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 purpose of the present study was to examine renal functional changes caused by chronic blockade of nitric oxide (NO) synthesis in young rats. Two types of NO synthase inhibitor were used: NG-nitro-L-arginine methyl ester (L-NAME) as a non-selective inhibitor and aminoguanidine (AG) as a selective inhibitor of the inducible isoform. Oral administration of L-NAME (20-80 mg/dL of drinking water), not AG (400 mg/dL), for 4 weeks induced systemic hypertension in the treated rats. Both inhibitors caused a significant reduction in urinary excretion of NO2-/NO3-. Rats treated with L-NAME developed proteinuria and tubular enzymuria (high excretion of N-acetyl-beta-D-glucosaminidase) in a dose-dependent fashion, with normal serum levels of creatinine, albumin and cholesterol. Chronic AG administration did not alter the urinary levels of protein and N-acetyl-beta-D-glucosaminidase or serum laboratory values. Overall, these observations highlight the importance of the continuous generation of NO by the constitutive isoform in the control of vascular tone and the maintenance of renal glomerular and tubular function. Oral administration of L-NAME may serve as a model of chronic NO-deficient hypertension with renal injury in young rats.
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PMID:Renal functional measurements in young rats with chronic inhibition of nitric oxide synthase. 900 96

1. The protective effect of ME3221, a surmountable AT1 antagonist, on the hypertension and its concomitant complications in aged (32 week old) stroke-prone spontaneously hypertensive rats (SHRSP) was studied following long-term (32 weeks) oral administration, and compared with those of losartan (metabolite EXP3174 is an insurmountable AT1 antagonist) and enalapril. 2. During the treatment period, ME3221, at a dose of 10 mg/kg per day steadily reduced the systolic blood pressure, and no tolerance was developed to the fall in blood pressure. The reference drugs showed similar activity, but the antihypertensive effect of ME3221 was more potent. 3. In the control group, rats began to die from 52 weeks of age and all rats had died by 64 weeks of age. In contrast, no rats treated with ME3221, losartan or enalapril died before 64 weeks of age. 4. ME3221, losartan and enalapril suppressed the hypertensive complications observed in control SHRSP, that is, cerebral apoplexy (stroke and cerebral oedema), renal injury (increased proteinuria, total N-acetyl-beta-D-glucosaminidase activity and ascites) and heart failure (cardiac hypertrophy and pleural effusion). 5. These results indicate that ME3221 has a stable anti-hypertensive effect, prevents hypertensive complications and prolongs survival in aged SHRSP equally as well as losartan and enalapril.
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PMID:Effect of chronic treatment with ME3221 on blood pressure and mortality in aged stroke-prone spontaneously hypertensive rats. 907 29

Taurine was used in the present study to evaluate its beneficial effects against proteinuria and hyperlipidemia associated with nephrotic syndrome. Rats made nephrotic with adriamycin had a high excretion of protein, albumin, and N-acetyl-beta-D-glucosaminidase compared with nonnephrotic rats. Nephrotic rats manifested hyperlipidemia with significant elevation in all major lipoprotein fractions. Treatment with taurine significantly suppressed adriamycin-induced proteinuria, albuminuria, and urinary excretion of N-acetyl-beta-D-glucosaminidase. Treatment of rats wit taurine for 7 days before adriamycin, and daily thereafter, significantly lowered plasma cholesterol, triglycerides, phospholipids, lipid peroxides, and malondialdehyde associated with lipoprotein fractions. Similarly, total lipids, cholesterol, triglycerides, lipid peroxides, hydroperoxides, and hydroxyl radicals in the liver and kidneys of taurine-treated adriamycin rats were decreased significantly compared with adriamycin alone. Lecithin cholesterol acyl transferase activity and free fatty acid levels in plasma, lipoprotein lipase activity, glutathione, total thiol, and ascorbic acid in the liver and the kidneys of taurine-treated adriamycin groups were significantly elevated compared with adriamycin alone. These results suggest that taurine might be applicable as a protective agent for proteinuria and hyperlipidemia associated with nephrotic syndrome.
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PMID:Protection by taurine against adriamycin-induced proteinuria and hyperlipidemia in rats. 918 3

We studied 23 children with steroid-sensitive nephrotic syndrome (SSNS), 21 children with steroid-resistant types of nephrotic syndrome and 32 children with other types of nephritis. Our controls were 43 apparently healthy children. We measured the urinary excretion of N-acetyl-beta-D-glucosaminidase (NAG) and the low molecular weight (LMW) protein beta 2-microglobulin (B2M), retinol-binding protein (RBP), alpha 1-microglobulin (A1M) and urine protein 1 (UP1). Results for B2M were considered only for a urine pH greater than 6.0. Comparisons were made with urine albumin excretion, glomerular filtration rate (GFR) and tubular abnormalities in selected renal biopsy samples. We found that abnormalities of LMW protein excretion occurred in between 50% (B2M) and 88% (UP1) of all subjects. In children with SSNS, A1M (r = 0.73), UP1 (r = 0.65) and NAG (r = 0.54) excretion were significantly correlated with albumin excretion, but not RBP or B2M excretion. Increased fractional excretion of A1M, B2M and UP1 and increased plasma A1M were demonstrated in 9 children with SSNS, suggesting competition for tubular reabsorption with albumin, most marked for UP1. In the steroid-resistant nephrotic and nephritic syndromes, correlation with albumin was found for all proteins. In these subjects, RBP (r = 0.37), B2M (r = 0.42) and A1M (r = 0.28) were inversely correlated with GFR, but not UP1, NAG or albumin. We found that RBP excretion was significantly greater in the presence of severe tubular abnormalities in 11 children with recent renal biopsies, but not A1M, UP1 or NAG. We conclude that LMW proteinuria is common in children with glomerular disease, and does not necessarily imply a poor prognosis. Factors other than histologically proven tubular abnormality may account for elevated LMW protein excretion. RBP is the LMW protein most closely associated with structural abnormality and least affected by increasing albuminuria.
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PMID:Low molecular weight protein excretion in glomerular disease: a comparative analysis. 920 74

Renal lesions have repeatedly been described in Wilson's disease (WD). We investigated the excretion of total protein, albumin, low (LMW) and high molecular weight (HMW) proteins, N-acetyl-beta-D-glucosaminidase (NAG), and calcium, as well as creatinine clearance, in 24-h urine samples of 41 patients with WD aged 6-37 (mean 17) years who had been treated for a period of 0-15 (mean 4.5) years with D-penicillamine (900 mg/day). The amount of all protein excreted was significantly increased compared with controls, 39% of patients presenting with total proteinuria more than two standard deviations from the mean of controls. The changes in protein excretion depended on the duration of treatment. LMW proteinuria was elevated almost exclusively in the first 2 years after the start of treatment, indicating early tubular damage. This is supported by an initially high excretion of beta 2-microglobulin, NAG, and calcium. Increased excretion of HMW proteins, including albumin, persisted over longer periods, which suggests glomerular injury in some patients, possibly related to the use of D-penicillamine. Creatinine clearance remained roughly within normal limits. We propose that renal function should regularly be checked in patients with WD.
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PMID:Proteinuria and other renal functions in Wilson's disease. 920 78

Post-exercise proteinuria is a common phenomenon in healthy subjects. Previous studies have used albumin (Alb) and beta 2-microglobulin (beta 2-m) molecules as representatives of high- and low-molecular-weight proteins. Recently, more specific markers of the human kidney proximal tubule have been used to identify the precise site of alterations. Active male subjects underwent two strenuous runs, one 400-m run and one 3000-m run. Urine was collected from the subjects before and after each event. Total protein (TP), Alb, alpha 1-microglobulin (alpha 1-m), beta 2-m, intestinal alkaline phosphatase (IAP), tissue-nonspecific alkaline phosphatase (TNAP) and N-acetyl-beta-D-glucosaminidase (NAG) were determined for each sample. The short-distance run (400 m) resulted in the largest increases (P < or = 0.05) in TP (31-fold), Alb (100-fold) and beta 2-m (164-fold) as compared to the long-distance run (3000-m). The alpha 1-m excretion rates were increased to a lesser extent by the exercises. The IAP activity was slightly increased (+90%) by the 400-m run while the TNAP and NAG activities showed a 6.8-fold and a 3.6-fold increase, respectively, after this event. Smaller increases were recorded for the long-distance run (P = 0.05). To conclude, the present investigation showed that: (1) post-exercise proteinuria is related to the absolute intensity of exercise; (2) the impairment of protein reabsorption is revealed better by changes in Alb and beta 2-m; (3) changes in TNAP and NAG activities could reveal biochemical modifications that occur in the proximal tubule, particularly at the S1-S2 segment.
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PMID:Evidence of differential renal dysfunctions during exercise in men. 924 75

Nephrotoxicity of free hemoglobin (Hb) based blood substitutes still awaits full elucidation. Previous reports attributed Hb passage through the renal glomeruli to a tendency of the Hb tetramer to dissociate into dimers. Now it has become more evident that the Hb tetramer is able to extravasate. It appears that the electrical charge of proteins plays an important role, with electronegativity and a low isoelectric point favoring intravascular persistence. This effect was utilized in the development of an improved blood substitute, comprising Hb reacted with o-ATP and o-adenosine, to form an intra- and intermolecularly cross linked product, which is reduced with glutathione. The modification reagents possess the desired pharmacologic activities and produce an increase in the electronegative charges on the Hb surface. All Hb polymers and chemically modified tetramers present in this solution have a uniform electronegative charge, with a pl of 6.1-6.2. In this present study, unmodified bovine Hb and an improved blood substitute were used for the replacement of 40% of the total blood volume in rats. The nephrotoxic effect was investigated by the determination of urinary output, glomerular filtration rate (GFR), fractional excretion of sodium (FENa), potassium (FEK), and chloride (FECl), urine/plasma osmolality ratio, and urine N-acetyl-beta-D-glucosaminidase (NAG) level. The free Hb and non heme protein contents in the urine were analyzed by using isoelectric focusing and size exclusion liquid chromatography methods. The results indicate that unmodified Hb is nephrotoxic. An initially elevated urinary output was followed by a significant oliguria associated with decreased GFR, FEK, and FECl and elevated FENa and NAG. Severe hemoglobinuria was associated with proteinuria. Analysis of urine from unmodified Hb treated rats revealed the presence of Hb tetramers. Histopathological examination of the kidneys showed cytoplasmic vacuolization of proximal tubular epithelium. On the contrary, an improved blood substitute did not produce any nephrotoxic reactions. It was found that this Hb solution did not pass through the renal glomerular barrier and was not present in urine samples. In conclusion, such a chemical and pharmacological alteration of Hb molecules reduced their interaction with renal glomeruli and suspended nephrotoxicity.
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PMID:An improved blood substitute. In vivo evaluation of its renal effects. 936 Jan 40

Proteinuria is one of the bad prognostic indices in renal disease. This study compares the pattern of protein excretion in 10 patients with IgA nephropathy (IgAN), 10 patients with chronic glomerulonephritis approaching end-stage renal failure (ESRF) who still had proteinuria and 10 other patients with diabetic nephropathy (DN) with proteinuria but normal renal function. The pattern of proteinuria was analysed by sodium dodecyl sulphate polyacrylamide gel electrophoresis (SDS-PAGE), isoelectric focusing (IEF) and assayed for orosomucoid, alpha-1-microglobulin, retinol-binding protein, lysozyme, beta-2-microglobulin and N-acetyl-beta-D-glucosaminidase activity. Our data showed much similarity in the pattern of proteinuria between the DN and ESRF groups but significant differences with the IgAN group. The pattern of proteinuria in the IgAN group reflects glomerulonephritis whereas the similar pattern between the ESRF and DN groups may reflect hyperfiltration as well as tubular injury.
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PMID:Pattern of proteinuria in tubular injury and glomerular hyperfiltration. 939 12

In order to investigate the effect of triathlon and renal function of normal subjects, we evaluated the excretion of urinary enzymes and proteins before and after triathlon. From 6 subjects samples were obtained 24 hours after the first urine collection. We performed quantification of urinary total protein, beta2-microglobulin (beta2-M), N-acetyl-beta-D-glucosaminidase activity (NAG), and concentration of urinary creatinine from each participant. There was a significant increase in urinary total protein excretion immediately after triathlon (p<0.01). The urinary beta2-M and NAG excretions after triathlon were higher than the initial values. Post-exercise proteinuria in one subject persisted until the next morning, whereas the increased excretion of urinary beta2-M and NAG returned to the pre-exercise level at least 24 hours after triathlon. It appears to be reasonable to presume that glomerular damage may persist in some subjects who do heavy exercise.
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PMID:The effect of triathlon on urinary excretion of enzymes and proteins. 960 77

Markers of renal tubular injury are difficult to interpret in patients with proteinura. The 24-hour urinary N-acetyl-beta-D-glucosaminidase (NAG) concentration was measured in 167 patients with dissimilar renal disease, function, and proteinuria. NAG isoenzymes were also separated in 69 patients, using a modified fast protein liquid chromatography technique. The 'A2' isoenzyme predominated at all levels of renal function and in all diagnostic groups. Urinary NAG and proteinuria were well correlated at all levels of renal function, as was NAG 'A2' isoenzyme. Proteinuria and urinary NAG were similarly correlated in patients with different glomerulonephritides, hypertensive nephrosclerosis, and chronic pyelonephritis, but not in those with diabetic nephropathy.
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PMID:Proteinuria and renal tubular damage: urinary N-acetyl-beta-D-glucosaminidase and isoenzymes in dissimilar renal disease. 962 32


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