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)

Angiotensin II is the main regulator of both glomerular haemodynamics and glomerular capillary permeability. An alteration in the function of intrarenal angiotensin II seems to be the cause of diabetic glomerulopathy in animals and humans. In order to investigate the renal effects of the angiotensin converting enzyme (ACE) inhibitor enalapril (5 mg once a day), 24 normotensive diabetic patients with persistent proteinuria, after a 3-month run-in period, were randomly allocated to receive the active drug (12 patients) or the corresponding placebo, for the 6 months. Effective renal plasma flow, glomerular filtration rate, renal vascular resistance and filtration fraction were measured at the end of the run-in and the treatment periods. Blood pressure, heart rate, urinary albumin excretion, plasma renin activity and aldosterone, blood glucose, serum fructosamine and body weight were checked monthly during the run-in and every 2 months during the treatment period. Enalapril decreased urinary albumin excretion in the normotensive diabetic patients without any changes in systemic blood pressure or glomerular haemodynamics. These results indicate that ACE inhibition interferes with the glomerular capillary permeability induced by angiotensin II.
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PMID:Angiotensin converting enzyme inhibition with a low dose of enalapril in normotensive diabetics with persistent proteinuria. 285 53

The authors studied clinical and biological data occurring in 165 patients observed during 23 years and afflicted with polyarteritis nodosa. Hypertension was present in 52 patients (31.5%) and seven of them suffered from malignant hypertension (4%). Mean age of patients (6 male, 1 female), with malignant hypertension was 38 +/- years old. Mean follow up was 49 +/- 28 months including 26 +/- 21 months after discontinuation of treatment of polyarteritis nodosa. Malignant hypertension occurred during the first year of evolution of polyarteritis nodosa. Renal insufficiency was present in 5 of 7 patients. Proteinuria was greater than 1 gr/d in 4 cases. Renal arteriography was performed in 6 patients and showed in every case renal ischemia and microaneurysms in five. In 4 patients measurements of plasma renin activity and of aldosterone were obtained. A stimulation of those hormones was demonstrated. Some symptoms of polyarteritis nodosa were present with a high incidence in case of malignant hypertension: digestive signs (6/7), orchitis (3/6). HBs antigen was present in 6 cases and hepatitis in 5. Captopril was effective in every case, alone or associated with other treatments. Follow up of hypertension went from 8 months to 4 years. At present time 6 patients are alive and one is lost of follow up. A treatment is necessary in 6 of 7 patients. Creatininemia is greater than 300 micromol/l in 4 patients. A successful kidney transplantation was performed in one case. Our study shows a close relation between malignant hypertension observed in polyarteritis nodosa, vascular nephropathy, digestive and urologic signs. Hepatitis B virus could be responsible of those manifestations.
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PMID:[Malignant arterial hypertension in periarteritis nodosa. Incidence, clinicobiologic parameters and prognosis based on a series of 165 cases]. 287 20

The classic conception of the pathophysiology of the nephrotic syndrome (NS) is now being seriously questioned, on the basis of current research findings. New conceptions of the syndrome, with its proteinuria, hypoalbuminemia, and edema, are providing explanations for the discrepancies between the original theory and clinical data from individual patients, particularly related to edema formation. Many of the edema-preventing mechanisms are normal in patients with NS, but may fail when plasma osmotic pressure falls significantly. Plasma volumes, blood volumes, and blood pressures of patients with NS have been found to be generally normal or slightly increased, in contrast to the classic "hypovolemia" theory. Activation of the renin-angiotension-aldosterone system is variable and cannot fully explain the sodium and water retention. The decreased renal filtration rates and abnormal sodium retention/excretion rates are now best explained by an intrarenal defect, on the basis of multiple research approaches. These research conceptions of the pathophysiology of NS are significant for nurses because they can be used in patient assessment, interpretation of patient data, monitoring during treatment, collaboration about the plan of care, development of nursing care plans, and patient teaching. Several nursing diagnoses may be appropriate for patients with NS: alteration in fluid volume: excess; potential for infection; alteration in nutrition: less than body requirements, potential alteration in comfort; knowledge deficit; and potential disturbance in self-concept: body image.
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PMID:Nephrotic syndrome: a nursing care plan based on current pathophysiologic concepts. 291 29

Hypertension is more frequently found in patients with diabetes mellitus than in subjects with normal glucose tolerance. On the other hand, concomitant hypertension accelerates the progression of diabetic nephropathy. To examine whether human atrial natriuretic peptide (human ANF-[99-126], hANP) is involved into the pathogenesis of hypertension and nephropathy of diabetic patients and to find out whether the detection of increased hANP levels can serve as an early marker, helping to identify diabetic patients at increased risk of developing these diabetes complications, we studied 107 randomly selected patients with Type 1 or Type 2 diabetes mellitus (53 women, 54 men). There were no differences between patients with normal hANP levels and patients with hANP levels above normal range regarding age, diabetes duration, metabolic control, kidney function (creatinine clearance and proteinuria), electrolytes, and in plasma renin activity, aldosterone, epinephrine and norepinephrine levels in plasma. However, higher blood pressure was measured and antihypertensive therapy was found more frequently in patients with increased hANP levels (p less than 0.05). This was confirmed by analyzing the subgroup of patients with normal blood pressure without antihypertensive therapy: Again, diastolic blood pressure was found to be higher (p less than 0.05) in patients with elevated hANP than in patients with normal hANP levels. In this subgroup, increased creatinine clearance tended to be found more frequently among patients with increased hANP levels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[What pathophysiologic significance does increased plasma levels of human atrial natriuretic peptide have in patients with diabetes mellitus?]. 297 Jan 66

Atrial natriuretic peptide (ANP) and the renin-angiotensin-aldosterone system are important regulatory hormones in sodium homeostasis. We have measured these hormones during volume expansion produced by water immersion in diabetic subjects without and with microalbuminuria or frank proteinuria and compared the response with normal controls. Diabetic subjects excreted about half the amount of sodium that was excreted by the normal subjects (39 vs 21 mmol) over 4 h. Diabetic subjects and normal ones showed a twofold rise in ANP during immersion and a marked suppression of both plasma renin activity and aldosterone. There was no difference in the hormonal response between diabetic and normal subjects or between those diabetic subjects with and those without incipient (microalbuminurics) or established nephropathy.
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PMID:The relationship of the renin-angiotensin-aldosterone system to atrial natriuretic peptide and the natriuresis of volume expansion in diabetics with and without proteinuria. 297 18

Angiotensin-converting enzyme (ACE) inhibitors are a new class of drugs, whose main indications are the treatment of hypertension and of heart failure. Data obtained with captopril, the first orally active ACE inhibitor, affords an understanding of the rationale of their therapeutic use based on the knowledge of their mechanisms of action, efficacy, contraindications and precautions, dosage and frequency of administration, side-effects, interactions and advantages. ACE inhibitors appear to exert their haemodynamic effect mainly by inhibiting the renin-angiotensin-aldosterone system, but also by modulating sympathetic nervous system activity and by increasing prostaglandin synthesis. Therefore they act both on vasoconstrictor and volume factors, since they cause vasodilation (the main effect) and mild natriuresis without affecting the heart rate and contractility and, probably, favourably influencing renal, coronary and cerebral circulation. So far it appears that ACE inhibitors can be usefully employed in the treatment of heart failure, in which they reduce both pre- and after-load, and mainly of hypertension. In the past captopril has been used to treat only severe and or resistant hypertension and some secondary forms, like renal parenchymal and renovascular hypertension, but now it seems that captopril is useful also to treat mild to moderate essential hypertension. Their efficacy in reducing blood pressure is similar to that of thiazide diuretics and of beta-blockers, the two drugs now considered of first choice and they exert their hypotensive action without the development of pseudotolerance or tolerance. ACE inhibitors seem, at the moment, contraindicated in pregnancy and in hyperkalaemic syndromes and must be used with caution in patients with collagen disease (mainly associated with renal failure), with severe bilateral renal artery stenosis (and with severe artery stenosis of a solitary kidney) and with severe sodium depletion. It is now established that captopril has a flat dose response curve and that it must be given (twice daily) at a dose not exceeding 150 mg/day. The same pharmacological approach must be used with future ACE inhibitors in order to establish the right posology and the frequency of administration. In this respect enalapril seems to be a promising ACE inhibitor with a prolonged action (at least 24 hours). The exact posology of ACE inhibitors might be crucial, since it has been shown that the side-effects of captopril (skin rashes, fever, taste disturbances, proteinuria and neutropenia) are dose dependent.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Angiotensin-converting enzyme inhibitors in hypertension: a review. 300 82

The purpose of this study was to define the effect of the angiotensin-converting enzyme inhibitor, enalapril maleate, on blood pressure, renal function, protein excretion, and potassium homeostasis in patients with hypertension associated with moderate to severe renal dysfunction. Nine patients, having an initial inulin clearance between 9 and 48 mL/min/1.73 m2, were treated with enalapril monotherapy (n = 6) or enalapril/furosemide (n = 3) combination therapy. Systolic and diastolic blood pressures were well controlled. Supine plasma renin activity was stimulated; the supine plasma aldosterone level was suppressed, with a resultant increase in the serum potassium level. Clinical hyperkalemia was not observed. Glomerular filtration rate, assessed by inulin and creatinine clearances, was not significantly changed. Effective renal plasma flow, assessed by paraaminohippurate clearance was significantly increased, with a resultant decrease in filtration fraction. Importantly, urinary protein excretion was markedly reduced. These results suggest that enalapril therapy produces efferent arteriolar dilitation with preservation of the glomerular filtration rate. Enalapril therapy may also blunt the effects of angiotensin II on transglomerular passage of protein, as demonstrated by reduced proteinuria. These findings suggest that interruption of the renin-angiotensin system in patients with preexisting renal disease may have renal protective effects.
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PMID:Effect of enalapril in subjects with hypertension associated with moderate to severe renal dysfunction. 302 60

This case report deals with an eight-year duration severe high renin hypertension and its consequences. In 1975, a 13 years old girl was found to have blood pressure (BP) levels of 240/150 mmHg with bilateral papilloedema. Hypokalemic alkalosis, a 45 mm Sokolow index (SI) and very high peripheral renin activity (PRA) were also noticed. Renal vein renin sampling (RVRS) suggested secretion from the left kidney but intravenous pyelography and renal arteriography were normal. BP levels were first controlled by triple treatment but rose one year later, despite adjunction of beta-blockers. High PRA was again found, but without hormonal gradient on a second RVRS. From 1977 to 1982, BP never fell to normal levels despite quadruple treatment. In 1982, a stage II optic fundus, a 58 mm SI and 2 g/day proteinuria are noticed, so that a new complete etiologic work up is undertaken in 1983: PRA is still high, with a dramatic acute BP fall after captopril and no gradient on a third RVRS, but intravenous pyelography, tomodensitometry and selective arteriography disclose a 4 cm diameter poorly vascularized tumour on the surface of the lower pole of the right kidney. BP levels are controlled for three months by captopril + chlorothiazide. The tumour is removed in january 1984. RVRS by direct peroperative punction indicates (a posteriori) hormonal secretion from the right kidney lower pole. Histologic examination and immunofluorescence with antirenin serum corroborate the juxtaglomerular origin of the tumour. Eighteen months later, BP is permanently normal, SI is 30 mm, and there is no proteinuria.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Natural history of arterial hypertension due to primary hyperreninism]. 314 36

Although most patients respond well to loop diuretics, poor response is sometimes a problem and some underlying mechanisms were addressed in this study. The renal response to continuous infusion of furosemide was investigated in eight healthy volunteers during controlled isotonic dehydration and after full restoration of volume losses. A rapidly reversible acute tolerance developed in parallel with dehydration and activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS). Dehydration also reduced the renal clearance of furosemide substantially, but only decreased the urinary delivery rate of the drug (the principal determinant of the diuretic effect) to a minimal extent. Delayed tolerance to an i.v. bolus dose of furosemide was found in 12 healthy volunteers after 1 week of oral furosemide treatment with and without angiotensin converting enzyme inhibition. No pharmacokinetic changes were seen. This type of tolerance was not related to dehydration or activation of RAAS. Thus, the induced decrease in renal sensitivity to furosemide was probably due to an intrarenal (structural?) adaptation. The pharmacokinetics and pharmacodynamics of piretanide were studied in six healthy volunteers and 22 patients with chronic renal failure (glomerular filtration rate 1-28 ml/min). Poor response to the diuretic action of the drug was found in the patients. This was entirely due to a decrease in the fraction of piretanide excreted unchanged in the urine, and the renal sensitivity to the drug was normal. Multiple daily doses of piretanide of maximally 24 mg are recommended for optimal efficiency in renal failure. Substantial changes in pharmacokinetics of furosemide were found after manipulation of plasma albumin in five patients with nephrosis, while the urinary delivery of the drug scarcely changed. Neither the induced alterations in proteinuria nor those in plasma volume influenced the renal sensitivity to furosemide significantly. Some methodological observations proved to be of significance. Creatinine was found to be an unreliable marker of GFR because of its substantial tubular secretion and reabsorption, both of which were related to the degree of hydration. Likewise, lithium was considered an unreliable marker of proximal tubular reabsorption, since there were reasons to suspect furosemide-sensitive distal lithium reabsorption.
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PMID:Mechanisms of reduced effects of loop diuretics in healthy volunteers and in patients with renal disease. 320 Nov 62

1. Normal rats and passive Heymann membranous glomerulonephritic rats were chronically treated with DOCA/NaCl for 9 weeks. Normal and untreated nephritic rats were used as controls. Urinary kallikrein excretion (UKE), proteinuria and tail blood pressure (BP) were determined in awake rats. Glomerular filtration rate (GFR), plasma renin activity (PRA), and plasma potassium (PK) concentration were measured at the end of the experiment. 2. Comparison between basal and 9th-week measurements indicated that DOCA/NaCl administration significantly increased (P less than 0.05) UKE (3.96 +/- 0.30 vs 7.60 +/- 1.51 U/24 h) and BP (118 +/- 2 vs 135 +/- 6 mmHg) in normal rats, whereas in nephritic DOCA/NaCl-treated rats, UKE was unaltered (3.80 +/- 0.50 vs 3.40 +/- 0.30 U/24 h) and BP increased to higher levels (117 +/- 2 vs 152 +/- 3 mmHg) than in the normal DOCA/NaCl group (P less than 0.05). Passive Heymann nephritis alone did not affect UKE (3.56 +/- 0.40 vs 3.60 +/- 0.80 U/24 h) or BP (124 +/- 2 vs 125 +/- 2 mmHg). 3. At the end of the study, PK was decreased and PRA totally suppressed in both normal and nephritic DOCA/NaCl-treated rats. Proteinuria was more pronounced in nephritic DOCA/NaCl-treated rats (44.8 +/- 5.2 mg/day) than in control nephritic animals (15.1 +/- 2.4 mg/day) and GFR was increased equally in both DOCA/NaCl-treated groups. 4. The failure of nephritic rats to respond to DOCA/NaCl by increasing UKE was not associated with any significant derangement of renal function or structure and may have been related to the aggravation of arterial hypertension in this group.
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PMID:Nephritis blunts urinary kallikrein excretion and aggravates DOCA/NaCl hypertension in rats. 324 40


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