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)

Seventeen hypertensive patients were treated with captopril, an orally active inhibitor of converting-enzyme. All patients showed a fall in blood pressure (BP), although in some patients only after the addition of diuretics. In 2 patients a skin rash developed. One patient developed proteinuria. A renal biopsy revealed membranous glomerulopathy. Correlations were found between pretreatment plasma renin activity (PRA) and the decrease in BP, and between pretreatment PRA and the decrease in plasma aldosterone concentration (PAC). Filtration fraction (FF) fell, indicating a decrease in renal vascular resistance. Captopril decreased the sensitivity to exogenous angiotensin I (AI), dependent on the captopril dose used. The sensitivity to exogenous bradykinin increased impressively even on the lowest dose of the drug. These observations suggest extrapulmonary conversion of AI to angiotensin II (AII).
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PMID:Treatment of moderate to severe hypertensive patients with an orally active converting-enzyme inhibitor. 23 14

The effect of captopril on proteinuria was evaluated in twenty patients with various glomerular diseases excreting heavy proteinuria (> 3.0 g/day). Captopril in a daily dose of 37.5 mg was administered orally three times a day to all patients and they were followed for eight weeks. Twenty-four hour urinary excretion of protein, creatinine, sodium, selective protein index (SPI), and blood chemistry including serum electrolytes were measured every two weeks. Twenty-four hour urinary protein excretion per gram creatinine started to fall within two weeks of captopril administration and became nearly stable after four weeks of therapy (p < 0.05). Mean 24-hour urinary protein excretion decreased significantly from a pretreatment value of 9.0 +/- 6.0 gm/gm of cr. to 4.4 +/- 3.5 gm/gm of cr. after eight weeks of captopril treatment. The serum albumin level increased progressively at six and eight weeks after the captopril treatment period and was significantly higher than the pretreatment value (p < 0.05). The decrease in proteinuria did not coincide with a fall in blood pressure or any changes in creatinine clearance. We conclude that captopril does have a significant antiproteinuric effect in patients excreting heavy proteinuria with various glomerular diseases. However, the long term therapeutic efficacy and any renal protective effect of this drug remain to be proven.
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PMID:Effect of captopril on heavy proteinuria in patients with various glomerular diseases. 129 47

Angiotensin converting enzyme inhibitors was given to 16 patients with glomerular nephritis in whom a complete remission of nephrotic syndrome could not be achieved with immunosuppressive-anti-inflammatory therapy. Captopril in the daily dose of 25-75 mg and enalapril in the daily dose of 10 mg were administered for 1-36 months (mean 12.6 months). Daily proteinuria decreased by 40-80% comparing with baseline value in 2/3 of patients. Total protein and albumin serum levels increased simultaneously. No changes in blood creatinine were noted in patients with initially normal renal functioning except one patient. Renal functioning was stable in 50% of patients with increased blood creatinine levels (mean 200 mumol/L). Blood creatinine was increasing in the remaining patients.
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PMID:[Effect of ACE inhibitors on proteinuria and renal functioning in primary glomerulopathies]. 130 32

The effects of a daily administration of an anti-converting enzyme inhibitor. Captopril (CPT) (100 mg/kg/orally), on the development of functional and morphological alterations induced in rats by a single injection (7.5 mg/kg/iv) of Doxorubicin (DXR) (Adriamycin*), were investigated. Twenty-four-hour protein excretion, urine output, food intake, water intake, and body weight gain were measured weekly for 30 days. Transmission and scanning electron microscopy observations were performed on kidney samples after 30 days. Four groups were studied. Group 1 were control rats. Group 2 were rats injected with DXR. Group 3 were rats injected with DXR and treated with CPT for 30 days. Group 4 were rats injected with DXR and treated with CPT for 15 days (CPT treatment started 15 days after DXR injection). Group 1 did not show significant functional or morphological changes. Group 2 showed severe proteinuria, significant increase in urinary volume within 2 weeks, significant body weight reduction and diffuse morphological changes. These changes mainly consisted of podocyte swelling, severe foot process fusion, and presence of casts within tubular lumen. Group 3, with respect to group 2, showed a significant reduction of the 24 h protein excretion and urine output. This group displayed morphological changes similar to those observed in group 2, but with a focal distribution. Group 4 showed functional and morphological changes comparable with those of group 2. It is concluded that CPT partially inhibits the development of the functional and morphological damage induced by DXR in the rat kidney. However, CPT did not influence the natural development of nephropathy when treatment started 15 days after DXR injection.
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PMID:Effects of captopril on the development of rat doxorubicin nephropathy. 151 5

The effects of the angiotensin converting enzyme inhibitor captopril on blood pressure, proteinuria, creatinine clearance and metabolic control in diabetic nephropathy have been evaluated. Captopril 144 mg per day was given to 8 longstanding, insulin-dependent, diabetic females with nephropathy. The blood pressure was significantly reduced (systolic 45.4, diastolic pressure 30.6 and mean arterial pressure 33.8 mm Hg after 24 weeks of treatment). Plasma renin activity rose significantly from a basal value of 1.60 to 6.71 ng.ml-1.h-1, and so did serum potassium (from 4.57 to 4.83 mEq.1-1). Serum aldosterone fell from 161 to 70.9 pgm.ml-1 and from 27.3 to 15.3 micrograms.24 h-1 in plasma and urine, respectively, after 6 months on captopril therapy. Urinary protein excretion was decreased by about 48% and creatinine clearance remained unchanged throughout the study. Plasma triglycerides and cholesterol also remained unchanged, and glycosylated haemoglobin was significantly reduced from 13.8 to 10.2% after captopril. The results suggest that captopril is a useful drug to treat hypertension in patients suffering from diabetic nephropathy, as the decline in kidney function can be reduced without impairing glucose tolerance or the lipid profile.
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PMID:Effects of captopril on diabetic nephropathy in hypertensive women. 176 Oct 66

We retrospectively analysed the effects of a 12-month treatment with captopril (Tensiomin) in 46 patients. All of the patients had hypertension lasting for years (9 essential, 37 with chronic renal failure), 32 of them had proteinuria. Captopril was given in addition to, or in exchange for, other antihypertensive drugs. Under treatment with ACE-inhibitors, a small but significant decrease in diastolic blood pressure (0.4 torr/month) and in proteinuria (0.19 g/month) was seen (regression analysis). Discriminant analysis showed proteinuria and diastolic blood pressure to be the more modifiable, the younger the patients, the higher the proteinuria at the beginning and the longer the history of hypertension. Serum creatinine, blood urea nitrogen, serum protein and serum potassium did not change.
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PMID:[Effect of the ACE-inhibitor captopril on the blood pressure and kidney function of patients with essential and renal hypertension]. 177 7

In an attempt to evaluate the influence of hypertension and antihypertensive agents on IgAN, IgAN and hypertension experimental models were induced in SD rats and divided into 4 groups: (1) IgAN(n = 8); (2) IgAN+by hypertension(n = 8); (3) captopril 4mg/100gBW/d, for 42 days administered to rats as group (2) (n = 8); (4) nifedipine 300ug/100gBW/d, for 42 days administered to rats as group (2) (n = 8). Blood pressure was measured at the 12th, 14th, 16th, 18th and 20th week. Urinary protein, serum angiotensin II (AT II) and renal pathologic changes were examined at the 20th week. Our results suggest that hypertension worsens IgAN by glomerular mesangial proliferation in early stages. Though Captopril has the same therapeutic effect on hypertension as Nifedipine does, the former has been proven to have potentially beneficial effects on diminishing proteinuria as well as mesangial lesions. This is consistent with the suppression of serum ATII which favours glomerular microcirculation.
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PMID:[The influence of hypertension and antihypertensive agents on experimental IgA nephropathy (IgAN)]. 180 38

Angiotensin-1 converting enzyme inhibitors (ACEI) have been shown to reduce proteinuria in azotaemic diabetics and in other glomerulopathies, and such treatment has also slowed the development of experimentally-induced glomerulosclerosis in animals. We have treated 13 patients with focal segmental glomerulosclerosis (FSGS) and IgA nephropathy (IgAN) with Captopril 12.5 mg twice daily for six months and assessed their response in terms of 24 hour urinary protein excretion, blood pressure, glomerular filtration rate, effective renal plasma flow and derived values for filtration fraction and renal vascular resistance. A mean fall of 29 per cent in urinary protein excretion was observed over the six months treatment schedule. No significant changes were observed in other parameters of renal haemodynamics measured. We conclude that Captopril therapy in patients with FSGS and IgAN reduces urinary protein excretion consistently over a six month period, and that this may in the longer term retard the progression of their renal failure.
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PMID:Reduction of proteinuria with captopril therapy in patients with focal segmental glomerulosclerosis and IgA nephropathy. 181 Aug 99

Strenuous physical exercise causes transient proteinuria and renal hemodynamic changes: decrease of renal blood flow and to a lesser extent of the glomerular filtration rate, and an increase of the filtration fraction. However, the mechanisms of these modifications are still poorly understood. In order to elucidate them we performed maximal exercise tests on 8 untrained healthy volunteers after inhibition of the renin-angiotensin system (RAS) by captopril, the sympathetic nervous system by a beta-blocking drug (acebutolol) or an alpha-blocking drug (prazosin) and the prostaglandin system by indomethacin. Urinary albumin excretion was measured in every subject first at rest (AB) and then after exercise (AA) performed successively without and with blockade by each of theses drugs. AA-AB difference in the captopril test (12.04 +/- 6.11 micrograms/min) compared to that in the control test (68.91 +/- 25.18 micrograms/min) was significantly reduced (p less than 0.02). This difference remained unchanged after acebutolol (59.87 +/- 21.91 micrograms/min, p = 0.62), prazosin (35.23 +/- 27.80 micrograms/min, p = 0.21) and indomethacin (55.21 +/- 28.43 micrograms/min, p = 0.35). There was a negative correlation between the lowering of AA elevation and the rise in plasma renin activity in the captopril test (r = 0.64; p less than 0.03). Only acebutolol decreased systolic blood pressure significantly. These results suggest that the RAS plays a major role in postexercise proteinuria. We hypothesize that stimulation of this system induces an increase of efferent glomerular artery constriction and consequently of glomerular transcapillary pressure and the filtration fraction. Captopril seems able to prevent these hemodynamic changes.
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PMID:Captopril but not acebutolol, prazosin or indomethacin decreases postexercise proteinuria. 192 9

The effect was studied of the converting enzyme inhibitor (captopril) on the gentamicin nephrotoxicity in rats. Captopril 25 mg/kg b.w. and gentamicin 100 mg/kg b.w. were injected subcutaneously in a single daily dose. Three groups of Wistar male rats were studied: 1) treated with gentamicin 3 and 7 days, 2) treated with gentamicin and captopril, 3) treated with captopril. The mean serum creatinine and urea levels and proteinuria in the second group were significantly higher than in the first one. Light and electron microscopy examinations demonstrated increased renal cortex damage in the second group. There were not differences between mean urea and creatinine levels in the third examined group and normal rats. Mechanism of gentamicin nephrotoxicity enhancement in the second group is unknown.
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PMID:[Nephrotoxicity of aminoglycosides. III. Preventive studies with subcutaneous administration of converting enzyme inhibitor, captopril]. 203 72


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