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)

An examination of the principal physiological actions of angiotensin II should make it clear why in vivo attempts to inhibit the rate of angiotensin II generation have been an attractive avenue in pursuing control of high blood pressure. The major physiological effect of angiotensin II relates to its direct pressor effect, but there are supplementary blood pressure regulating actions. Therefore, if we limit the rate of angiotensin II generation by inhibiting the angiotensin converting enzyme (ACE) we should expect to control high blood pressure in a number of clinical syndromes. This paper reviews the future of ACE inhibitors in the treatment of conditions such as hypertension associated with unilateral renal artery stenosis, essential hypertension and severe and previously unresponsive hypertension, with respect not only to efficacy but also to the side-effect profile and ancillary properties. Side effects seen with this class of drug are cough, rashes (both morbilliform and urticarial) and, rarely, angio-oedema. Proteinuria, nephrotic syndrome, leukopenia and taste disturbance were previously reported with captopril but only taste disturbance, and that less frequently, is apparent at the lower doses now employed. Several studies have examined the 'quality-of-life' aspects of ACE therapy and have usually but not always reported favourably. There are features of the ACE inhibitors which make them attractive drugs, and while we should be cautious because of limited experience, we should critically and creatively examine their properties over the next years.
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PMID:Angiotensin converting enzyme inhibition in hypertension. 331 25

It had been previously thought that protein excretion in hypertensive nephrosclerosis was less than 0.5 to 1.0 g/24 h. Furthermore, it was believed that proteinuria in the nephrotic range associated with hypertension was probably due to primary renal disease, malignant hypertension, renal artery stenosis, or pheochromocytoma. We report eight patients with biopsy-proven hypertensive nephropathy and heavy proteinuria in the absence of malignant hypertension or renal artery stenosis. The 24-hour protein excretion ranged from 2.7 to 4.3 g. All patients had renal insufficiency, with serum creatinine ranging from 2.0 (176.8) to 7.8 mg/dL (689.5 mumol/L). Renal function worsened in most patients during the follow-up period despite adequate control of the hypertension, and three patients had to be started on hemodialysis. Three patients died during the follow-up period. We conclude that hypertensive nephrosclerosis must be included in the differential diagnosis of marked proteinuria in patients with essential hypertension and that heavy proteinuria, along with renal insufficiency, are poor prognostic indicators in such patients.
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PMID:Proteinuria in hypertension. 368 33

Sixty-five renal transplant recipients underwent digital vascular imaging of the graft and simultaneous selective venous sampling for plasma renin activity. Renal artery stenosis was found in seven patients but did not appear to be functionally important. Diffuse intrarenal arterial attenuation was found in seven patients and was associated with impaired graft function and perfusion; it may indicate chronic rejection. Lower pole hypoperfusion was found in nine patients without impaired graft function or perfusion; its clinical relevance is uncertain. Aneurysmal dilatation of the main renal artery was found in two patients. Severe hypertension was common in patients with these three major abnormalities, but a causal association between the abnormality and hypertension could rarely be inferred. It may be the abnormalities on digital vascular imaging, especially diffuse intrarenal arterial attenuation and lower pole hypoperfusion, are secondary to severe hypertension. Digital vascular imaging with simultaneous selective venous sampling for plasma renin activity is useful in evaluating the vascular anatomy of the grafted kidney and in assessing any abnormality found. The combined procedure was well tolerated by all patients with no complications and no incidence of acute tubular dysfunction or proteinuria after the investigation.
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PMID:Digital vascular imaging and selective renin sampling in evaluation of vascular anatomy in renal transplant recipients. 640 69

The effect of laboratory evidence of renal parenchymal abnormality on the results of renal revascularization in 83 patients with renovascular hypertension was determined. Primary renal disease (PRD) was defined as an abnormal urinalysis (proteinuria, hematuria, or casts) in the absence of urinary infection, or decreased renal function (elevated serum creatinine level greater than 1.5 mg/dl and/or decreased creatinine clearance). All patients were hypertensive on medical therapy preoperatively. Patients were defined as cured if postoperative diastolic blood pressure (BP) was less than 90 mm Hg on no medication and improved if BP less than 90 mm Hg on medication. Sixty-six patients (80%) were cured or improved following revascularization. Of 45 patients (63%) with evidence of PRD preoperatively, 28 (62%) were cured or improved compared with 33 patients without PRD, of whom all (100%) were cured or improved (p less than 0.001). Each of five patients with transplant renal artery stenosis had two operations; four were cured or improved. The serum creatinine level was elevated preoperatively in 37 cases. Eighteen of the 37 (49%) improved to within normal limits following operation. Fifteen patients had simultaneous bilateral renal artery revascularization, and 12 (80%) were cured or improved. Fourteen patients (17%) had concomitant vascular procedures: aortobifemoral bypass (seven), abdominal aneurysm resection (five), femoral endarterectomy (one), and aortoiliac bypass (one). Twelve of these 15 patients had PRD, and 8 of the 12 (67%) were cured or improved. Only one death occurred in the perioperative period. Thirty-eight patients (46%) had been treated for hypertension for more than 12 months before referral.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of primary renal disease in patients with renovascular insufficiency. 648 98

Exacerbation of hypertension and a marked excretion of protein in the urine were observed in three patients in the absence of underlying renal parenchymal disease or other causes of proteinuria. Stenosis of a renal artery and hyperreninemia were present in all three patients. Correction of the stenosis by arterial bypass or nephrectomy resulted in a rapid decrease in urinary protein excretion. The relationship between the levels of renin activity and the proteinuria in one patient and long-term follow-up in the other two patients are reported, and the mechanisms of this proteinuria are reviewed. Renal artery stenosis may be the underlying cause in some cases of idiopathic nephrotic syndrome.
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PMID:Proteinuria and nephrotic syndrome induced by renin in patients with renal artery stenosis. 700 41

Nephrotic range proteinuria occurred in a 60-year-old woman with renal artery stenosis and marked hyperreninemia. Treatment by nephrectomy produced resolution of both proteinuria and hypertension. The gradual resolution of the proteinuria postoperatively suggested the proteinuria, at least in part, came from the contralateral kidney. Foot process fusion in the nephrectomy specimen suggested it too was a source of proteinuria. A marked degree of hyperreninemia, as was present in this case, may be necessary before massive proteinuria occurs in renal artery stenosis.
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PMID:Reversible nephrotic range proteinuria with renal artery stenosis: a clinical example of renin-associated proteinuria. 705 Jul 50

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

Ischemic nephropathy encompasses renal insufficiency due to 3 different diseases, namely renal artery stenosis, so-called benign nephrosclerosis, and renal cholesterol embolism. All 3 disease entities may lead to a progressive loss of renal excretory function. If a patient presents with renal failure of unknown origin, renal artery stenosis should be looked for by color-coded duplex scanning or arteriography. The clinical presentation of benign nephrosclerosis in caucasians has no typical clues. Usually, a renal biopsy identifies this renal disorder in a patient with long-standing hypertension, moderate proteinuria and renal insufficiency. Cholesterol embolism typically affects several arterial trees, and is induced by arteriography in patients with arteriosclerosis of the aorta. The best treatment for ischemic nephropathy due to renal artery stenosis [conservative, angioplasty, surgery] is unknown because appropriately controlled trials are lacking. Invasive therapy should be considered in patients with bilateral renal artery stenosis or stenosis of a single functioning kidney, particularly if the affected kidney is not contracted. Arguments in favor of invasive therapy include the progressive nature of renal artery stenosis and the poor outcome of dialysis patients with this diagnosis as underlying renal disease.
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PMID:[Ischemic nephropathy]. 778 95

A considerable number of hormones control renal perfusion to preserve glomerular filtration. We used the "captopril test" to characterize patients with renal-vascular hypertension. This study revealed a group of patients which reacted to 25 mg of captopril with a significant increase of plasma renin activity, but angiography excluded a renal artery stenosis. These patients had significantly more hypertensive organ damage than a control-group, including a significant microalbuminuria. Consequently, we infused a subpressure dose of angiotensin II to investigate its impact on albuminuria in these patients. Although angiotensin II induced hyperfiltration, microalbuminuria was not increased. Because this finding could have therapeutic relevance, we investigated the significance of different antihypertensive drugs (beta-blocker, alpha-blocker, Calcium antagonists, ACE-inhibitor) on microalbuminuria in patients with arterial hypertension. Renal hemodynamics were influenced as expected, but blood-pressure and microalbuminuria were reduced to the same extent by all antihypertensives. In contrast to these results, we could demonstrate significantly different influences of a beta-blocker and an ACE-inhibitor on proteinuria in patients with primary glomerulonephritis. These results suggest different effects of antihypertensive drugs on renal protein excretion depending on the actual disease.
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PMID:[Modification of renal hemodynamics and proteinuria in patients with arterial hypertension and kidney diseases]. 790 76

ACE inhibitors have been shown to worsen the kidney damage occurring distal to a renal artery stenosis. To determine if this effect was due to the decrease of arterial pressure or to an inhibition of the formation of angiotensin, we compared the effects of equihypotensive doses of an angiotensin converting enzyme inhibitor (enalapril) and a long-acting calcium antagonist (Ro 40-5967) in 2K-1C rats. The rats were treated for five weeks with either enalapril, Ro 40-5967, or were left untreated. A group of sham operated rats was used as control. At the end of the five-week treatment period, proteinuria, plasma urea and creatinine were measured and quantitative morphometry of the clipped and unclipped kidneys was performed. Ro 40-5967, despite an absence of inhibition of the renin-angiotensin system, worsened the lesions of the clipped kidney to the same extent as enalapril. In contrast, the effects of both drugs on the unclipped kidney were different. Ro 40-5967, and not enalapril, increased the weight and the glomerular surface area of the unclipped kidney. Ro 40-5967 did not change the glomerulosclerosis index, which was improved by enalapril. In contrast with enalapril, Ro 40-5967 decreased plasma urea and creatinine concentrations. Only enalapril decreased proteinuria which originated from the unclipped kidney as shown by nephrectomy experiments. We conclude that during ACE inhibition the fall in renal perfusion pressure seems to be the main determinant of the renal damage distal to a renal artery stenosis, independently of a blockade of the renin-angiotensin system.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Calcium blockade versus ACE inhibition in clipped and unclipped kidneys of 2K-1C rats. 796 54


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