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 therapeutic effect of long-term enalapril administration was studied in 20 patients with severe essential hypertension (EH), resistant to intensive therapy with a combination of 3 or 4 antihypertensive drugs. Addition of enalapril (Renitec MSD from 5 to 40 mg/day) to the previous therapy allowed to maintain blood pressure within limits not exceeding 150/95 mmHg during a 12-month study in more than 80% of previously resistant patients. Left ventricular hypertrophy regressed in all patients and dilatation of the left ventricle seen in 4 patients disappeared during enalapril treatment. Serum sodium creatinine did not change significantly. Serum potassium increased slightly but remained within the normal range. Proteinuria had a tendency to diminish and N-acetyl-beta-D-glucosaminidase activity in the urine dropped within normal limits. Based on their results, the authors conclude that enalapril is suitable for the long-term treatment of patients with severe EH, resistant to intensive antihypertensive therapy, with minimal side effects, good tolerance and a tendency for amelioration of cardiac and renal function.
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PMID:The effect of long-term treatment by the angiotensin I-converting enzyme inhibitor enalapril on renal function and left ventricular hypertrophy in severe essential hypertension. 198 Oct 38

Several studies have shown that long-term therapy with angiotensin-converting enzyme inhibitors may reduce urinary protein excretion and decrease the rate of progression of renal disease in patients with insulin-dependent diabetes mellitus more effectively than conventional antihypertensive drugs. Only few studies, however, have been performed in patients with non-insulin-dependent diabetes mellitus (NIDDM). To compare the effects of captopril with more conventional drugs on proteinuria and progression of renal disease, we conducted a prospective, 18-month study in 42 proteinuric (> 500 mg/day) NIDDM and, for comparison, in 31 nondiabetic patients with a variety of renal diseases (NDRD). Twenty-four NIDDM patients were treated with captopril and 18 with conventional drugs. Eighteen NDRD patients received captopril, and 13 received conventional drugs. Baseline proteinuria and glomerular filtration rate (GFR) were not different among groups. The blood pressure decreased equally in all group of patients, irrespective of whether they received captopril or conventional drugs. Urinary protein excretion, however, decreased significantly only in NIDDM and NDRD patients treated with captopril. The GFR decreased only in patients treated with conventional drugs, but not in those treated with captopril. The rate of decline in GFR in NIDDM patients treated with captopril was significantly lower than in patients treated with conventional drugs. However, in NDRD patients treated with captopril, the rate of decline in GFR was not different from that in patients treated with conventional drugs. The reduction of urinary protein excretion was poorly correlated with changes in blood pressure or with changes in renal function and renal hemodynamics. Serum potassium increased significantly in patients treated with captopril.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of long-term therapy with captopril on proteinuria and renal function in patients with non-insulin-dependent diabetes and with non-diabetic renal diseases. 789 96

This 1.5-year prospective study compared the effects of angiotensin II receptor blocker, candesartan(n = 21), and ACE inhibitor(ACEI, n = 23) on proteinuria and renal function in patients with moderate renal impairment due to chronic glomerulonephritis. Blood pressure reductions were comparable between both groups. Proteinuria was significantly reduced from 2.1 +/- 0.4 (mean +/- SE) to 0.6 +/- 0.2 g/day(p < 0.001) with candesartan, and the reduction was significantly larger than with ACEI(p < 0.01). Serum creatinine did not increase with candesartan or ACEI, suggesting the renoprotective effect. Serum potassium increased significantly with both drugs from 6 months. Plasma aldosterone concentrations(PAC) showed a stronger suppression with candesartan(150 pg/ml before treatment and 51 at 1.5 years) than with ACEI(104 pg/ml at 1.5 years). Plasma renin activity with candesartan(1.0 ng/ml/hr before treatment) decreased from 3.9 ng/ml/hr at 6 months to 1.3 at 1.5 years, whereas PRA remained elevated with ACEI. We speculate that the stronger reduction of PAC contributed to suppression of growth of mesangial matrix and the interstitial fibrosis in the candesartan group.
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PMID:[Comparison of ARB and ACEI for renoprotection in chronic glomerulonephritis]. 1239 99

We have studied the effects of add-on spironolactone treatment (100 mg/day) in 11 patients with idiopathic membranous nephropathy (IMN) and > 3 gm proteinuria/day despite angiotensin converting enzyme (ACE) inhibitor therapy titrated to a systolic/diastolic blood pressure < 120/80 mmHg. Blood pressure, 24-hour urinary protein excretion, and creatinine clearance were measured prior to, after two months of combined therapy, and after a 2-month withdrawal period of spironolactone. While systolic and diastolic blood pressure decreased significantly after spironolactone therapy, proteinuria did not improve. Serum potassium increased significantly as well, with three patients requiring resin-binding therapy. Thus, spironolactone seems to have no additional antiproteinuric effects over ACE inhibitor therapy in patients with IMN and nephrotic syndrome and carries the risk of significant hyperkalemia.
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PMID:Spironolactone Plus Full-Dose ACE Inhibition in Patients with Idiopathic Membranous Nephropathy and Nephrotic Syndrome: Does It Really Work? 2771 39