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)

N-acetyl-beta-D-glucosaminidase (NAG) urine activities of 63 patients with stable and unstable chronic renal failure have been investigated. The values of NAG activity obtained from these patients were compared with NAG activity of 33 normal controls. Abnormal NAG values (> 70 nmol/mg of creatinine) were found in 60 (95.2%) patients with chronic renal failure and the median of all values was 327.8 nmol/mg of creatinine. It was 14-fold greater than the median of values for normal controls. There were any significant differences of NAG values between the patients with massive proteinuria (> 1.5 g/24 h), moderate proteinuria and those without 24 hour proteinuria or non-significant proteinuria (respectively 423.5 +/- 286.3 vs 414.4 +/- 334.8 vs 453.0 +/- 451.3 nmol/mg of creatinine). There was no significant difference between the two subgroups of patients with NAG values above and below 280 nmol/mg of creatinine in age, gender, serum urea and uric acid levels. However, the incidence of patients with NAG values higher than 280 nmol/mg of creatinine was statistically significant in unstable course of renal insufficiency and raised serum creatinine levels. It is suggested that the measurement of NAG excretion may be helpful to monitor unstable process in renal failure.
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PMID:[Renal proximal disfunction based on activity of n-acetyl-beta-d-glucosaminidase in urine of patients with kidney failure]. 964 82

1. Progression to renal failure may be linked to the degree of proteinuria through tubulo-interstitial mechanisms. However, there are no data in man on the kinetics of proximal renal tubular protein catabolism or markers of tubular injury before and after lisinopril. We developed a method to allow such studies, and found increased tubular catabolism of 99mTc-labelled aprotinin (Trasylol) in patients with nephrotic range proteinuria which was associated with increased ammonia excretion. 2. In this study, 10 patients with mild renal impairment (51Cr-EDTA clearance 63.7 +/- 8.3 ml.min-1.1.73 m-2) and heavy proteinuria (8.2 +/- 2.3 g/ 24 h) were given lisinopril (10-20 mg) for 6 weeks. Renal tubular catabolism of intravenous aprotinin was measured before and after lisinopril by renal imaging and urinary excretion of the free radiolabel over 26 h. Fractional degradation was calculated from these data. Fresh timed urine collections were also analysed for ammonia excretion every fortnight from 6 weeks before treatment. Total urinary N-acetyl-beta-D-glucosaminidase and the more tubulo-specific N-acetyl-beta-D-glucosaminidase 'A2' isoenzyme were also measured. 3. After lisinopril proteinuria fell significantly as expected (from 9.5 +/- 1.6 to 4.5 +/- 1.0 g/24 h, P < 0.01). This was associated with a reduction in metabolism over 26 h (from 1.7 +/- 0.1 to 1.2 +/- 0.1% dose/h, P < 0.01) and in fractional degradation of aprotinin (from 0.08 +/- 0.02 to 0.04 +/- 0.007/h, P < 0.04). Ammonia excretion also fell significantly (from 1.2 +/- 0.1 to 0.6 +/- 0.1 mmol/h, P < 0.0001), as did both total urinary N-acetyl-beta-D-glucosaminidase (P < 0.0001) and the N-acetyl-beta-D-glucosaminidase 'A2' isoenzyme (P < 0.015). These observations after lisinopril treatment have not been described previously. There was no significant change in blood pressure nor in glomerular haemodynamics.
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PMID:Proximal renal tubular peptide catabolism, ammonia excretion and tubular injury in patients with proteinuria: before and after lisinopril. 964 Mar 48

The predictive value of tubular proteinuria and/or enzyme excretion for the development of microalbuminuria in patients with diabetes mellitus was investigated over a period of 7.5 years in 64 children and adolescents without microalbuminuria at baseline. An abnormal urinary excretion of N-acetyl-beta-D-glucosaminidase (NAG) preceded the increase of albumin excretion in all 8 patients (12.5%) developing microalbuminuria during this period (positive/negative predictive value 0.2 and 1.0, respectively). Also both, the actual as well as the long-term glycemic control (HbAlc) up to the onset of abnormal NAG excretion were predictive for the development of microalbuminuria. Fifty percent of those patients with both an elevated NAG excretion and an HbAlc > or = 9% developed micro-albuminuria within the next 5 years. Therefore, periodic monitoring of urinary NAG excretion should be incorporated into the follow-up of patients with type 1 diabetes mellitus.
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PMID:Predictive value of tubular markers for the development of microalbuminuria in adolescents with diabetes. 967 93

Rosiglitazone (BRL 49653), a peroxisome proliferator-activated receptor-gamma (PPAR-gamma) agonist and potent insulin action-enhancing agent, was given in the diet (50 micromol/kg of diet) to male Zucker rats ages 6-7 weeks for 9 months (prevention group). In this treatment mode, rosiglitazone prolonged the time to onset of proteinuria from 3 to 6 months and markedly reduced the rate of its subsequent progression. Progression was also retarded when treatment was commenced (intervention group) after proteinuria had become established (4 months; ages 24-25 weeks). In either treatment mode, rosiglitazone normalized urinary N-acetyl-beta-D-glucosaminidase activity, a marker for renal proximal tubular damage, and ameliorated the rise in systolic blood pressure that occurred coincidentally with the development of proteinuria in Zucker fatty control rats. The renal protective action of rosiglitazone was verified morphologically. Thus in the prevention group there was an absence of the various indexes of chronic nephropathy that were prominent in the Zucker fatty control group, namely, glomerulosclerosis, dilated tubules containing proteinaceous casts, a loss of functional microvilli on the tubular epithelium, and varying degrees of chronic interstitial nephritis. An intermediate pathology was observed in the intervention group. Also, pancreatic islet hyperplasia, ultrastructural evidence of beta-cell work hypertrophy, and derangement of alpha-cell distribution within the islet were prominent features of Zucker fatty control rats, but these adaptive changes were ameliorated (intervention group) or prevented (prevention group) by rosiglitazone treatment. These data demonstrate that treatment of Zucker fatty rats with rosiglitazone produced substantial protection over a prolonged period against the development and progression of renal injury and the adaptive changes to pancreatic islet morphology caused by sustained hyperinsulinemia.
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PMID:Peroxisome proliferator-activated receptor-gamma agonist, rosiglitazone, protects against nephropathy and pancreatic islet abnormalities in Zucker fatty rats. 970 35

Photodynamic therapy (PDT) is now being used more frequently in carefully selected cases of malignancies. The drugs used for PDT are mostly derivatives of haematoporphyrine (HPD) and its active component photofrine II. Another compound prepared by total synthesis is meso-tetra-(4-sulfonatophenyl)-porphine (TPPS4) but its application in human medicine was rejected because of its neurotoxicity. Our TPPS4 was prepared by the method of Busby et al. in the modification of Jirsa and Kakac (1987). This product is purer and without neurotoxic effects. In this study, we concentrated our attention on the effect of TPPS4 on nephrotoxicity and its accumulation in some organs. As the parameters of toxic kidney damage we used urine levels of N-acetyl-beta-D-glucosaminidase (NAG), serum creatinine levels, glomerular filtration rate (GFR) and proteinuria. TPPS4 was administered i.v. in a dose of 25 mg/kg b.w. The animals were observed for 21 days after drug application. Urine and blood samples were collected over 24-hour periods on days 0, 5 and 21. The serum creatinine level was significantly higher only on day 5 (65.0+/-1.46 micromol/l vs 56.5+/-2.69 micromol/l on day 0, p<0.05). There were no significant changes in GFR, proteinuria or NAG activity in the urine during the experiment. AST serum activity was increased. We determined the concentration of TPPS4 (pmol/mg w.w.) in rat organs on the 21st day after the injection. The concentration of TPPS4 was high in kidneys (30.8+/-5.5), liver (13.5+/-2.0), lungs (11.7+/-4.6) and spleen (9.7+/-1.5), while the concentration in heart and brain was low. We conclude that TPPS4 has the highest concentration in the kidney 21 days after its administration and does not exert any nephrotoxic effects during this period.
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PMID:The localisation of TPPS4 in some organs and its possible nephrotoxicity in rats. 972 80

The Otsuka Long-Evans Tokushima Fatty (OLETF) rat is a new genetic model of non-insulin-dependent diabetes mellitus (NIDDM). We investigated whether treatment with an angiotensin II (ANGII) subtype-1 receptor antagonist delays the onset of NIDDM and attenuates diabetic nephropathy in the OLETF rat. OLETF rats fed a regular chow were treated with ANGII subtype-1 receptor antagonists (E4177 or TA606) for 22 weeks. Hemodynamic changes, glucose metabolism, and the effects on diabetic nephropathy were examined. Systolic blood pressure increased in OLETF rats in an age-dependent manner. OLETF rats exhibited increases in plasma concentrations of glucose and insulin and developed glucosuria at the age of 28 weeks. The changes in glucose metabolism were associated with proteinuria and an increase in urinary excretion of N-acetyl-beta-D-glucosaminidase (NAG). Morphologic investigation revealed nodular lesions in glomeruli in the OLETF rats. The ANGII receptor antagonist treatment abolished the blood pressure elevation. However, the treatment did not affect plasma glucose and insulin levels and did not significantly reduce glucosuria. Nodular lesions in glomeruli were not improved by the treatment. However, the receptor antagonists significantly reduced proteinuria and urinary NAG excretion. Multivariate analyses revealed that proteinuria was determined by systolic blood pressure, lipid metabolism, and glucose levels in plasma. ANGII subtype-1 antagonism does not improve glucose metabolism in the OLETF rat model of NIDDM, which has abnormalities in the glucose-uptake system. Blood pressure elevation and part of the proteinuria associated with NIDDM depends on the renin-angiotensin system rather than glucose metabolisms per se.
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PMID:Angiotensin II subtype-1 receptor antagonists improve hemodynamic and renal changes without affecting glucose metabolisms in genetic rat model of non-insulin-dependent diabetes mellitus. 1007 80

Increased urinary excretion of N-acetyl-beta-D-glucosaminidase (NAG) and beta2-microglobulin (beta2M) is considered a marker of tubulo-interstitial disease. This study assessed urinary excretion of NAG and beta2M in children with nephrotic syndrome (NS), 14 with cortico-sensitive nephrotic syndrome (CSNS), five with cortico-resistant NS (CRNS) and 30 healthy controls matched for sex and age. At onset urinary excretion of NAG was significantly higher in children with CSNS than controls (p=0.0001) but during remission values were superimposable. Conversely in CRNS at onset urinary excretion of NAG and beta2M was significantly higher than CSNS and remained unchanged at the end of steroid treatment (p < 0.05 and p < 0.01). Urinary NAG values in CSNS were correlated with proteinuria (r = 0.63), serum total proteins (r = -0.54), serum albumin (r = -0.55) and serum cholesterol (r = 0.67). These data suggest that urinary excretion of NAG and beta2M may be useful as a marker of tubular dysfunction in nephrotic syndromes which often characterises cortico-resistant patients.
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PMID:N-acetyl-beta-D-glucosaminidase and beta2-microglobulin: prognostic markers in idiopathic nephrotic syndrome. 1020 5

The purpose of the study was to determine the effect of initiation of gold therapy on glomerular and tubular integrity. Urine albumin was used as a marker of glomerular damage. N-acetyl-beta-D-glucosaminidase (NAG) urinary excretion served as an indicator of proximal tubular damage. This study was an adjunct to a clinical trial that investigated the safety and the efficacy of Depo-Medrone during the induction phase of gold therapy. The NAG activities and albumin levels in the urine of 36 patients with active rheumatoid arthritis treated with sodium aurothiomalate weekly up to a total of 1 g were investigated. NAG was assayed in 565 early morning urine samples of these patients at weekly intervals for 24 weeks. The mean NAG level rose from 50.2 nmol/mg of creatinine on entry to peak NAG excretion of 120.4 nmol/mg of creatinine at week 4 and then fell to 56.3 nmol/mg of creatinine at week 24. Urinary albumin was assayed in 252 early morning urine samples at monthly intervals during gold treatment. Values greater than 20 mg/l were observed in 7.5% of urine samples. Microalbuminuria was present in 9% of patients at baseline. Two patients who were withdrawn because of proteinuria and macroalbuminuria had normoalbuminuria on entry. We conclude that raised levels of NAG associated with tubular damage are more frequent than glomerular damage on entry to, and during, treatment with gold salts.
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PMID:N-acetyl-beta-D-glucosaminidase urinary excretion as an early indicator of kidney damage in rheumatoid arthritis patients starting on parenteral gold and Depo-Medrone/placebo injections. 1035 14

The aim of this longitudinal study was to evaluate tubular proteinuria in rats with unilateral (UPO) and bilateral (BPO) partial ureteral obstruction with the dimercaptosuccinic acid (DMSA) scan as the gold standard for measuring renal tubular damage. We studied 70 female Wistar rats: 28 animals with UPO, 28 animals with BPO, 7 sham-operated animals, and 7 controls. All animals with obstructed ureters showed renal dilatation on the diethylenetriaminepentaacetic acid DTPA images 1 and 5 weeks postoperatively. One week following UPO and BPO, tubular proteinuria and urinary N-acetyl-beta-D-glucosaminidase (NAG) activity increased (P < 0.01) and the absolute DMSA uptake decreased (P < 0.01). Persistently (week 6) high tubular proteinuria was found in 29% of the animals and was related to severe damage on the DMSA scan (P < 0.01) and to albuminuria (P < 0.05). Renal tubular damage was demonstrated by measuring renal enzymes, tubular proteins, and DMSA uptake after UPO and BPO. Persistent elevated tubular proteinuria was related to severely damaged kidneys.
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PMID:Urinary excretion of tubular proteins and the technetium-99m dimercaptosuccinic acid (DMSA) absolute renal uptake in partial ureteral obstruction in rats: a functional evaluation of hydronephrotic kidneys. 1042 94

A computerized Urine Protein Expert System (UPES) measuring creatinine, total protein, albumin, IgG, alpha(1)-microglobulin, alpha(2)-macroglobulin, and N-acetyl-beta-D-glucosaminidase, together with urine dipstick testing for granulocyte esterase and hemoglobin pseudoperoxidase, and measurement of serum creatinine had been found to be useful in adults for differentiating between renal disorders. The objective of this study was to investigate UPES for identifying the different types of proteinuria and their underlying prerenal, glomerular, tubular, and postrenal causes in 146 children characterized by routine and invasive nephrological investigations. UPES proved to be a useful tool in pediatric renal patients after refinements were implemented in the program. Comparing UPES with the pediatric nephrologist's interpretation of all available clinical and laboratory data, UPES diagnosed glomerulopathies in 46 (75%) of 61 patients. In a further 23% it suggested glomerular involvement by indicating either a disturbed glomerular permeability or increased excretion of albumin. Tubular proteinuria was correctly described by UPES in 23 (100%) patients with different tubulopathies. UPES revealed normal kidney function in all healthy children and all children with remission of renal disorders. Therefore, UPES can be regarded as a useful tool in the automated differentiation of renal diseases in children.
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PMID:Evaluation of pediatric nephropathies by a computerized Urine Protein Expert System (UPES). 1060 45


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