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)

1. In four patients with nephrotic syndrome indomethacin not only reduced proteinuria but also inhibited the natriuretic effect of high doses of frusemide. 2. The inhibition of natriuresis by indomethacin could not be antagonized by albumin infusions. 3. Only the combined use of spironolactone and frusemide induced a natriuresis during indomethacin treatment. Spironolactone alone was ineffective. 4. It is suggested that inhibition of prostaglandin synthesis by indomethacin, in the presence of a stimulated renin-angiotensin system and hyperaldosteronism, may cause this strong tendency to sodium retention.
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PMID:Inhibition of frusemide-induced natriuresis by indomethacin in patients with the nephrotic syndrome. 84 48

A 5-year-old boy is presented who exhibited the classical symptoms of the syndrome described by BARTTER et al. in 1962: growth retardation, hypokalemic alkalosis, hyperplasia of the juxtaglomerular apparatus with normotensive hyperreninism-hyperaldosteronism, polydipsia with impaired renal concentration ability resistant to pitressin. In addition, the patient showed the typical proximal tubular defects of the Fanconi syndrome: hyperphosphaturia with hypophosphatemic ricktts, generalized hyperaminoaciduria, proteinuria and glucosuria. In the cases of Bartter's syndrome described to date, no uniform pathogenetic mechanism could be identified. Proximal tubular salt wasting generally is assumed to be the primary defect. The studies carried out in this case support this hypothesis and indicate that the complete clinical picture of Bartter's syndrome may occur within the framework of multiple proximal tubular defects.
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PMID:[Bartter's syndrome and tubular functional disturbances]. 115 68

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

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

Unilateral renal artery stenosis can lead to a non-functional kidney which secretes large amounts of renin. Four cases are presented in which the high renin state resulted in hypertension, proteinuria from the intact contralateral kidney, and secondary aldosteronism. The proteinuria was in the nephrotic range, which is unusual in renovascular hypertension, but gradually disappeared after correction of the high renin state by removal of the renin-secreting kidney or administration of an ACE inhibitor. Accordingly, when there is marked proteinuria in the presence of new-onset or rapidly progressive hypertension, hypokalaemic alkalosis, and a high peripheral PRA, renal artery stenosis should be considered since the proteinuria may be reversible after nephrectomy, repair of the ischaemic kidney or medical therapy.
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PMID:Reversible nephrotic syndrome due to high renin state in renovascular hypertension. 773 87

The renin-angiotensin-aldosterone system (RAAS) participates in the injury sustained by the remnant kidney. Our studies assessed the importance of aldosterone in that model and the response of aldosterone to drugs interfering with the RAAS. Initially, four groups of rats were studied: SHAM-operated rats, untreated remnant rats (REM), REM rats treated with losartan and enalapril (REM AIIA), and REM AIIA rats infused with exogenous aldosterone (REM AIIA + ALDO). The last group was maintained with aldosterone levels comparable to those in untreated REM rats by constant infusion of exogenous aldosterone. REM rats had larger adrenal glands and a > 10-fold elevation in plasma aldosterone compared to SHAM. REM AIIA rats demonstrated significant suppression of the hyperaldosteronism as well as marked attenuation of proteinuria, hypertension, and glomerulosclerosis compared to REM. REM AIIA + ALDO rats manifested greater proteinuria, hypertension, and glomerulosclerosis than REM AIIA rats. Indeed, by 4 wk of observation all of these features of the experimental disease were similar in magnitude in REM AIIA + ALDO and untreated REM. In separate REM rats spironolactone administration did not reduce glomerular sclerosis but did transiently reduce proteinuria, lowered arterial pressure, and lessened cardiac hypertrophy. In summary, aldosterone contributes to hypertension and renal injury in the remnant kidney model.
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PMID:Role of aldosterone in the remnant kidney model in the rat. 877 Aug 80

Interruption of the renin-angiotensin-aldosterone system (RAAS) by converting enzyme inhibition or angiotensin II (ANG II) receptor antagonism dramatically reduces injury in the remnant kidney model. Furthermore, converting enzyme inhibition reduces proteinuria and slows the decline in renal function in clinical disease. Hemodynamic actions of ANG II in the kidney in conjunction with a more poorly defined effect of the RAAS on systemic hypertension have been posited as the major mechanisms for maintenance of elevated glomerular pressure. Reductions in glomerular pressure have been attributed, at least in part, to removal of intrarenal effects of ANG II. Growth and fibrotic actions of ANG II may also contribute to progressive renal injury and relief from them reduce injury. The participation of circulating aldosterone in the remnant kidney model has been recently raised. Hyperaldosteronism and adrenal hypertrophy attend the hypertension, proteinuria, and glomerulosclerosis of this model. Although the hemodynamic actions of aldosterone probably account for some of the adverse effects it has in this model, other direct cellular actions may participate in its renal, as well as cardiac and fibrotic consequences. Thus, the RAAS, working through both ANG II and aldosterone, contributes to chronic progressive renal injury.
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PMID:Role of the renin-angiotensin-aldosterone system in the progression of renal disease: a critical review. 931 11

The aetiology of hypertension in type 1 diabetes is commonly due to the presence of diabetic nephrology. A rare case of hypertension in a patient with type 1 diabetes and no proteinuria is reported, where the investigation of borderline hypokalaemia allowed us to make a diagnosis of hyperaldosteronism due to bilateral adrenocortical hyperplasia. Secondary causes of hypertension should always be considered in all diabetic patients, particularly in the absence of clinical proteinuria.
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PMID:Aldosterone excess: a rare non-nephrophathic cause of hypertension in type I diabetes. 968 79

The first application of angiotensin converting enzyme (ACE) inhibitors it was the treatment of arterial hypertension. Latter news application appears such as: heart failure, myocardial infarct, nephropathy and diabetic proteinuria. Captopril, the first oral ACE inhibitor was used, since 1986, in the diagnostic screening of renovascular hypertension (RVH). Since then other authors recognised the importance of captopril test in the detection of RVH, advising also it's application in the diagnosis of primary aldosteronism and pheocromocithoma. Based in different publications the sensitivity of captopril test is 40%-100% and the specificity 72%-100%. There are several reasons to explain the differences between these results. In our opinion, these observations appeared as a consequence of the different methodology used. Despite the fact that alternative procedures to captopril test in the screening of RVII do exist this is, in our opinion, the most simple, cheap, safe and efficient test available at the moment.
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PMID:[Converting enzyme inhibitors in the diagnosis of secondary arterial hypertension --focus on the captopril test]. 1130 9

The cause of residual hypertension after adrenalectomy for primary aldosteronism (PA) is unknown. The purpose of this study is to investigate the characteristic pathological kidney features associated with PA. Between 1977 and 1999 at our hospital, 26 patients with PA caused by a unilateral adrenal cortical adenoma (Conn's syndrome) underwent unilateral adrenalectomy with concurrent open-wedge renal biopsy. Patients were categorized into two groups: (1) those with normotension with diastolic blood pressure less than 90 mm Hg who were not administered antihypertensive drugs, and (2) those with residual hypertension with diastolic blood pressure of 90 mm Hg or greater who were administered medication for 6 months after surgery. Thirteen patients were cured of hypertension postoperatively, and 12 patients were administered antihypertensive medications. Glomerulosclerosis, renal arteriolosclerosis, and preoperative left ventricular mass (LVM) index were worse in the group with residual hypertension than in that with normotension (17.8% +/- 7.8% versus 9.6% +/- 3.8%; P = 0.01; 2.5 +/- 0.5 versus 1.6 +/- 0.4, Bader's grade; P = 0.005; and 165 +/- 31 versus 139 +/- 24 g/m(2); P = 0.02, respectively). Severity of tubulointerstitial injury, preoperative duration of hypertension, preoperative severity of proteinuria, plasma aldosterone level, and serum potassium concentration were not significantly different between the two groups. In conclusion, severity of glomerulosclerosis and arteriolosclerosis and LVM are related to blood pressure after adrenalectomy in patients with PA.
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PMID:Cause of residual hypertension after adrenalectomy in patients with primary aldosteronism. 1132 68


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