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)

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

A 55-year-old man developed renovascular hypertension that was characterized by high plasma renin activity. This was accompanied by nephrotic range proteinuria. Treatment with nifedipine and furosemide lowered the blood pressure to normal values, but proteinuria persisted. However, treatment with an ACE-inhibitor brought resolution of the proteinuria, suggesting a role for angiotensin II in urinary protein loss.
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PMID:Disappearance of renin-induced proteinuria by an ACE-inhibitor: a case report. 222 56

The pathophysiology of the nephrotic syndrome (NS), characterized by protenuria, edema, sodium retention and hyperlipidemia, is not clear. We studied the role of some systemic factors on sodium retention in an experimental model of NS. NS was induced in rats by a single subcutaneous injection of puromycin aminonucleoside (PA) (15 mg/100 g); control animals received vehicle. All rats were kept in metabolic cages for 24 days (3 days before and 21 days after PA-injection). Urine was collected daily. Blood samples were obtained every day until day 10, and then every other day up to the end of the study. The rats showed the following alterations after PA injection: a) a rise in serum angiotensin converting enzyme activity (ACEA) and plasma aldosterone (PAldo) at day 1; b) a rise in urinary aldosterone (UAaldoV), azotemia and sodium retention at day 2; c) massive proteinuria (UProt) and decrease in plasma angiotensinogen concentration (PAC) at day 4; d) increases in plasma renin activity (PRA), plasma renin concentration (PRC) and serum creatinine as well as hypoproteinemia, hypercholesterolemia, hypertriglyceridemia, ascitis and edema at day 5; e) increase in urine volume at day 6. PAldo became normal at day 7; urine sodium (UNaV), PRA and PRC at day 8; UAldoV at day 9; serum urea and ACEA at day 10; urinary volume at day 11; PAC, serum total protein and creatinine at day 12. The edema disappeared at day 11. UProt, hypercholesterolemia and hypertriglyceridemia persisted, though they decreased substantially by the end of the study (day 21). Light microscopy studies revealed normal glomerular morphology, but electron microscopy showed fusion of podocytes before proteinuria. These data suggest that: a) sodium retention was not a consequence of proteinuria or hypoproteinemia; b) sodium retention seems non-related to renin secretion, but may be partially mediated by a fall in glomerular filtration rate or by an increased tubular resabsorption secondary to other factors; c) the increase in PAldo, UAldoV and ACEA are non-related to renin secretion: all occurred before PRA rose; d) water retention, increase in PRA and PRC, hypercholesterolemia and hypertriglyceridemia are secondary to the hypoproteinemia.
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PMID:Pathophysiology of experimental nephrotic syndrome induced by puromycin aminonucleoside in rats. I. The role of proteinuria, hypoproteinemia, and renin-angiotensin-aldosterone system on sodium retention. 223 72

Plasma active renin (PARC) and plasma total renin (PTRC) were measured in 72 patients with childhood-onset IDDM and 37 control subjects in the supine posture. The diabetic patients were divided into three groups: group A, 55 patients with normoalbuminuria; group B, 11 patients with microalbuminuria; and group C, 6 patients with overt proteinuria. The levels of PTRC were 125 +/- 51, 240 +/- 124 and 580 +/- 285 ng/l in groups A, B and C, respectively; all of which were significantly higher than 114 +/- 33 ng/l in the control subjects. On the other hand, the ratios of plasma active to total renin, ARC/TRC, were 18.1 +/- 12.5, 10.7 +/- 6.7, and 2.9 +/- 1.4% in groups A, B and C, respectively; all of which were in turn significantly lower than 24.8 +/- 8.7% in the control subjects. Among the diabetic groups, PTRC became higher and ARC/TRC became lower in conjunction with the degree of albuminuria. The acute increments of PARC and PTRC during a standing load test were subsequently observed in 7 patients of group A, 5 of group B, 4 of group C, 13 patients with non-diabetic glomerulonephritis, and 6 control subjects. The ratios of increments of PARC to that of PTRC, delta ARC/delta TRC, were 48.3 +/- 22.3, 35.1 +/- 10.4 and 8.4 +/- 8.1% in groups A, B, C, respectively; all of which were significantly lower than 84.2 +/- 48.6% in the control subjects. Patients with non-diabetic glomerulonephritis showed, to a lesser degree, low ratio of delta ARC/delta TRC (60.4 +/- 37.9%) in conjunction with higher level of PTRC (249 +/- 89 ng/l).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Altered synthesis of renin in patients with insulin-dependent diabetes: plasma prorenin as a marker predicting the evolution of nephropathy. 226 47

In vitro release of renin, angiotensinogen and aldosterone was studied in control (CT) and nephrotic rats. Nephrotic syndrome (NS) was induced by a single injection of puromycin aminonucleoside (PA). The in vitro systems used were: renal cortical slices (RCS), liver slices (LS) and adrenal glands, all incubated in Krebs-Ringer buffer. Renal renin content (RRC) and isoproterenol-induced renin secretion (RS) also were studied. RS, RRC and angiotensinogen release were measured indirectly by radioimmunoassay (RIA) of angiotensin I (ANG I); aldosterone was estimated by direct RIA. Basal RS was not modified in NS: 385 +/- 196 (CT) vs 344 +/- 149 ng ANG I/mg protein/h (NS), p greater than 0.05. Isoproterenol increased RS significantly in both CT and NS groups: 535 +/- (CT) and 685 +/- 231 ng ANG I/mg protein/h (NS) (p less than 0.05 vs. basal RS). RRC was similar in both groups: 2.17 +/- 0.62 (CT) vs 2.05 +/- 0.49 micrograms ANG I/mg protein/h (NS), p greater than 0.05. Angiotensinogen release from LS increased in nephrotic rats from 10 +/- 3.2 (CT) to 12 +/- 1.9 pmoles angiotensinogen I/mg tissue/2h (NS), p less than 0.05. Aldosterone release increased markedly from adrenal glands of rats with NS (1649 +/- 1111 pg aldosterone/mg tissue/h) with respect to control rats (257 +/- 85), p less than 0.05 In vitro studies were performed six days after PA-injection, when nephrotic rats had ascitis, edema, proteinuria, hypoproteinemia, hypercholesterolemia, hypertriglyceridemia, low sodium and aldosterone excretion, low levels of plasma angiotensinogen and high levels of plasma renin and aldosterone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pathophysiology of experimental nephrotic syndrome induced by puromycin aminonucleoside in rats. II. In vitro release of renin, angiotensinogen and aldosterone. 226 44

The effect of the converting enzyme inhibitor (CEI) (captopril, 50 mg/kg/day) on proteinuria (UProt), urinary aldosterone (UAldoV), plasma renin activity (PRA), plasma renin concentration (PRC), plasma angiotensinogen concentration (PAC), urinary sodium (UNaV), serum total protein, and body weight was studied for 21 days in an experimental nephrotic syndrome (NS) model induced in rats by a single injection (15 mg/100g) of puromycin aminonucleoside (PA). The effect of captopril on control rats without NS was also characterized. In control rats, captopril increased PRC and PRA, and decreased PAC; it had no effect on UNaV, UAldoV, UProt, total serum protein and body weight. In rats with NS, captopril had no effect on sodium retention, hypoproteinemia, and UProt; it abolished the increased UaldoV and favored weight loss. Captopril also rose PRA and PRC, and decreased PAC in PA-nephrotic rats; these changes were similar to those produced by captopril in control rats. The mortality rate was higher in nephrotic rats treated with captopril (37%) than in untreated nephrotic rats (13%). It is concluded that captopril has no beneficial effects on the course on NS induced by PA during the first 21 days, and supports the contention that sodium retention is not related to the renin-angiotensin-aldosterone system activity in these rats.
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PMID:Pathophysiology of experimental nephrotic syndrome induced by puromicyn aminonucleoside in rats. III. Effect of captopril, an angiotensin converting enzyme inhibitor, on proteinuria and sodium retention. 227 Mar 68

Recombinant human erythropoietin (r-HuEPO) therapy for anemia in chronic renal failure patients could have unfavorable renal effects since reversal of anemia can raise blood pressure and accelerate experimental glomerular injury. Thus, the effects of r-HuEPO on renal and systemic hemodynamics and the progression of renal disease were studied in predialysis chronic renal failure patients. The clearances of inulin and p-aminohippurate, fractional excretions of albumin and immunoglobulin G, cardiac output, plasma renin activity and aldosterone concentration were assessed at baseline, after short-term r-HuEPO (n = 4) or placebo (n = 4) therapy, and after long-term r-HuEPO for all patients (n = 8). In addition, the slope of l/serum creatinine with time was determined before and during continued r-HuEPO therapy. In contrast to placebo therapy, hematocrit increased with r-HuEPO from 32 to 37% after 7.6 +/- 2.7 weeks (mean +/- SD). Antihypertensive drug therapy was increased in 2 patients in each group. Renal function, cardiac output, plasma renin activity and aldosterone did not change significantly in either group. After 18 +/- 9 weeks of therapy for all patients, hematocrit increased from 31 to 39%. Antihypertensive drug therapy was increased in 5 patients and decreased in 1. Renal function decreased while proteinuria tended to increase. Cardiac output, plasma renin activity and aldosterone did not change. During 37 +/- 22 weeks of r-HuEPO therapy, the slope of l/serum creatinine did not worsen in any patient.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal function during erythropoietin therapy for anemia in predialysis chronic renal failure patients. 234 56

This study was undertaken to investigate the role played by renal functional and structural changes in the development of radiation-induced hypertension. Four groups of rats were studied: 1) left kidney radiated, 2) sham procedure, 3) uninephrectomy followed 3 weeks later by radiation of the contralateral kidney, and 4) uninephrectomy followed by sham procedure 3 weeks later. All radiated rats became hypertensive at 12 weeks (p less than 0.05) and had higher protein excretion (p less than 0.05). In the presence of an intact contralateral kidney, radiation causes mild-to-moderate histological abnormalities, and therefore, creatinine clearance and water and sodium handling do not change. Plasma renin activity increased in this group (p less than 0.05). Radiated uninephrectomized rats showed decreased creatinine clearance (p less than 0.05), but renin activity remained unchanged. These rats developed severe histological abnormalities in glomeruli, interstitia, tubuli, and vessels resulting in increased sodium and water output. The average of individual tubular and interstitial scores correlated significantly with both water intake and output but not with sodium excretion. These studies suggest that in the presence of an intact kidney, renin is an important determinant in the development or maintenance of radiation hypertension, whereas in the absence of the contralateral kidney, severe histological changes and renal failure are prominent despite increased water intake and output. The more severe glomerular sclerosis and proteinuria in the latter model could be related to diminished renal mass.
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PMID:Mechanisms of hypertension in renal radiation. 240 56

The glomerular size-selective properties in a patient with "hyponatremic hypertensive syndrome" were investigated before and after administration of the angiotensin-converting enzyme inhibitor enalapril. Hyponatremic hypertensive syndrome is a rare condition of renovascular hypertension characterized by electrolyte abnormalities (hyponatremia, hypokalemia), polyuria, and high renin activity. In this patient a marked increase in urinary protein excretion was observed. Treatment with enalapril normalized BP, corrected electrolyte abnormalities, and reduced proteinuria. Glomerular filtration rate (GFR), renal plasma flow (RPF), and the clearance of neutral dextrans of graded sizes were measured before and after 6 months of enalapril (20 mg/d) administration. Theoretical analysis of dextran and inulin clearance data with a model of glomerular size selectivity were adopted to separate effects of hemodynamic changes on macromolecule filtration from changes of intrinsic membrane selective properties. After enalapril urinary protein excretion decreased, GFR was unchanged and RPF almost doubled. Fractional clearance values of dextran molecules were markedly elevated in comparison with the corresponding values measured in a group of normal controls and were normalized by enalapril. Theoretical calculation of membrane pore characteristics showed that enalapril treatment reduced the radius of all membrane pores by approximately 1 nm. Altogether these results indicate that enalapril normalized glomerular filtration of neutral macromolecules and circulating proteins in a human condition of angiotensin II-induced proteinuria. Enalapril effectively restored glomerular size-selective function, reducing dimensions of membrane pores, independently of its effect on renal hemodynamics.
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PMID:Angiotensin-converting enzyme inhibition ameliorates the defect in glomerular size selectivity in hyponatremic hypertensive syndrome. 247 29

We compared the effect of nicardipine, a dihydropiridine derivative calcium entry blocker (CEB), with that of captopril (CAP), a converting-enzyme inhibitor (CEI), and that of the two drugs combined, on blood pressure (BP), heart rate (HR), and renal function in 12 hypertensive type II diabetic outpatients with nephropathy (persistent proteinuria greater than 500 mg/24 h) according to a 2 x 2 factorial design. For 4-week treatments, the patients received nicardipine (NIC) 20 mg t.i.d., CAP 50 mg b.i.d., NIC plus CAP, and matched placebo. Each active treatment significantly reduced BP, with an additive effect of NIC and CAP combined versus either drug alone. HR did not change. Effective renal plasma flow (RPF) and glomerular filtration rate (GRF) were unmodified, but renal vascular resistances (RVRs) were significantly reduced by the three active treatments. Filtration fraction (FF) did not change with NIC or with NIC plus CAP and was significantly reduced with CAP. Urinary albumin excretion (UAE) was significantly reduced by each active treatment to a similar extent. Plasma renin activity (PRA) increased significantly with NIC plus CAP only and did not change when the drugs were administered singly. Plasma aldosterone, glucose, potassium, fructosamine, and urinary sodium and volume did not change during the trial. We conclude that the two drugs singly and combined are useful for treatment of hypertensive non-insulin-dependent diabetes (NIDD) patients with persistent proteinuria.
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PMID:Hemodynamic, renal, and humoral effects of the calcium entry blocker nicardipine and converting enzyme inhibitor captopril in hypertensive type II diabetic patients with nephropathy. 248 72


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