is poor if blood pressure is not adequately controlled.
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PMID:Efficacy and adverse effects of captopril in severe refractory hypertension. 617 29

Captopril (Capoten; Squibb) is a specific orally active antagonist of peptidyl-dipeptide carboxyhydrolase, the enzyme which converts angiotensin I to angiotensin II and which inactivates bradykinin. Captopril therefore reduces blood pressure in a variety of animal models of hypertension. In 96 studies on 1570 patients, captopril has been shown to be superior to placebo and equivalent to either propranolol or a diuretic in the treatment of essential hypertension. In the management of severe treatment-resistant hypertension, the response to captopril (alone or in combination with a diuretic and/or propranolol) was better than the response to standard triple therapy. Captopril, with digitalis and a diuretic, also improved the haemodynamic and clinical status of patients with refractory congestive heart failure. Side-effects include skin rashes (15%), proteinuria (1,1%, or 0,4% of patients with no prior renal disease) and the nephrotic syndrome (0,9%, or 0,3% of patients with no prior renal disease). Nearly all patients with the nephrotic syndrome in whom renal biopsies were performed were found to have membranous glomerulopathy. Neutropenia (total white cell count less than 1,000/microliter) was found in 33 of over 6,000 patients (0,4%), but in all cases there were other possible causes for this. Captopril is the first of an important group of antihypertensive and afterload-reducing drugs; its major indications are likely to be in the treatment of refractory severe hypertension or congestive heart failure.
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PMID:Captopril--an overview. 621 58

Proteinuria is a side effect of captopril treatment in hypertensive patients. The possibility of reproducing the same renal abnormality with captopril was examined in SHR. Oral administration of captopril at 100 mg/kg for 14 days failed to aggravate proteinuria pre-existing in SHR. Also, captopril treatment failed to potentiate or facilitate development of massive proteinuria invoked by puromycin aminonucleoside in SHR. Captopril had little or no demonstrable effects on serum electrolyte concentrations, excretion of urine, sodium and potassium, endogenous creatinine clearance, body weight, and food and water consumption. However, ketone bodies were consistently present in urine and several lethalities occurred during multiple dosing of captopril in SHR.
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PMID:Effect of captopril on pre-existing and aminonucleoside-induced proteinuria in spontaneously hypertensive rats. 645 43

1 Forty-one patients with essential hypertension, stages I, II, and III, were treated with captopril alone or in combination with hydrochlorothiazide. Forty two percent were responsive to captopril alone, while the remaining 58% also required the diuretic. The need for the diuretic was related to the phase of hypertension. 2 There was no significant relation between drug response and plasma renin activity. Serum concentrations of creatinine and potassium remained normal, and there were no pathological changes in serum glucose, cholesterol, uric acid concentrations, erythrocyte count, packed cell volume, haemoglobin, or heart rate. 3 Captopril was well tolerated. One patient developed a rash and another ageusia, which disappeared spontaneously. A third, who was also taking allopurinol, developed leucopenia but it disappeared after treatment was withdrawn. There were no cases of proteinuria attributable to captopril; and proteinuria disappeared in four of five patients who were proteinurin before the start of treatment. 4 These findings suggest that doses of captopril of 150 mg to 300 mg (with or without a diuretic) may be adequate for controlling the blood pressure of most patients with essential hypertension.
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PMID:Captopril in essential hypertension. 675 90

1 Forty-one patients with primary (essential) hypertension were treated with captopril alone or in combination with hydrochlorothiazide for 12-36 months. 2 During an initial dose-titration period mean blood pressure fell from 174/111 mm Hg to 134/88 mm Hg supine and from 170/116 mm Hg to 126/93 mm Hg standing after 3 months' treatment. 3 During long-term treatment with unchanged or reduced doses of captopril or hydrochlorothiazide, or both, blood pressure remained substantially reduced. Mean supine blood pressure at 24 months was 136/90 mm Hg and at 36 months 138/90 mm Hg. 4 In 12 patients with clearly defined low renin (essential) hypertension initial blood pressure reduction was less than in patients with normal renin hypertension after 1 month's treatment (162/102 mm Hg v 143/92 mm Hg). After 24 months of treatment, however, the treatment results were similar in the two groups. 5 Except for one case of reversible proteinuria no serious side effects were seen during treatment periods of up to three years. 6 Captopril alone or in combination with hydrochlorothiazide seems to be an effective and safe drug in the long-term treatment of primary hypertension.
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PMID:Long-term experience of captopril in the treatment of primary (essential) hypertension. 675 94

Captopril, an angiotensin converting enzyme inhibitor, was used to treat 25 patients with treatment-resistant hypertension of long duration. Seven patients had essential hypertension, 10 renovascular hypertension and 8 renoparenchymatous hypertension. All patients had GFR greater than 25 ml/min/1.73 m3 BSA. The acute blood-pressure-lowering response to the drug was shown to be dependent on the prevailing activity in the renin-angiotensin system. Its long-term effect was not correlated to the activation of the renin-angiotensin system as the mean blood-pressure decrease was not significantly different for high renin and normal renin patients (21 +/- 3% vs. 19 +/- 2%). All patients needed addition of diuretics and betablockers for optimum control. Nine patients have been well controlled for one year and several of them are now approaching two years' treatment. A few adverse effects were observed, including taste disturbances and increased proteinuria. The latter side effect occurred in two patients with decreased renal function and pre-existing proteinuria. Upon reduction of the dose the proteinuria returned to pre-treatment levels within a few months. We conclude that altogether 78% of these patients with treatment-resistant hypertension obtained greatly improved long-term blood-pressure control on treatment including captopril.
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PMID:Captopril in treatment-resistant essential and renal hypertension. 676 60


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