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)

A prospective open clinical trial was carried out with 23 hypertensive type I diabetics (13 men, ten women, mean age 49 +/- 9.1 years, duration of diabetes 18 +/- 9.1 years) with early nephropathy. Glomerular and tubular renal function and metabolic parameters were monitored during 8 months' treatment with the angiotensin converting enzyme (ACE) inhibitor, captopril, in addition to previous antihypertensive treatment with one or more drugs. Blood pressure control tended to improve on captopril (systolic pressures 152 +/- 13 vs 140 +/- 13 mm Hg, P < 0.05; diastolic pressures 89 +/- 10 vs 87 +/- 10 mm Hg, not significant). Proteinuria (> 0.5 g/24 hours) fell into the microalbuminuria range (albumin excretion 2-20 mg/mmol creatinine) in four out of 13 patients, and microalbuminuria disappeared in four out of ten patients. Urinary levels of the brush border enzyme N-acetyl-beta-D-glucosaminidase (NAG), a marker of tubular dysfunction, were initially raised and fell significantly after 8 months' treatment with captopril (20.3 +/- 14.4 vs 8.8 +/- 8.1 U/g creatinine; P < 0.01). Captopril did not affect metabolic control (HbA1, total, HDL and LDL cholesterol, triglycerides, apolipoproteins A1 and B) or the insulin dosage. These results show that long-term treatment with captopril may favourably influence both albumin excretion and NAG activity, a marker of tubular dysfunction, in type I diabetics with nephropathy.
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PMID:[The effect of blood pressure-reducing therapy with captopril on tubular marker excretion in type-1 diabetics with nephropathy]. 820 41

The antiproteinuric effect of the angiotensin-I-converting enzyme inhibitor, captopril, was studied in 14 patients (10 men and 4 women, age range of 24 to 60 years) with chronic glomerulonephritis in whom IgA nephritis had been confirmed by renal biopsy. Eight of the 14 patients had received antihypertensive drugs such as calcium channel blockers, diuretics or beta-blockers. Captopril was added to these regimens at 25 mg twice daily in 3 patients, and 37.5 mg in 11 patients. Proteinuria decreased from 2.55 +/- 0.48 g/day to 1.58 +/- 0.35 g/day within three months after the start of administration. In 4 patients (28.6%), the extent of reduction was over 50%, and in 8 patients (57.1%), over 25%. Blood pressure, creatinine clearance and serum creatinine were not changed significantly. There was a positive linear correlation between the extent of reduction of proteinuria and the increase in plasma renin activity (r = 0.93, p < 0.001). We conclude that captopril reduces proteinuria in some patients with IgA nephritis whose plasma renin activity responds to the drug.
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PMID:Effect of the angiotensin converting enzyme inhibitor, captopril, on proteinuria in chronic glomerular disease. 825 7

Proteinuria after strenuous exercise is common in healthy subjects. The pathophysiologic mechanism of postexercise proteinuria (PEP) is not clear, although the phenomenon has long been known and many explanatory theories have been proposed. It is widely recognized that angiotensin II may increase filtration of protein through the glomerular membrane, and that its concentration in plasma increases during exercise. The aim of this study was to evaluate possible involvement of angiotensin II in the pathogenesis of PEP. Of 25 young volunteers who performed maximal aerobic exercise, eight showed PEP. The exercise was repeated after an interval of at least one week, now 90 minutes after administration of captopril (25 mg). Captopril did not affect the achieved work load of the maximal blood pressure and heart rate during the exercise, but PEP was not found. As it was possible to prevent PEP by administering an angiotensin-converting enzyme inhibitor, the study supports the theory that the renin angiotensin system is involved in the pathogenesis of PEP.
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PMID:Involvement of the renin angiotensin system in the pathogenesis of postexercise proteinuria. 829 Sep 7

In 15 type I diabetics with manifest diabetic nephropathy the authors investigated the antihypertensive and antiproteinuric effect of captopril and in seven patients of this group also its effect on renal haemodynamics. Captopril treatment or its combination with hitherto used antihypertensive treatment was associated after two months with a significant drop of the systolic and diastolic blood pressure from 150/95 (120/70-195/110) to 130/90 (110/65-180/115) mmHg, (p < 0.005 < 0.05). The median aortic pressure declined from 118.5 (92-140.8) to 106.5 (84-1334.8) mm Hg (p < 0.005). Nine of 11 patients (82%) could be changed to reduced antihypertensive therapy. The antiproteinuric effect was manifested in 11 patients (73%). Quantitative proteinuria dropped from 2.7 (0.83-8.65) to 1.85 (0.38-8.84) g/24 h., (p < 0.05) without a significant change of serum creatinine: 109 (70-342) vs. 135 (90-288) mumol/l, p = n.s.). The change of proteinuria, as compared with the baseline value, was -41 (-77 - +88)%, (p < 0.05) and did not correlate with the change of the median aortic pressure (correlation coefficient = -0.165, p = n.s.). In the group of seven patients the change of the median aortic pressure was -15% (-26.1 - +6.6), (p < 0.05). No statistically significant change of glomerular filtration was observed: 0.96 (0.32-1.38) vs. 0.96 (0.19-1.71) ml/s, p = n.s.); effective renal plasma flow: 6.32 (2.24-7.74) vs. 7.22 (1.68-10.55) ml/s, (p = n.s.); filtration fraction: 0.136 (0.123-0.220) vs. 0.130 (0.110-0.236), change 0.0 (-43.0 - +31.0)% (p = n.s.) and renal vascular resistance: 15429 (12907-54148) vs. 13243 (7099-77832)%, (p. = n.s.).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Changes in blood pressure, proteinuria and renal hemodynamics in type I diabetes with manifestations of diabetic nephropathy after 2 months of captopril therapy]. 834 43

Inhibition of non-immune progression of renal insufficiency for control of glomerulonephritis was attempted via hemodynamic, metabolic and hypolipidemic means. Hemodynamic correction was conducted using inhibitors of angiotensin-converting enzyme capoten and renitek. The action on metabolic factors of progression was realized by lovastatin mevakor. Capoten and renitek exhibited in 57 patients with chronic nephritis not only a hypotensive effect, but also reduced intraglomerular hypertension and proteinuria. A long-term (7-12 months) hypolipidemic therapy (diet and lovastatin) in 20 patients with chronic glomerulonephritis with nephrotic syndrome resulted in lowering of serum cholesterol concentrations and proteinuria, raised serum albumin. 9 patients achieved remission of nephrotic syndrome. The highest effect occurred in non-inflammatory nephropathy: membranous nephropathy, focal-segmental glomerulosclerosis, nephrosclerosis.
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PMID:[Means for the inhibition of the nonimmune progression of nephritis]. 857 23

Captopril (Tenziomin) treated rats after subtotal (5/6) nephrectomy showed conspicuously better function of kidney tissue remnants than untreated animals. Histology was the same in both groups--focal glomerulosclerosis, anisocytosis and anisokaryosis of tubular epithelial cells, hyperplasia of proximal tubuli. Proteinuria was substantially lower in treated animals. Lectin histochemistry showed differences between superficial and juxtamedullary nephrons in glycoprotein contents and function. An important finding was selective binding of WGA lectin in brush border of proximal convoluted tubuli of juxtamedullary nephrons. Differences in lectin binding between nephrectomized and intact control animals were rather quantitative than qualitative.
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PMID:[The effect of Tenziomin on function, morphology and lectin binding in rat kidney remnants after experimental subtotal nephrectomy]. 859 46

The present study describes a novel renal hypertensive guinea pig model for comparing different inhibitors of the renin-angiotensin system (RAS). Renal hypertension was induced by a two-step procedure consisting of ligation of the left caudal renal artery and right nephrectomy. Sham-operated animals were used as controls. Arterial blood pressure and heart rate were monitored in conscious animals. Left caudal renal artery ligation and subsequent right nephrectomy led to a significant increase (32% over sham-operated controls, p < .05) in mean arterial blood pressure (MABP), 3 to 4 weeks following surgery. Renal hypertensive animals had increased urine production (from 63 +/- 8 mL/kg per day to 143 +/- 29 mL/kg per day, p < .05) and an increased incidence of proteinuria (11/13 animals had urine protein levels higher than 20 mg/kg per day). Five of the 13 renal hypertensive animals also had hematuria. On autopsy, an 83% increase in the left kidney/body weight ratio and a 37% increase in the heart/body weight ratio were observed in the renal hypertensive animals, compared to the sham-operated controls. Changes in blood pressure and heart rate were assessed before and after an intravenous bolus injection of the drug to be tested. Captopril reduced MABP in both sham-operated and renal hypertensive animals with equal efficacy (up to a maximum of 42%). In contrast, BILA 2157 BS, one of our human renin inhibitors, produced a similar maximum MABP decrease but only in renal hypertensive animals. This selective antihypertensive effect was also observed with enalkiren, another renin inhibitor. These results indicate that the renal hypertensive guinea pig is an useful model for comparing and contrasting different RAS inhibitors.
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PMID:A novel renal hypertensive guinea pig model for comparing different inhibitors of the renin-angiotensin system. 872 34

In the present study we investigated the effect of a selective alpha 1-adrenergic blocker (doxazosin), an angiotensin-converting enzyme (ACE) inhibitor (captopril), and a calcium channel antagonist (nifedipine) on renal function in hypertensive non-insulin-dependent diabetic patients. 30 NIDD hypertensive patients (age = 50 +/- 3 years; BMI = 30 +/- 1 kg/m2) (mean +/- SEM) were studied before and after a 12-week period of antihypertensive treatment. Ten patients were treated with doxazosin (Cardura) (2-8 mg once daily or 8 mg b.i.d.), 9 with captopril (Capoten) (25-50 mg b.i.d.), and 11 with nifedipine (Procardia-XL) (30-60 mg once daily). Blood pressure, creatinine clearance, 24-hour urinary protein excretion, fasting plasma glucose concentration and glycosylated hemoglobin were measured before and after drug treatment. Fasting plasma glucose and glycosylated hemoglobin (HbA1c) were similar in all three groups prior to the start of antihypertensive therapy and did not change significantly from baseline in any treatment groups. In the doxazosin group creatinine clearance rose from 99 +/- 8 to 122 +/- 8 ml/1.73 m2.min (p < 0.01), while 24-hour urinary protein excretion declined from 2.66 +/- 0.05 to 1.76 +/- 0.02 mg/day/ml/1.73 m2.min (p < 0.01). In diabetics treated with captopril creatinine clearance rose from 93 +/- 6 to 109 +/- 9 ml/1.73 m2.min (p < 0.05), while the 24-hour urinary protein excretion fell from 2.70 +/- 0.05 to 2.03 +/- 0.04 mg/day/ml/1.73 m2.min (p < 0.05). In patients treated with nifedipine creatinine clearance did not change (97 +/- 6 vs. 94 +/- 7 ml/1.73 m2.min), while 24-hour urinary protein excretion decreased from 2.84 +/- 0.04 to 1.95 +/- 0.03 mg/day/ml/1.73 m2.min. Systolic and diastolic blood pressure were similar in doxazosin (150 +/- 3/95 +/- 2 mm Hg), captopril (153 +/- 3/93 +/- 1), and nifedipine (155 +/- 4/93 +/- 1) groups prior to the start of antihypertensive therapy and declined to 143 +/- 3/84 +/- 3 (doxazosin), 139 +/- 3/82 +/- 3 (captopril), and 141 +/- 3/84 +/- 1 (nifedipine) mm Hg (all p < 0.01 vs. pretreatment). In summary, both doxazosin and captopril treatment were associated with significant rises in GFR, while all three antihypertensive agents caused a significant decline in proteinuria. These results indicate that alpha-adrenergic blockers, ACE inhibitors, and calcium channel antagonists can safely and effectively be used in the clinical management of non-insulin-dependent diabetic patients with hypertension.
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PMID:Effect of alpha-adrenergic blockers, ACE inhibitors, and calcium channel antagonists on renal function in hypertensive non-insulin-dependent diabetic patients. 885 95

We and others have already reported that Onpi-to (TJ-8117), a Kampo medicine composed mainly of Rhei Rhizoma, has a beneficial effect on an adenine-induced renal failure model and 5/6 nephrectomized renal failure. However, little is known about the detailed mechanism of this medicine when used for renal failure. The present study was designed to clarify whether or not TJ-8117 affects TGF-beta 1 production or activation in glomeruli of 5/6 nephrectomized rats. TJ-8117 (400 mg/kg/ day) and captopril (50 mg/kg/day) were administered as drinking water from the day immediately after the operation and continued throughout the experiment. All rats were sacrificed at 4 weeks and renal cortical tissue was removed to quantify the protein and activity of TGF-beta 1 and activities of metalloproteinase. TIMP expression and extracellular matrix (collagen type I, IV) in the glomeruli were analysed histologically. TJ-8117 inhibited proteinuria, and the accumulation of collagen type I and IV in glomeruli of nephrectomized rats. In addition, TJ-8117 inhibited the TGF-beta 1 positive area in the glomeruli and the elevation of mature TGF-beta 1 level in the renal cortex of nephrectomized rats. In the TJ-8117 treated group, activities of metalloproteinase 1, 2 or 9 in the renal cortex were elevated compared with the control group. Captopril failed to affect the TGF-beta 1 level. We also found that the constitutive herbs in TJ-8117, Rhei Rhizoma and Ginseng radix, inhibited the process from inactive TGF-beta 1 to mature TGF-beta 1.
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PMID:[Effect of Onpi-to (TJ-8117) on TGF-beta 1 in rats with 5/6 nephrectomized chronic renal failure]. 895 1

The effects of captopril on morphologic changes and clinical course of adriamycin (ADR) nephropathy in spontaneously hypertensive rats (SHR) were examined. After ADR infections rats were divided into two groups: ADR-C group (n = 20) given captopril (60 mg/kg per day) and ADR group (n = 19) receiving no antihypertensive treatment. SHR were examined every 6 weeks. Captopril normalized systemic blood pressure, but failed to prevent proteinuria. It slowed down renal function deterioration in the early stage of ADR nephropathy (weeks 6 and 12), but at the end of the study both groups had the same degree of renal failure irrespectively of whether blood pressure was well controlled with captopril or hypertension persisted. Captopril slowed down mesangial expansion in the early stages of ADR nephropathy, but at the end of the study there was no statistically significant difference between these two groups. Treatment with captopril also reduced the development of glomerular sclerosis.
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PMID:[The effect of captopril on the development of adriamycin nephropathy in rats with spontaneous arterial hypertension]. 910 28


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