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)

The effects of angiotensin converting enzyme inhibitors (ACEI) on proteinuria, renal function, and serum proteins were evaluated in six children with steroid-resistant nephrotic syndrome and proteinuria of 3-15 g/24 h (277 +/- 47 mg/m2 per hour). Following ACEI, proteinuria decreased from 7,408 +/- 2,385 (mean +/- SEM) to 3,746 +/- 1,395 mg/24 h (P less than 0.05). Creatinine clearance was 87.8 +/- 22.6 before and 96.4 +/- 23.6 ml/min per 1.73 m2 after ACEI. In two patients, inulin and para-aminohippuric acid clearances were normal before and after ACEI, together with parallel reductions of urine protein of 50% and 46%. Clearance of total protein was reduced by 56% following ACEI, compared with reduction in the clearance of gamma globulin by 58% and albumin by 39.5%. No significant change was seen in blood pressure, serum albumin, or total protein following ACEI. After ACEI, diuretic doses were able to be reduced or eliminated in three patients. Reduction of proteinuria was sustained during a followup period of 11-20 months in three patients. ACEI may be of benefit in the clinical management of children with steroid-resistant nephrotic syndromes, allowing reduction in diuretic requirements.
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PMID:Angiotensin converting enzyme inhibitors for reduction of proteinuria in children with steroid-resistant nephrotic syndrome. 191 Nov 44

The relationship between tubulointerstitial nephritis and proteinuria was characterized in experimental nephrosis in rats. In one group, proteinuria induced by aminonucleoside of puromycin (PAN) was reduced by using an 8% protein diet and adding the angiotensin I-converting enzyme (ACE) inhibitor enalapril to the drinking water. Two control groups were injected with saline and PAN, respectively, and fed a 27% protein diet. The first group had significantly reduced albuminuria and a definite attenuation of tubular cell injury. There was a strong positive correlation between the number of interstitial macrophages and albuminuria. The beneficial effect was reproduced by dietary-protein restriction alone, whereas ACE inhibition alone had an insignificant effect on the degree of proteinuria. Depletion of circulating T lymphocytes in one group of nephrotic rats eliminated interstitial lymphocytes but did not affect interstitial macrophage influx. Inhibition of the in situ proliferation of resident interstitial macrophages by unilateral kidney irradiation failed to change the intensity of the macrophage infiltration. Treatment of rats with sodium maleate produced proximal tubular cell toxicity but interstitial inflammation did not develop, suggesting that the latter is not a nonspecific response to tubular injury. These studies demonstrate a strong relationship between tubulointerstitial nephritis and the severity of proteinuria in experimental nephrosis.
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PMID:A relationship between proteinuria and acute tubulointerstitial disease in rats with experimental nephrotic syndrome. 202 4

This analysis of IMG has focused on the long-term natural history and current approaches to therapy of this disorder. It seems clear that IMG is intrinsically a relatively benign disease, particularly in certain populations. Risk factors for an unfavorable course can often be identified at the discovery of disease. For example older age at onset, male sex, very heavy proteinuria (greater than 10 g/d), sustained hypertension, impaired renal function, and significant chronic tubulointerstitial lesions in the initial renal biopsy all portend an unfavorable outcome. Contrariwise, patients lacking these prognostic features usually do quite well with a high likelihood of spontaneous complete or partial remissions and stable renal function. Once a complete remission has occurred, whether spontaneous or therapy induced, the long-term evolution of the disorder is quite favorable. Some patients may present with what appears to be "idiopathic" MGN, only to later demonstrate underlying disease, such as neoplasia, chronic viral infection, or systemic lupus erythematosus. Glucocorticoids alone, particularly when administered orally, do not seem to have significant beneficial effects over the long term; however, high-dose intravenous methylprednisolone may at times reverse declining renal function in patients with severe nephrotic syndrome. A small subset of patients may display a remitting and relapsing course following treatment with oral glucocorticoids, resembling to some extent patients with minimal change disease. Combination of alkylating agents, either cyclophosphamide or chlorambucil with glucocorticoids is very likely beneficial for the group of patients having an intrinsically unfavorable prognosis or for patients who demonstrate progressive renal insufficiency. At the present time it is not known whether regimens that involve long-term therapy with oral cyclophosphamide combined with glucocorticoids are superior to, equivalent to, or inferior to regimens that involve the cyclical use of intravenous methyl-prednisolone oral prednisone, and oral chlorambucil. Very long-term use of cyclophosphamide, in excess of 12 months, is probably associated with unacceptable long-term risks, particularly the emergence of neoplasia. Long-term follow-up, more than 10 years, will be required to establish the magnitude of the oncogenic potential of existing shorter term regimens of cyclophosphamide-glucocorticoid combinations and for cyclical regimens using chlorambucil. Further data is required to establish the role of cyclosporine, nonsteroidal antiinflammatory agents and intravenous immunoglobulins in the treatment of patients with IMG. ACE inhibitors, sometimes combined with nonsteroidal antiinflammatory agents, may have some usefulness in patients with heavy proteinuria and declining but not advanced renal failure.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The therapy of idiopathic membranous glomerulonephritis. 203 23

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

The existence of tissue renin angiotensin system (RAS) has been widely suggested in the recent literature by 2 main approaches: first, a dissociation between antihypertensive effects of angiotensin converting enzyme (ACE) inhibitors and the levels of stimulation of the circulating RAS; secondly, by the demonstration of the presence of the 3 key-proteins of the system (angiotensinogen, creatinine, and converting enzyme) within the 3 main target-organs of hypertension (i.e. kidney, heart and vessels). Those organs are capable to synthetize locally angiotensin II. Ramipril, a new ACE inhibitor (Triatec), which possesses a high affinity for tissue CE of those organs, according to previous publications by Unger, has been used as a tool for the investigations of the inhibition of those systems in human hypertension: a decrease of micro proteinuria has been without antihypertensive effects. In binephrectomized patients, ramipril has been shown to possess an antihypertensive effect. Finally, an important improvement of myocardial hypertrophy has been shown in hypertensive patients. Furthermore, this effect has been observed in animals (rats with aortic stenosis) even with low doses without antihypertensive effects. Further studies with new methodological approaches are still necessary.
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PMID:[Tissue renin-angiotensin system. Physiology and physiopathological value of their inhibition by ramipril]. 214 94

Hypertension and renal mass reduction induce glomerular hypertension (GH), hyperfiltration (HF) and renal injury. GH may contribute to allograft loss in post-transplant hypertensive patients (PT x HT). HF and GH may be evaluated by renal response to acute protein intake (API). Since ACE inhibition may prevent GH, the effects of fosinopril (Fos) were evaluated in 10 PT X HT on azathioprine and prednisone. Patients received 5 to 40 mg/day of Fos during 12 months. Baseline MAP (111.1 +/- 2.9 mm Hg) was significantly reduced by 10 to 12 mm Hg, rising to 114.7 +/- 2.7 mm Hg after Fos was administered. GFR (63.7 +/- 5.9 ml/min) decreased after 4 (48.1 +/- 4.6, P less than 0.05) and 12 months (50.7 +/- 4.6, P less than 0.05), rising to 59.4 +/- 5.6 after Fos was given. There was no GFR response to API before and after one month of Fos, however, a clear response became apparent at 4 (+ 27% P less than 0.05), and 12 months (+ 18%, P less than 0.05), disappearing after Fos discontinuation. Proteinuria (918.8 +/- 710.6 mg/d) decreased after 4 (72.3 +/- 21.6 mg/d, P less than 0.05) and 12 months, rising to 297.8 +/- 172.3 mg/day after therapy. GFR response to API in 22 controls and 17 uninephrectomized donors was 13 and 11%, respectively. Lack of response to API in PT x HT suggests HF and GH. Reduction of GFR, restoration of response to API and reduction of proteinuria, indicate that ACE inhibition with fosinopril ameliorates HF and GH. This effect may be beneficial in preventing hemodynamic-mediated allograft injury.
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PMID:Fosinopril prevents hyperfiltration and decreases proteinuria in post-transplant hypertensives. 214 57

Puromycin aminonucleoside (PAN)-nephrotic rats have high serum angiotensin I-converting enzyme (ACE) activity. We studied ACE activity in serum, urine, and tissues from PAN-nephrotic rats on days 2, 6, 11, and 16 after PAN injection. Proteinuria and hypoproteinemia were evident on days 6 and 11. Though significantly decreased, proteinuria was still evident on day 16. Serum ACE activity increased on days 2, 6, and 11. Urinary ACE activity became evident on days 6, 11, and 16 and correlated positively with proteinuria, suggesting that the source of urine ACE is the blood serum. ACE activity increased in testis on days 2 and 6, in lungs and aorta on days 6 and 11, in adrenal glands and small intestine on day 11, and in kidney on days 11 and 16. Heart ACE activity decreased on days 2 and 6, and increased on day 16; brain ACE activity decreased on day 6 and increased on day 11. These data implicate that changes in tissue ACE content may contribute to elevate serum ACE in PAN-nephrotic rats.
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PMID:Angiotensin I-converting enzyme activity in puromycin aminonucleoside-nephrotic syndrome. 217 83

The purpose of this study was to measure components of the renin angiotensin system in patients with type 1 diabetes mellitus, with and without nephropathy, to study the renal sensitivity to angiotensin II in uncomplicated type 1 diabetes and to investigate the short and long-term renal effects of angiotensin II reduction with angiotensin converting enzyme inhibitors in patients with diabetic nephropathy. In patients with type 1 diabetes without complications, plasma renin activity, angiotensin II and aldosterone levels were normal. In patients with diabetic nephropathy, renin levels were elevated, probably partly as a result of diuretic treatment. However, renin levels were also elevated compared to patients with other renal diseases who had similar treatment and degree of azotemia. The renal sensitivity to angiotensin II was normal in patients with uncomplicated diabetes. The reduction in glomerular filtration rate and renal plasma flow and increases in filtration fraction during A II infusion were equal to those in healthy controls. Nine days' captopril treatment in 15 patients with diabetic nephropathy induced an increase in renal plasma flow and a decrease in filtration fraction. The glomerular filtration rate remained unchanged. During 8 weeks' randomised enalapril or metoprolol treatment in 40 patients with diabetic nephropathy, enalapril treatment reduced proteinuria to half the initial value. Metoprolol treatment had no effect on proteinuria. Furosemide was also used and the dosage was adjusted to give equally effective blood-pressure control in both groups. During long-term treatment with captopril in patients with diabetic nephropathy, the rate of decline in kidney function over time was reduced to one-fourth the initial value even though the blood pressure was only slightly reduced. The renin angiotensin system appears to be functionally intact in diabetes mellitus and interruption by ACE inhibition reduces proteinuria both by blood pressure reduction and by an effect independent of systemic blood pressure. Long-term treatment might protect kidney function in diabetic nephropathy to a greater extent than would be expected from the blood-pressure-lowering effect alone.
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PMID:The renin angiotensin system in diabetes mellitus. A physiological and therapeutic study. 219 80

A double-blind, placebo-controlled study was carried out to assess the effects of a three-month treatment with a new ACE inhibitor, Benazepril (BNZ), on systemic and renal hemodynamics, and urine protein excretion, in 20 patients with chronic glomerulonephritis, normal blood pressure (130/83 +/- 16/10 mm Hg), and normal renal function (creatine clearance 106 +/- 25 ml/min). Treatments with placebo or BNZ were assigned randomly. A wide range of proteinuria lowering effect was observed in overall population (from 1 to 84%, average 34%). Following the arbitrary level of a 30% reduction, two well-matched subgroups (10 patients for each one) were obtained: "good responders" (average decrease 51%), and "poor responders" (average decrease 17%). The main distinctive feature between the two groups was a higher plasma renin activity level in good than in poor responders. A positive correlation between the fall in proteinuria and blood pressure was found. Although the decrease in blood pressure seems to represent the major factor in determining the reduction in proteinuria, a multiple correlation analysis showed that the most prominent role (71%) was attributable to the combined decrease in blood pressure and filtration fraction, and then also to the efferent arteriole dilatation. Our conclusion is that ACE inhibitors are capable of also reducing proteinuria in patients with renal disease with normal blood pressure, the effect being more pronounced in those exhibiting humoral, systemic and renal hemodynamic patterns, indicating a greater activity of circulating and renal renin angiotensin system.
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PMID:Effects of ACE inhibition in normotensive patients with chronic glomerular disease and normal renal function. 220 Sep 24

ACE-inhibitors have many positive features, when treating patients with progressive renal failure. These patients have high mortality in cardiac and vascular complications. It is therefore important to treat hypertension in these patients with drugs which do not have negative effects on lipid-, glucose, or electrolyte-metabolism, and ACE inhibition fulfills these requirements. These drugs decrease left ventricular hypertrophy, which is a positive prognostic sign of hypertensive patients, too. Contrary to regular diuretics, ACE-inhibition does not cause the negative effects associated with activation of the renin-angiotensin system. In many patients ACE-inhibitors decrease proteinuria to a higher degree than other antihypertensive drugs, and this may be an important clinical advantage, particularly in nephrotic patients. ACE inhibition might slow progressive renal failure. This effect may be associated with advantageous intraglomerular hemodynamic changes, but may also associate with inhibition of negative effects of angiotensin II on mesangial hypertrophy and matrix proliferation.
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PMID:[ACE inhibitors' effect on kidney function]. 221 87


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