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)

Chronic renal insufficiency is a progressive, self-perpetuating process which is influenced in part by activation of the intrarenal renin-angiotensin system. Oral angiotensin-converting enzyme inhibitors are being studied in animals and humans to determine whether they slow the decline in renal function characteristic of progressive renal disease. In animals that have reduced renal mass, streptozotocin-induced diabetes mellitus, or puromycin aminonucleoside nephrosis, these agents can reduce proteinuria, decrease the frequency of sclerotic glomeruli, and normalize intrarenal hemodynamics. They also may decrease glomerular hypertrophy that occurs after renal ablation. In human trials, angiotensin-converting enzyme inhibitors decrease proteinuria by altering the glomerular capillary permeability. The effect of these agents on progressive disease may be influenced by how soon therapy is begun and how long it is continued.
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PMID:Use of angiotensin-converting enzyme inhibitors in chronic progressive renal disease. 202 23

Puromycin aminonucleoside (PA)-nephrotic rats have a high plasma renin activity (PRA) and low angiotensinogen levels. We measured proteinuria, urine renin, and urine angiotensinogen daily, for 11 days after PA injection. Proteinuria and urine angiotensinogen were evident on day 5, and urine renin on day 6. Peak levels of urine renin and angiotensinogen were attained on day 8. These data suggest that angiotensinogen urine excretion may contribute to its low plasma levels, and urine renin loss may limit a further increase in PRA.
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PMID:Urinary excretion of renin and angiotensinogen in nephrotic rats. 204 2

Fifty women with pyelonephritic renal scarring were prospectively followed for five years and the changes in renal function were related to blood pressure control, plasma renin activity, urinary albumin excretion and the incidence of urinary tract infections (UTI). Five patients (10%) developed end stage renal disease. All these patients had bilateral disease, proteinuria and anti-hypertensive treatment at presentation. The mean +/- SD glomerular filtration rate (GFR) of all patients with renal scarring was 74 +/- 27 ml/min x 1.73 m2 at presentation which was significantly lower than the GFR in 55 patients with a recent episode of acute pyelonephritis (p less than 0.001) and 10 healthy controls (p less than 0.001). GFR and age corrected GFR decreased significantly during follow-up (p less than 0.001) and p less than 0.02 respectively). The decrease in GFR was significantly higher in patients with bilateral scarring, in patients on blood pressure treatment and in patients with an episode of symptomatic UTI during follow-up. Eight patients (16%) had antihypertensive treatment at presentation and another 11 patients (26%), of whom 10 had bilateral scarring, developed hypertension (greater than 140/90 mmHg) during follow-up. Seventy-five per cent of all patients had symptomatic UTI and 40% had an episode of acute pyelonephritis during follow-up. In conclusion, patients with pyelonephritic scarring have a high incidence of UTI and are at high risk of developing renal failure and hypertension. It is essential that recurrent episodes of symptomatic UTI are treated promptly and that blood pressure is monitored carefully in these patients.
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PMID:A five-year prospective follow-up of women with non-obstructive pyelonephritic renal scarring. 204 74

Transient hyperkalemia has been reported to occur in patients with acute glomerulonephritis, but the pathogenetic mechanism has not been investigated systematically. We studied the mechanism of hyperkalemia (5.7 to 6.7 mmol/liter) in four men with post-infectious glomerulonephritis. All four patients had clinical findings consistent with acute glomerulonephritis (edema, hypertension, proteinuria, hematuria, and an elevated ASO titer) and a renal biopsy performed in three of the patients confirmed the diagnosis. In comparison to normal subjects (N = 18), plasma aldosterone (5.4 +/- 1.6 vs. 22.8 +/- 2.6 ng/dl, P less than 0.005) and plasma renin activity (0.3 +/- 0.2 vs. 4.3 +/- 0.6 ng/ml/hr, P less than 0.005) were reduced. Hyperkalemia resolved within one to two weeks in two patients as the nephritis resolved and diuresis ensued, and aldosterone and renin levels obtained at follow-up visits were normal. Hyperkalemia persisted despite furosemide-induced diuresis in the other two patients, but resolved with fludrocortisone treatment. Thus, hyperkalemia in patients with acute glomerulonephritis is a manifestation, in part, of hyporeninemic hypoaldosteronism. It is ameliorated by mineralocorticoid therapy and improves spontaneously with resolution of the glomerulonephritis.
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PMID:Hyperkalemia in acute glomerulonephritis due to transient hyporeninemic hypoaldosteronism. 207 57

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

In contrast to some other antihypertensive drugs, angiotensin-converting enzyme (ACE) inhibitors lower glomerular capillary pressure, decrease proteinuria, and may halt progressive glomerular injury and loss of renal function in experimental chronic renal failure (CRF). Although these favourable effects of ACE inhibition may result from alterations in glomerular haemodynamics, there is some evidence to show that ACE inhibitors may reduce glomerular injury through other mechanisms. CRF in man may result from a variety of insults to the kidney. However, it is not known whether, or under which conditions, glomerular capillary pressure is elevated in this heterogeneous population. Limited data suggest that renal haemodynamics (and perhaps glomerular capillary pressure) may depend in part on the level of systemic blood pressure. In addition, several studies have demonstrated a positive correlation between systemic blood pressure and the rate of progression of CRF. ACE inhibitor therapy generally lowers systemic blood pressure, does not alter renal function and decreases proteinuria in patients with CRF. The reduction in proteinuria appears to be variable and may depend on pretreatment glomerular haemodynamics and/or the activity of the renin-angiotensin-aldosterone system. Preliminary evidence also suggests that ACE inhibitors may slow the progression of renal disease in humans with CRF. However, this effect, like the reduction in proteinuria, has not been observed consistently in all patients. In addition, it is not clear whether these effects on proteinuria and progression of disease are unique to ACE inhibitor therapy, since the lowering of systemic blood pressure with other drugs may have similar effects. The heterogeneity of the response to ACE inhibition suggests that there may be interpatient differences in glomerular haemodynamics in CRF, perhaps related to systemic blood pressure or the underlying disease process. Studies to date indicate that ACE inhibitors exert their beneficial effect by lowering glomerular capillary pressure and that not all patients will benefit from therapy with regard to proteinuria or amelioration of disease progression. However, further investigation of the haemodynamic and non-haemodynamic effects of ACE inhibitors, as well as the variability of response, may ultimately allow the selection of those patients who would benefit from such therapy.
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PMID:Angiotensin-converting enzyme inhibitors in chronic renal failure. 218 23

Spontaneously hypertensive rats (SHR) were uninephrectomized (UNX) at 6 wk of age and given either standard chow (CON), low-sodium chow (LSC), or standard chow and hydrochlorothiazide (HCTZ) added to the drinking water. Severe hypertension developed in all three groups. Forty-two weeks after UNX, proteinuria and glomerular sclerosis were significantly lower in LSC than in CON or HCTZ. The protective effect of salt restriction did not depend upon alterations in plasma renin concentration or glomerular hemodynamics. Micropuncture revealed that glomerular pressure was high in all three groups. Renal hypertrophy assessed by kidney weight, kidney-to-body weight ratio, glomerular volume, and glomerular capillary radius were reduced by salt restriction. These findings suggest that, in the setting of glomerular hypertension, hypertrophy promotes sclerosis. Salt restriction inhibits compensatory kidney growth and protects the kidney.
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PMID:Superiority of salt restriction over diuretics in reducing renal hypertrophy and injury in uninephrectomized SHR. 219 43

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

The effects of dietary protein intake on the progression of renal insufficiency were studied in daunomycin (DMC) induced nephrotic rats (DMC rats) and also patients with chronic renal diseases. In the first study, the author examined which treatment among enalapril (E) and indomethacin (I) and dietary protein restriction was the most effective to prevent proteinuria and glomerulosclerosis, and then the effect of dietary protein restriction on renal content of malondialdehyde (MDA) and superoxide dismutase (SOD) in DMC rats. These rats were divided into four groups as follows: group PL and group PH were isocaloric diets containing either 5% or 24% protein, respectively and group PE and PI were given orally E (100 mg/l drinking water) or I (50 mg/l drinking water) with diets of 24% protein, respectively. In group PL, urinary protein excretion (U-Protein) rates and renal damage index were significantly lower than those in other three groups. In group PE, renal damage index was significantly improved although U-Protein showed no reduction in contrast with these in group PH. Renal MDA in group PL was lower than that in group PH was significantly lower than that in group PL. In this study dietary protein restriction was the most effective treatment for the prevention of progressive renal insufficiency. In the second study, patients with chronic renal diseases were divided into two groups according to their Ccr: group I; Ccr greater than or equal to 60 ml/min, group II; Ccr less than 60 ml/min. All patients orally received diets of high protein (1.4 g/kgBW) and subsequently of low protein (0.7 g/kgBW). Ccr, U-Protein, serum MDA and serum SOD were estimated at the end of each dietary period. In group I, Ccr was significantly lower on low protein diet than that on high protein diet, although these were no significant changes in Ccr in group II. The low protein diet caused a significant decrease in U-Protein in both groups. Serum MDA in group I was significantly lower on low protein diet than that on high protein diet, but not in group II. Serum SOD activity showed no changes. It is suggested that dietary protein restriction might reduce oxidant stress to the kidney, in addition to renal hemodynamic changes induced by prostaglandin and renin-angiotensin system, resulting in the prevent of progress of renal insufficiency.
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PMID:[Study on the pathogenetic factors of the progression of renal insufficiency, with special reference to the effects of dietary protein intake]. 221 17


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