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)

Captopril, a competitive antagonist of angiotensin converting enzyme, has been marketed in the United States for the treatment of resistant hypertension. Despite extensive study, its exact mechanism of action remains unclear; decreased renin-angiotensin-aldosterone and sympathoadrenal system activity as well as increased bradykinin and prostaglandin E and F activity have been postulated. The drug decreases peripheral vascular resistance. Controlled trials in resistant hypertension of various etiologies and chronic congestive heart failure have demonstrated sustained effectiveness and therapeutic benefits. Side effects include skin rash, loss of taste, proteinuria, and leukopenia; higher doses and concomitant renal dysfunction appear to be predisposing factors. The benefit-to-risk ratio for captopril clearly justifies its use in resistant cases of hypertension and congestive heart failure, but further experience is needed to evaluate its use in milder forms of these diseases.
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PMID:Captopril: clinical pharmacology and benefit-to-risk ratio in hypertension and congestive heart failure. 676 88

The effects of Captopril on blood pressure and renal function were evaluated in ten patients with different degrees of hypertension. In seven, blood pressure was reduced after 7 weeks of therapy; in three it remained practically unchanged. No correlation was found between the standing plasma renin activity before treatment and the hypotensive response. Plasma renin activity increased significantly from the median value of 5.4 (range 1-16.7) to 9.5 (range 2.6-19.8) ng ml-1 h-1 (P less than 0.05) and urine aldosterone significantly fell from 13 (range 2.3-52.5) to 7.4 (range 1.6-14) microgram 24 h-1 (P less than 0.01) during therapy. Renal plasma flow decreased from 534 (range 300-616) to 471 (range 333-606) ml min-1, but the difference was not significant, and glomerular filtration rate fell significantly form 122 (range 64-143) to 88 (range 71-116) ml min-1 (P less than 0.05). No urinary excretion of alpha 2-macroglobulin was observed during Captopril. 24 h proteinuria, albumin and transferrin clearance, alanine-amino transferase, gammaglutamyl transferase and alpha glucosidase excretion rate and malate-dehydrogenase clearance remained unaltered throughout the treatment. This indicates that neither glomerular permeability nor renal tubular function were affected by the drug.
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PMID:Hypotensive and renal effects of captopril. 680 Aug 13

To determine the effect of diabetes mellitus on the renin-aldosterone system, independent of age, nephropathy, or hypertension, 16 normotensive diabetics with long-term disease (mean duration, 15 years) and no (14) or minimal (2) proteinuria, were compared to nine age-matched, normotensive controls. Plasma renin activity (PRA) measured supine and after 4 hours of quiet ambulation, both on an ad libitum diet and on Day 4 of a 10 mEq low sodium diet, was always lower in the diabetics (31%-56% of control values). After the combined stimulus of sodium depletion and ambulation, PRA was 2.2 +/- 0.4 in the diabetics compared to 3.4 +/- 0.2 ng/ml/hr in controls (p less than 0.025). On the low sodium diet, PRA and the postural response of PRA correlated directly with the degree of autonomic dysfunction as quantitated by the velocity of esophageal peristalsis (r = 0.60, p less than 0.05; r = 0.75, p less than 0.005 respectively), suggesting that autonomic neuropathy was an important factor contributing to low PRA in these patients. No other parameters correlated with PRA. Plasma renin substrate (PRS) tended to be lower in diabetics (1053 +/- 95 vs 1358 +/- 132 ng AI/ml; p less than 0.07) but not sufficiently so to account for the substantial difference in PRA. Furthermore, PRS did not correlate with PRA. Fasting blood sugar, while higher in diabetics (209 vs 96 mg/dl), and creatinine clearance, which was lower (112 +/- 13 vs 78 +/- 4 ml/min; p less than 0.01), also did not correlate with PRA. Other factors, including serum creatinine, serum potassium, urinary aldosterone, blood pressure, and body weight, and the responses of these parameters to sodium depletion, were similar in diabetics and controls. These data implicate visceral neuropathy as a major factor in the hyporeninemia of these diabetics.
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PMID:Low plasma renin activity in normotensive patients with diabetes mellitus: relationship to neuropathy. 700 28

Captopril (SQ 14 225), an orally active inhibitor of angiotensin converting enzyme, was evaluated in the treatment of primary (essential) hypertension in a placebo-controlled long-term study. In 24 patients allocated to captopril treatment, mean supine BP fell from 174 +/- 18/110 +/- 7 to 151 +/- 22/96 +/- 12 mmHg. Ten patients achieved a supine diastolic BP of less than or equally 90 mmHg with a mean BP fall of 28/22 mmHg after 4 weeks' captopril dose titration (75-450 mg daily). In 14 patients, BP fell 19/9 mmHg. When hydrochlorothiazide (50-100 mg daily) was subsequently added, a total supine BP reduction of 51/20 mmHg was noted. In the placebo control group (n = 16), BP changed +1/-2 mmHg from 171/110 mmHg while addition of hydrochlorothiazide caused a mean supine BP fall of 19/10 mmHg. During long-term follow-up (mean 11.8 months), no resistance to therapy developed. A weak correlation, (p less than 0.05) was seen between pretreatment plasma renin activity and initial captopril-induced BP reduction. However, in patients with clearly defined low renin hypertension, the hypotensive effect of captopril was much less than in patients with higher renin values. Captopril induced a significant decrease in urinary aldosterone excretion, which was partially reversed by addition of hydrochlorothiazide. Observed side-effects were proteinuria (1 case), rash (2 cases) and taste disturbances (3 cases). During long-term follow-up, seven patients have dropped out, four due to side-effects and three because of non-compliance.
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PMID:Captopril, an orally active converting enzyme inhibitor, in the treatment of primary hypertension. A controlled long-term study with reference to initial plasma renin activity. 701 95

Plasma renin activity (PRA) and plasma aldosterone (PA) were measured under conditions of bed rest and after administration of furosemide and/or angiotensin II to adult-onset diabetics and age-matched controls. Seventeen of the diabetics had no proteinuria (non-proteinuria group) while in the other ten subjects, there was a persistent proteinuria, but no hypertension and renal dysfunction (proteinuria group). In the non-proteinuria group, changes in PRA and PA levels during both bed rest time and after the stimulation with furosemide did not significantly differ from findings in the control group. In the proteinuria group, PRA and PA levels were significantly lower than in the other two groups. PA and diastolic pressure responses to angiotensin II were slightly increased in diabetics (N.S.). PA responses to furosemide had significant positive correlation with those to angiotensin II. These findings suggest that the renin-aldosterone system responds normally in adult onset diabetics without proteinuria, but shows lower response in diabetics with persistent proteinuria, even without complications of hypertension and a decreased renal function.
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PMID:Plasma renin and aldosterone in adult-onset diabetics with persistent proteinuria. 704 Jul 51

The incidence of vascular complications in 224 patients with aldosterone-producing adenoma (APA) which was proven on adrenal surgery, was compared to that in 224 sex- and age-matched patients with essential hypertension (EHT). The incidence of cerebral hemorrhage was significantly higher (p < 0.05) in the patients with APA when compared to the EHT group. On the other hand, the incidence of myocardial infarction and/or congestive heart failure in the APA group was lower, although this difference did not reach statistical significance. Diastolic blood pressure in the APA group was significantly higher (p < 0.001) in the EHT group. However, a significant difference in diastolic blood pressure was not detected between the APA groups with and without vascular complications, whereas in the EHT group diastolic blood pressure was significantly higher (p < 0.001) in cases with vascular complications as compared to those without complications. As a possible factor contributing to the higher incidence of cerebral hemorrhage in the APA group, proteinuria was suggested. It was recommended that patients with primary aldosteronism should undergo operation when localization of the APA is established.
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PMID:Vascular complications in patients with aldosterone producing adenoma in Japan: comparative study with essential hypertension. The Research Committee of Disorders of Adrenal Hormones in Japan. 759 26

The cause of sodium retention in nephrotic syndrome is unclear. Hypovolaemia has traditionally been labelled as the cause but there is evidence in adults of a renal disturbance as the main cause. We aimed to find out whether children with early nephrosis can be classified as hypovolaemic by objective measures. We measured blood volume, kidney function, and hormone concentrations in children with early relapse of minimal-change nephrosis. Three presentations could be defined. The first was patients with incipient proteinuria and normal plasma protein, characterised by sodium retention, increased renal plasma flow, and slightly increased aldosterone, but normal noradrenaline. The second was patients with severe proteinuria, hypoproteinaemia, and hypovolaemic symptoms, who had oedema, sodium retention, and high concentrations of plasma renin, aldosterone, and noradrenaline, low atrial natriuretic peptide, and low glomerular filtration rate. The third was patients with equally severe proteinuria and hypoproteinaemia, but without hypovolaemic symptoms; they had oedema, but no active sodium retention, and normal plasma hormones and glomerular filtration. Neither blood pressure nor blood volume discriminated patients with or without hypovolaemic symptoms. These findings show that children with early full-blown nephrosis can present both with and without hypovolaemic symptoms and laboratory signs, despite equally severe hypoproteinaemia, and also that sodium retention precedes the reduction in serum protein.
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PMID:Volume regulation in children with early relapse of minimal-change nephrosis with or without hypovolaemic symptoms. 760 25

Exercise induces profound changes in the renal hemodynamics and protein excretion. Strenuous exercise provokes a major fall of the renal plasma flow and a reduction of the glomerular filtration rate. Despite these changes, the filtration fraction doubles at maximal exercise preserving the transfer of metabolites or substances through the glomerulus. A higher production of vasopressin and aldosterone enhances the tubular processes of water and electrolyte reabsorption, stabilising therefore the homeostasis during exercise. Urea, uric acid and lactate reabsorption are also increased. Postexercise proteinuria is directly related to the intensity of exercise rather than to its duration. This transient state may be explained by an increased glomerular membrane permeability and a partial inhibition of tubular reabsorption of plasma proteins. Postexercise proteinuria appears to be age-dependent. Exercise has an additional effect on protein excretion in patients with nephropathies (diabetes, renal diseases, kidney transplants).
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PMID:[Renal response to exercise in healthy and diseased patients]. 763 Apr 70

A male patient with hyperplasia of the juxtaglomerular apparatus, hypokalemia, an associated increase in plasma renin activity and hyperaldosteronism without hypertension was diagnosed as having Bartter's syndrome at the age of three. He was treated with spironolactone, indomethacin and potassium supplements. However hypokalemia, increased plasma renin activity and hyperaldosteronism persisted. Proteinuria was observed at the age of fifteen. Because of the gradual reduction of his renal function, the patient was admitted to our hospital and underwent hemodialysis at the age of twenty-one. He was normotensive. Serum potassium was within the normal range. Plasma renin activity and aldosterone concentration levels were still elevated. Renal biopsies, which had been carried out four times throughout his treatment, revealed an increase in sclerosis of the glomerular mesangial region, and interstitial fibrosis in proportion to narrowing of the small arteries in association with the juxtaglomerular hyperplasia. These findings suggested that changes in the glomeruli and interstitium of the kidney were secondary to long-standing hypokalemia, stenosis of the small arteries and the effects of the prescribed drugs for Bartter's syndrome.
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PMID:[A patients with chronic renal failure due to Bartter's syndrome]. 763 11

A twenty-one-year-old male was admitted to our hospital because of hypertension and proteinuria. He had felt general fatigue and low grade fever for one month. Blood pressure was 180/120 mmHg on admission. Laboratory findings showed 3+ proteinuria and 1+ occult blood in urinalysis; an accelerated erythrocyte sedimentation rate (ESR) of 39 mm/hr; elevation of LDH to 755 IU/l. Antinuclear antibody was positive with a titer of 1: 160, with a speckled pattern. Plasma renin activity and serum aldosterone were markedly elevated to 25.8 ng/ml/hr and 585.3 pg/ml, respectively. Renal function had declined mildly; endogenous creatinine clearance was 60 ml/min. Renal arteriogram demonstrated multiple intrarenal aneurysms in the bilateral kidneys. Aneurysms, 5-8 mm in diameter were located in the arteries from the interlobar to interlobular region. He was diagnosed as having polyarteritis nodosa (PN) and was then treated with 20 mg/day of prednisolone and monthly pulse therapy of cyclophosphamide. After steroid, cyclophosphamide and anti-hypertensive therapy, he became well and had normal blood pressure. The patient was considered a rare case of PN with multiple intrarenal aneurysms and accelerated hypertension. We discuss aneurysms in PN and accelerated or malignant hypertension documented in the literature.
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PMID:[A case of polyarteritis nodosa presenting with multiple intrarenal aneurysms and accelerated hypertension]. 769 55


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