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)

In 11 hypertensive patients with chronic renal failure we studied the short-term effects of the calcium antagonist nitrendipine, the angiotensin-converting enzyme inhibitor cilazapril, and the combination of both drugs on blood pressure, renal hemodynamics, and proteinuria in a randomized, double-blind, placebo-controlled way. After one week of treatment, blood pressure at 2-5 h after drug administration amounted to 159 +/- 5/101 +/- 3 mm Hg (means +/- SEM) during placebo. Nitrendipine, cilazapril, and the combination lowered mean arterial pressure by 1.4 +/- 1.6 (NS), 6.0 +/- 1.7 (p less than 0.10), and 10.3 +/- 2.1% (p less than 0.01), respectively. Glomerular filtration rate did not change. As compared to placebo, renal blood flow increased and renal vascular resistance decreased significantly during the combination. Filtration fraction amounted to 22.7 +/- 1.2% during placebo and was 22.0 +/- 1.4 (NS), 20.4 +/- 1.2 (p less than 0.01), and 20.5 +/- 1.4% (p less than 0.05) during nitrendipine, cilazapril, and the combination, respectively. During nitrendipine, albuminuria was slightly higher than during placebo: 0.86 +/- 0.39 vs. 0.58 +/- 0.25 mg/min (NS). During cilazapril alone and during the combination of both drugs, albuminuria was lower as compared to nitrendipine: 0.38 +/- 0.14 mg/min (p less than 0.01) and 0.44 +/- 0.18 mg/min (p less than 0.01), respectively. The data suggest that the combination of nitrendipine and cilazapril is an effective treatment in renal hypertension. In addition, cilazapril alone as well as the combination with nitrendipine reduced albuminuria, possibly by decreasing filtration fraction and/or reduction of blood pressure.
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PMID:Effects of nitrendipine and cilazapril on renal hemodynamics and albuminuria in hypertensive patients with chronic renal failure. 170 85

Captopril and Enalapril, angiotensin converting enzyme inhibitors, were used in the treatment of grave renal hypertension. The treatment concerned 40 randomly selected patients with the average creatinine clearance of 55.7 ml/min. The patients were divided in two groups: the first groups was ril. The good regulation of blood pressure was achieved only in combination with furosemide and protreated with captopril and the second with enalappranolol. Furosemide was given to all patients, and propranolol to all treated with captopril and to 12 subjects treated with enalapril. The angiotensin converting enzyme increased plasma renine activity and decreased aldosterone concentration in the serum. No change in renal function was noted. Proteinuria was decreased. Side-effects were manifest in two patients only treated with captopril. In conclusion it can be said that angiotensin converting enzyme inhibitors are efficient in the treatment of renal hypertension.
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PMID:[Captopril and enalapril in the treatment of renal hypertension]. 209 77

There has been no useful treatments for chronic vascular rejection (CVR) after kidney transplantation until now. Recently, however, some reports have suggested that the thromboxane A2 synthetase inhibitor, OKY-046, is useful in reducing proteinuria in nephrotic syndrome and preventing progression of CVR. Five patients with CVR (serum creatinine range: 1.7-2.6 mg/dl) were treated with OKY-046 for over one year and the effect of OKY-046 was evaluated. One patient developed acute rejection and another renal hypertension during this study. Except for the cases of acute rejection and renal hypertension, serum creatinine slightly decreased in 1 case and remained unchanged in 2 cases. Urinary excretion of protein and thromboxane B2 decreased significantly but prostaglandin E2 did not change in the treatment of the deterioration with OKY-046. We concluded that OKY-046 was effective in preventing graft function and decreasing urinary protein excretion in kidney transplant recipients with CVR.
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PMID:[The effects of thromboxane A2 synthetase inhibitor on chronic rejection of kidney transplantation]. 240 13

In our study we investigated 36 out-patients with renal disease, 22 of whom were hypertensive. In all patients proteinuria was present (4.30 +/- 5.05 g protein/day) and kidney diseases were verified by renal biopsy. Blood cadmium in non-smokers was significantly (p less than 0.05) lower than in smokers. We found a positive correlation between cadmium-concentration of blood and urine (p less than 0.01, R = 0.44) and between cadmium-concentration of blood and blood uric acid (p less than 0.01, R = 0.44). Proteinuria was weakly correlated with cadmium concentration of urine (p less than 0.05, R = 0.35). Patients with renal hypertension showed a significantly higher (p less than 0.05) urine cadmium excretion per day (1.60 +/- 1.12 micrograms/day) compared to normotensives with a disease of the kidney (1.14 +/- 1.47 micrograms/day). Our results indicate that cadmium may be involved in the development of hypertension in patients with renal disease.
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PMID:Does cadmium contribute to the development of renal parenchymal hypertension? 259 74

In our study we investigated 36 out-patients with renal disease; 22 of them were hypertensive. In all patients proteinuria was present (4.30 +/- 0.82 g protein/d) and renal involvement has been proved by renal biopsy. Blood cadmium in nonsmokers was significantly (P less than .05) lower than in smokers. Patients with renal hypertension showed a significantly higher (P less than .05) urine cadmium excretion/d (1.60 +/- 0.23 micrograms/d) compared to normotensives with a disease of the kidney (1.14 +/- 0.38 micrograms/d). Our results indicate that cadmium may be involved in the development of hypertension in patients with renal disease.
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PMID:Role of cadmium in hypertensive patients with renal parenchymal disease. 275 5

A case of renal hypertension after pyelolithotomy cured by segmental nephrectomy is reported. The patient, a 39-year-old man had had pyelolithotomy performed by the lumbodorsal approach at another hospital. Two months after operation he started to complain of headache and palpitation. The blood pressure was markedly high when he visited our hospital and peripheral plasma renin activity was also elevated. Urinalysis was normal except for slight proteinuria. The excretory urogram demonstrated cortical scarring in the lower portion of the left kidney. The renal scintigram demonstrated low uptake in this area, suggesting renal infarction. Renal arteriogram showed decreased vascularity in this area. Plasma renin activity was measured on the blood drawn from the renal vein of both sides and the ratio was about 2.4, and renin activity of the segmental renal vein from the left lower portion was elevated. Segmental nephrectomy of the lower pole was performed. The blood pressure three weeks after lower pole resection was estimated to be normal and renin activity returned to an almost normal level. Discussion was made on the cause of renal hypertension after renal surgery. In this case, it was suggested that renal hypertension is caused by subinfraction due to lesions of the dorsal renal artery in surgery for renal calculus.
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PMID:[A case of renal hypertension after pyelolithotomy cured by segmental nephrectomy]. 383 24

The usefulness of renal biopsy in investigating persistent asymptomatic proteinuria was assessed by a study of 87 out 1245 adults referred for pre-employment medical examination and individuals proposing to take life insurance policies. Out of these 87 persons with initial proteinuria on dipstik test, 25 were found to have persistent asymptomatic proteinuria. Unequivocal abnormalities were seen on light microscopy in 15 of the 25 specimens of renal tissues examined. Focal proliferative glomerulonephritis was the commonest abnormality, being present in 7 out of 15 renal tissues. Overall, 12 persons subsequently developed hypertension. Glomerulonephritis as a cause of asymptomatic proteinuria in the tropics has not been studied in detail; this study suggests that it may be an important cause of renal hypertension. Renal biopsy is an important procedure in evaluating glomerular disease in asymptomatic proteinuria which may subsequently cause hypertensive renal disease.
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PMID:Persistent proteinuria in asymptomatic individuals: renal biopsy studies. 401 54

Data concerning blood pressure, kidney weight, heart weight and proteinuria were obtained from different groups of BW mice. Relatively early in life, systolic blood pressures as measured by a tail-cuff method, were above the upper limits of normal, continued to rise with increasing age and had peak average values coinciding with the peak death period and increased proteinuria. Any relationships which might exist among age, body weight and heart weight or kidney weight were sought by computerized polynomial multivariate analysis. It was found that, although there was only a slight effect with increasing body weight, both heart weight and kidney weight showed a steady increase with increasing age. These data support the proposal that the BW female mouse is a good model of spontaneous renal hypertension.
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PMID:A mouse model of spontaneous renal hypertension. blood pressure, heart weight, kidney weight and proteinuria relationships in NZB x OUW F1 hybrid female mice. 743 14

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

Renal diseases as glomerulonephritis, diabetic nephropathy, interstitial nephritis (e.g. analgetic nephropathy) or systemic disease with renal involvement are responsible for renal hypertension. High blood pressure remains the most important factor for progression of chronic renal failure. On the other hand, effective anti-hypertensive therapy results in inhibition of progression. Clinical and experimental studies show a renoprotective effect of ACE inhibitors due to lowering of systemic blood pressure, reduction of glomerular capillary pressure, reduction of proteinuria and antiproliferative effects.
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PMID:[ACE inhibitors and the kidney]. 892 21


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