Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0730345 (microalbuminuria)
 4,018 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a double-blind, randomized trial with 26 male white patients with essential hypertension in World Health Organization Stages I and II, we examined the impact of calcium entry blockade (5 to 10 mg/day isradipine, N = 14) and beta-blockade (100 to 200 mg/day metoprolol, N = 12) on early markers of hypertensive nephropathy before and after 7 weeks' treatment. Excretion of total protein, albumin, alpha 1-microglobuline, and N-acetyl-beta-glucosaminidase (NAG) were measured in the 24-h urine by radial immunodiffusion and fluorimetric method, respectively. Before therapy, 8 of 26 patients had microproteinuria (31%), six had microalbuminuria (22%), six had elevated urinary NAG activity (22%), and three had elevated alpha 1-microglobulin excretion (11%). In these subjects anti-hypertensive therapy led to a fall in proteinuria (296 +/- 56 v 127 +/- 116 mg/day, P less than .01), albuminuria (44 +/- 24 v 25 +/- 12 mg/day, P less than .05), and NAG excretion (45 +/- 22 v 28 +/- 5, P less than .05). The higher the pretreatment value, the greater the fall was in proteinuria (r = +0.55, P less than .01), albuminuria (r = 0.80, P less than .001), and NAG excretion (r = 0.60, P less than .01). We did not observe any significant difference in clinical characteristics, blood pressure, or urinary excretion of protein, albumin, or NAG between the two treatment groups, either before or after therapy. Thus, antihypertensive therapy reduced excretion of total protein, albumin, and NAG activity in hypertensive patients with elevated pretreatment values, potentially indicating reversal of early hypertensive nephropathy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Impact of antihypertensive therapy with isradipine and metoprolol on early markers of hypertensive nephropathy. 153 71

Urinary albumin excretion (UAE) was determined by radioimmunoassay in two 24 h urine collections from 125 diabetic children and adolescents and from 71 normal children matched for age and sex. Thirteen patients (10.4%) aged greater than 12 years had microalbuminuria, i.e. log transformed UAE levels above the upper normal range (24.5 mg/24 h). UAE values were positively correlated with age, GH secretion, but not with duration of disease, glycosylated hemoglobin, renal size or N-acetyl-beta-glucosaminidase excretion. Diabetic normoalbuminuric children aged 10 years and older had significantly higher UAE than controls and than younger diabetic patients matched for duration of disease. HLA DR3/DR4 heterozygosity frequency was significantly higher (p less than 0.01) in the microalbuminuric group than in the normoalbuminuric. All microalbuminuric subjects (n = 8) with short duration of disease (3.92 +/- 3.43 yr) developed diabetes at puberty. In conclusion, our cross-sectional study suggests: if a number of factors are combined, i.e. HLA DR3/DR4 heterozygosity, onset of disease at puberty and higher GH values, the probability of developing abnormal levels of UAE will increase.
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PMID:Microalbuminuria in diabetic children and adolescents. Relationship with puberty and growth hormone. 219 Apr 42

Three laboratory indicators of impaired renal function (microalbuminuria (MA), N-acetyl-beta-glucosaminidase (NAG), beta-2-microglobulinaemia (beta-2-M)) were studied in sixty diabetics of type 1. 10 times higher MA levels were found in a subgroup of diabetics with identifiable diabetic retinopathy (DR). In a subgroup of diabetics with normal values of excreted albumin the mean MA value was significantly higher than in those who had already contracted DR. Pathological levels of NAG and beta-2-M were mostly seen in those patients who also had pathological MA results. In only four cases were increased NAG or beta-2-M values as the first and only pathological parameter indicative of possible renal involvement due to diabetic nephropathy.
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PMID:Laboratory detection of the early stages of diabetic nephropathy. 252 Jan 56

Serum erythropoietin (Epo) activity, hemoglobin (Hb), and hematocrit (Ht) were determined in 21 cross-country skiers during the training season. The Epo levels were not significantly reduced in the skiers relative to the normal population (P less than 0.01 and P less than 0.001, respectively). In 11 athletes Epo, Ht, urinary gamma-glutamyltransferase, N-acetyl-beta-glucosaminidase, and microalbuminuria were determined before and after a 50-km ski race at 1600 m above sea level. A significant increase of these variables (except for Ht) was found after the competition (P less than 0.001). It is concluded that while the reductions in Hb and Ht, which are typical of several endurance exercises, are not accompanied by a renal hypoxia sufficient to stimulate Epo overproduction, the renal hypoxia reached during the strenuous exercise of the race at altitude may be effective in determining blood increases in Epo.
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PMID:Serum erythropoietin in cross-country skiers. 338 28

N-acetyl-beta-Glucosaminidase activity in serum and urine and microalbuminuria were measured in 70 type-I diabetics and compared with glycated serum protein as well as with the finding of diabetic retinopathy. A significantly increased N-acetyl-beta-glucosaminidase activity in serum correlated positively with glycated protein but not with the development of retinopathy. Urinary N-acetyl-beta-glucosaminidase activity and albuminuria were significantly increased in diabetics with (p less than 0.001) or without (p less than 0.01) retinopathy as compared to healthy controls. A significant positive correlation was observed between urinary N-acetyl-beta-glucosaminidase activity and albuminuria (r = 0.73, p less than 0.01) as well as between blood pressure and albuminuria (r = 0.51, p less than 0.05).
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PMID:Comparison of N-acetyl-beta-glucosaminidase and albuminuria with clinical finding of microangiopathy in type I diabetes mellitus. 362 94

Renal function tests were performed in 101 unselected patients who had been on lithium for two weeks to 12 years. None had a recorded episode of lithium intoxication. The glomerular filtration rate (GFR), was not correlated with the cumulative dose of lithium or the duration of use of other psychotropic drugs. Nine patients had creatinine clearances lower than predicted; in six of these, no cause was identified and the small reductions in GFR may have been related to lithium use. Urinary concentrating ability (Umax) declined with age, and total dose of lithium received. Although the concurrent use of neuroleptics did not significantly reduce the Umax, the total duration of treatment with these drugs showed a negative correlation. The results suggest that prolonged use of neuroleptics, particularly in patients treated with lithium, may be responsible for an irreversible reduction in urine concentrating ability. Microalbuminuria was present in 40 per cent of the patients, although the rate of albumin excretion was not correlated with duration of use of psychotropic drugs. beta 2 microglobulin excretion was only raised in nine of these patients, suggesting that increased glomerular permeability rather than impaired proximal tubular protein reabsorption was responsible for the proteinuria. The urinary excretion of beta 2 microglobulin and N-acetyl-beta-glucosaminidase were slightly increased in small numbers of patients, indicating little evidence for proximal tubular damage. Increased NAG excretion did not correlate with reduced distal tubular function. However, there was a tendency to higher urinary beta 2 microglobulin excretion in patients with a reduced Umax.
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PMID:Renal function during lithium treatment. 648 19

Serum ascorbic acid (AA) is reduced in diabetic patients. Aim of this study was 1) to verify whether such a decrease might be due to an altered urinary excretion of AA, and 2) whether this latter was modified in presence of early diabetic nephropathy with microalbuminuria (albumin excretion rate [AER] > 20 micrograms/min) in a group of 21 patients affected by insulin-dependent (type 1) diabetes mellitus (IDDM) as compared with 13 healthy controls matched for sex, age, dietary AA intake, and creatinine clearance per 1.73 m2 (CCl). Mean serum AA (+/- SD) was lower in diabetics (40.3 +/- 14 microM/l) than in controls (85.1 +/- 23.5 microM/l; p = 0.0001) and there was no difference between serum AA of patients with or without microalbuminuria. Urinary excretion of AA to creatinine x 100 (UAA/Cr) was higher in micro- (n = 6; 4.6 +/- 1.7) as compared to normoalbuminurics (n = 15; 1.6 +/- 0.9) or controls (1.5 +/- 1.2; p = 0.0001). For values exceeding renal threshold of tubular AA reabsorption (39 microM) the regression line of serum AA to UAA/Cr was significantly (p = 0.001) steeper in diabetics than in controls, suggesting an impaired tubular reabsorption of filtered AA in IDDM. The ratio of AA clearance to CCl was moreover related to AER (r = 0.48; p = 0.03) and to blood glucose (r = 0.51; p = 0.01), being unrelated to uric acid clearance, glycosuria and to urinary excretion of both alanine aminopeptidase and N-acetyl-beta-glucosaminidase.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal excretion of ascorbic acid in insulin dependent diabetes mellitus. 796 Apr 90

The authors investigated a group of 47 type I diabetics in a prospective study extending over 8 years. Every year they evaluated the albuminuria and the N-acetyl-beta-glucosaminidase (NAG) activity in serum and urine and the results were compared with the state of compensation of diabetes and with the clinical finding on the ocular fundus. During the eight-year period newly manifested microalbuminuria developed in 8 of 32 patients (25%) who at the onset had a normal finding. In patients with newly manifested microalbuminuria the authors found a significant rise of the fructosamine serum concentration (p < 0.05) and at the same time a rise of serum NAG activity (p < 0.05). A positive correlation was proved between the serum NAG activity and glycated haemoglobin (r = 0.67, p < 0.01). In 13 patients (28%) in the course of the eight-year period the finding on the ocular fundus deteriorated. In these patients the NAG serum activity was elevated already at the onset of the investigation, while albuminuria rose in the course of the mentioned period. Dynamic changes of the NAG serum activity along with albuminuria can serve as bio-chemical markers of developing microangiopathy the manifestation of which is hastened by deteriorated compensation of diabetes.
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PMID:[Albuminuria and N-acetyl-beta-glucosaminidase activity in a prospective study of type I diabetics]. 837 66

Hypertensive nephropathy is an important complication of arterial hypertension, being a cause of chronic renal insufficiency in a considerable number of patients. For years it has been attempted to find an useful marker of nephropathy in the incipient phases of the disease. We revised the main biochemical indicators of renal damage, paying special attention to hyperuricemia, microalbuminuria, and urinary excretion of beta-2-microglobulin and N-acetyl-beta-glucosaminidase. Each one of them expresses alterations in the glomerular filtrate, lesion of capillary endothelium or anomalies of the tubular function. None of them demonstrated to be specific to nephroangiosclerosis, but they guide us on the structural and functional alterations occurring in the first stages of hypertensive nephropathy.
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PMID:[Early biochemical indicators of renal damage in arterial hypertension]. 962 77

Urinary pancreatic stone protein (PSP) levels were measured in 68 diabetic patients and 170 healthy controls to investigate the relationship between the progression of diabetic nephropathy and PSP excretion. Urinary albumin, N-acetyl-beta-glucosaminidase (NAG), alpha1-microglobulin, creatinine clearance, and the blood PSP level were also determined in the diabetic patients. The urinary glucose level and glycemic control did not influence the urinary PSP level. In patients with normoalbuminuria (urinary albumin <20 mg/gCr, n=31), microalbuminuria (20-200 mg/Cr, n=19), and macroalbuminuria (>200 mg/gCr, n=18), the mean urinary PSP level was 347, 507, and 860 microg/gCr, respectively. These levels were significantly higher than the level in normal volunteers (168 microg/gCr, p<0.01). A significant positive correlation was observed between the urinary PSP level and the NAG or alpha1-microglobulin levels (p<0.01). There was a stronger correlation with alpha1-microglobulin. Blood PSP levels were also elevated in patients who had renal impairment with a decreased creatinine clearance. In conclusion, urinary PSP excretion was increased from the initial stage of diabetic nephropathy and this increase became more marked as nephropathy progressed. Increased PSP excretion may reflect renal tubular dysfunction.
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PMID:Urinary excretion of pancreatic stone protein in diabetic nephropathy. 967 81


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