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)

The present investigation was performed to confirm the relationship between the circadian variation of microproteinuria and physical activity. Urine samples from 10 normal male volunteers, collected during six consecutive 4-h periods, were examined for albumin, alpha 1-, beta 2-microglobulin, NAG, electrolytes and hormones. The fluctuations in heart rate (HR) and blood pressure (BP) over 24-h were measured at 30-min and 1-h intervals, respectively. Energy expenditure (EE) was calculated using the equation of regression between HR and oxygen uptake measured on another day. The variations of HR (delta HR) and EE (delta EE) based on a 24-h average (bpm and kcal/kg/h) were used as indices of change in physical activity during an ordinary day. The correlation coefficients between delta HR and the variations of albumin (delta Alb) and beta 2-microglobulin (delta beta 2M) from the 24-h average (micrograms/h.cr 1 mg) were 0.619 and 0.670 (p less than 0.001), respectively. Increased excretions of both glomerular and tubular proteins were correlated with the increase in HR and/or EE during daytime activity. During rest time at night, the variations in alpha 1M, beta 2M and NAG excretion were different from the variations in albumin. A temporary inhibition of tubular protein excretion was observed only in the early morning (04:00-08:00), although albumin excretion was inhibited throughout the nighttime. These findings suggested that physical activity may influence the diurnal variations in protein excretions, that albuminuria may be more sensitive to daytime activity, and that fluctuation of tubular protein excretion may be preferably controlled by an endogenous mechanism. Timed overnight or first-morning urine may be recommendable as a sample for determination of microalbuminuria for screening of clinical diabetic nephropathy.
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PMID:[Circadian variations of urinary excretions of microproteins and N-acetyl-beta-D-glucosaminidase (NAG) during the ordinary activity day]. 169 14

Microalbuminuria in diabetics is considered to be a sensitive indicator of early diabetic nephropathy. In this paper, 24 h-urinary excretions of albumin, BMG and NAG activity were measured in forty-one children with insulin-dependent diabetes mellitus. Moreover, the relationships between the urinary excretions of these substances and various clinical parameters of diabetes were analyzed. The mean values (mean +/- SD) of 24 h-urinary albumin, BMG and NAG activity in the diabetic children were 8.0 +/- 10.6 mg/day, 61.2 +/- 69.0 micrograms/day and 1.87 +/- 1.30 U/day, respectively. No significant differences were found between diabetic children and normal controls for these mean values. Nor were significant correlations between the various clinical parameters of diabetes and the urinary excretions of any of these substances found. However, nine of the forty-one diabetic children (22.0%) had higher levels of these urinary substances than those (mean + 2SD) in normal controls. Screening of the 24 h-urinary albumin, BMG and NAG activity should be performed routinely in young patients with diabetes.
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PMID:The 24 h-urinary excretions of albumin, beta 2-microglobulin and N-acetyl-beta-D-glucosaminidase activity in children with IDDM. 266 32

Excretion of urinary N-acetyl-beta-D-glucosaminidase has been found to be elevated in diabetic humans and rats. This urinary glycosidase may reflect blood sugar control over time, since it has been significantly and positively correlated with hemoglobin A1 in children with insulin-dependent diabetes. Other studies have suggested that urinary NAG may predict diabetic nephropathy. In order to more carefully define the relationship between urinary NAG excretion and blood and urine sugars, hemoglobin A1, and microalbuminuria, 48 rats were made diabetic by the use of streptozotocin. All rats were uninephrectomized at 3 weeks. Of these, 23 were treated with daily insulin injections, 25 were untreated, and both groups were compared to 13 control, nondiabetic rats. Urine volume, glucose, albumin, and blood sugar were all significantly (P less than 0.05) elevated in the untreated rats compared to the treated and control groups. Urinary NAG:UCr was significantly (P less than 0.01) elevated in the untreated group with lower but still elevated levels (P less than 0.05) in the treated rats. To further define the time course of the increase in UNAG:UCr 12 rats were followed serially at 12-hr intervals for 92 hr after streptozotocin. Urinary NAG increased significantly (P less than 0.05) at 12 hr after streptozotocin injection and reached a plateau at 36 hr while hemoglobin A1 did not rise until 2 weeks after onset of hyperglycemia. Urinary NAG increases more rapidly than hemoglobin A1 after onset of hyperglycemia and glycosuria.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Urinary N-acetyl-beta-D-glucosaminidase in streptozotocin-induced diabetic rats. 647 35

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

The urinary excretions of salivary and pancreatic amylase were studied in 718 type I diabetic patients and 51 control subjects, as part of a multicenter study on diabetic nephropathy in 15 Spanish hospitals. It was found that the urinary ratio of salivary to pancreatic amylase (S/P ratio), that in normal subjects is always below 1, was elevated in 35.4% of diabetic patients, whereas microalbuminuria was present in 19.8%. The prevalence of elevated S/P ratio was also higher than that of microalbuminuria at the first years from the onset of the disease, but the prevalence of microalbuminuria was higher in patients with a long duration of the disease. alpha 1-microglobulin and microalbuminuria paralleled their prevalences during the disease, when measured in a group of patients. Overnight urine samples were obtained on three consecutive weeks from the diabetic patients, and a nested ANOVA analysis showed that the intra-individual variation of the urine parameters measured (albumin, salivary and pancreatic amylase, and beta-NAG) was very small and not statistically significant. All these findings suggest that in type I diabetes mellitus, loss of negative charges of GBM would induce preferential excretion of the anionic salivary amylase over the more cationic pancreatic amylase, and that this phenomenon is more frequent and appears earlier than microalbuminuria. The mechanisms for the increased excretion of salivary amylase and albumin into urine seem to be at least partly different. On the contrary, increase in urinary excretion of albumin and alpha 1-microglobulin in these patients are correlated, suggesting a tubular participation in the mechanisms of production of microalbuminuria.
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PMID:Charge selectivity and urine amylase isoenzymes. 753 43

To evaluate the renal structural changes in non-insulin-dependent diabetes mellitus (NIDDM), we studied the renal histological findings and urinary albumin excretion in 75 patients with NIDDM. They were divided into two groups according to excretion of urinary albumin: 40 cases of normoalbuminuria and 35 cases of microalbuminuria. Renal biopsy specimens were evaluated by light microscopy. Diffuse glomerular lesions were graded on a scale of D0 through DIV (Gellman's criteria). The incidence of microalbuminuria was 19.2% in D0, 53.3% in DI, 61.5% in DII and 100% in DIII. Grade IV lesions were not present in either group. Creatinine clearance differed significantly between the groups with and without microalbuminuria. There was no difference between the groups with normoalbuminuria and microalbuminuria in the incidence of retinopathy and hypertension, or in the urinary excretion of beta 2MG and NAG. We conclude that microalbuminuria in NIDDM indicates the early morphological changes of glomerular lesions.
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PMID:Glomerular lesions in patients with non-insulin-dependent diabetes mellitus and microalbuminuria. 801 66

Urinary albumin concentration (U-alb) and N-acetyl-beta-D-glucosaminidase (U-NAG) and glomerular basement membrane antibodies (a-GBMs) in serum samples were measured in 77 chloralkali workers previously exposed to mercury (Hg) vapour and 53 age matched referents. The exposure ceased on average 12.3 (range 1-35) years before the study. The mean exposure time was 7.9 (range 1.1-36.2) years. The mean yearly urinary Hg concentration (U-Hg) was 531 nmol/l. The concentrations of the urinary isoenzymes NAG A (U-NAG A) and NAG B (U-NAG B) were determined in 30 highly exposed subjects and 30 referents. No differences in U-alb or U-NAG, U-NAG A, or U-NAG B were found between the groups. Higher concentrations of a-GBMs were found among subjects who stopped exposure a short time before the study, but there was no association between a-GBMs and U-alb. The U-NAG and U-NAG A were negatively correlated with storage time. The results may suggest that microalbuminuria and enzymuria reported in subjects with ongoing exposure to Hg vapour are reversible in most instances.
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PMID:Assessment of renal dysfunction in workers previously exposed to mercury vapour at a chloralkali plant. 821 45

The knowledge of renal function in the course of BMT is poor. We prospectively investigated glomerular and tubular function in 42 children who underwent BMT because of malignancy. Seventeen children were transplanted autologously. Investigations were performed before and immediately after the conditioning regimen. Inulin and creatinine clearance, albuminuria, urine excretion of alpha 1-microglobulin, beta-N-acetylglucosaminidase, alanine-aminopeptidase, intestinal alkaline phosphatase, and Tamm-Horsfall-Protein as well as sodium- and phosphatreabsorption were measured. The patients were classified regarding use of total body irradiation (tTBI) in the conditioning regimen. BEFORE CR: Glomerular filtration rate (GFR) was not influenced by the underlying diagnosis or previous treatment. Mean GFR was elevated compared with the reference group. Microalbuminuria was elevated in 15% of patients, and mean levels were higher than in the reference group. Proximal tubular dysfunction was indicated by an elevated excretion of alpha 1-MG in 54%, of beta-NAG in 66%, of AAP in 40%, and of IAP in 47%. Fractional sodium excretion was abnormal in 21%, phosphate reabsorption in 5% and THP-excretion in 7% of the patients. AFTER CR: Creatinine clearance was not affected by CR. After CR alpha 1-MG, beta-NAG, FENa, AAP, and IAP were increased compared with values before CR. TP/Clcr was decreased. Excretion of THP was not altered by CR. In patients without fTBI there was a greater increase in alpha 1-MG excretion and decrease in phosphate reabsorption after CR compared with patients conditioned with fTBI. We conclude that significant proximal tubular dysfunction is present in about 50-60% of patients before and in nearly all alter CR. Distal tubular function was less severely affected. Severity of nephrotoxicity after CR did not correlate with pre-existing abnormalities.
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PMID:Renal function after conditioning therapy for bone marrow transplantation in childhood. 907 24

Insulin resistance and hyperinsulinemia cluster with microalbuminuria in both diabetic and nondiabetic subjects, but the mechanism underlying this association is unknown. To test the hypothesis that insulin influences protein permeability, we measured the albumin transcapillary escape rate (TER) by the (131)I-labeled albumin technique in 12 healthy volunteers and 12 normoalbuminuric NIDDM patients (fasting plasma glucose, 10.9 +/- 1.3 mmol/l) during 4 h of isoglycemia with high (1.1 mU x min(-1) x kg(-1)) or, on a different day, low (0.1 mU x min(-1) x kg(-1)) insulin infusion. In both patients and control subjects, high insulin was associated with a 7% decrease in blood volume (P = 0.006) and a 6% decrease in diastolic blood pressure (P < 0.02), these two changes being related to one another (r = 0.56, P < 0.01). Basal albumin TER was similar in patients (8.4 +/- 0.5% x h(-1)) and control subjects (7.7 +/- 0.7% x h(-1)) and was not significantly changed by high insulin in either group (patients vs. control subjects, 7.3 +/- 0.9 vs. 6.2 +/- 0.4% x h(-1); NS vs. low insulin). In contrast, high insulin increased renal albumin excretion (from 3.6 +/- 0.8 to 5.4 +/- 1.1 microg/min, P < 0.01) and clearance rate (0.09 +/- 0.02 to 0.13 +/- 0.03 microl/min, P < 0.001) in patients but not in control subjects. To localize the effect of insulin along the nephron, we measured the urinary excretion of N-acetyl-beta-D-glucosaminidase (beta-NAG), released by the proximal tubule; retinol-binding protein (RBP), reabsorbed by the proximal tubule; and Tamm-Horsfall protein (THP) and epidermal growth factor (EGF), both secreted by the distal tubule. For both beta-NAG and RBP, but not EGF or THP, insulin enhanced urinary excretion (diabetics vs. controls: beta-NAG, 0.48 vs. -0.15 microU/min [P = 0.03]; RBP, 78 vs. -32 ng/min [P = 0.05]). In conclusion, physiological hyperinsulinemia does not affect systemic albumin permeability in healthy subjects or normoalbuminuric NIDDM patients. In contrast, in NIDDM patients, but not in healthy subjects, insulin increases the urinary excretion of albumin and protein markers of proximal tubular function. The significance of this finding for the pathogenesis of diabetic nephropathy remains to be established.
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PMID:Effect of insulin on systemic and renal handling of albumin in nondiabetic and NIDDM subjects. 913 57

Diabetic nephropathy (DN) is usually characterized by glomerular dysfunction, with microalbuminuria as an early indicator. Urinary excretion of smaller molecular weight proteins such as n-acetyl-beta-glucosaminidase (beta-NAG) and retinol binding protein (RBP) indicate proximal tubular dysfunction, and may identify diabetic patients at risk of developing diabetic nephropathy. In a trial to assess renal tubular function, urinary excretion of beta-NAG (by colorimetric assay) and RBP (by ELISA) were determined in 59 type 1 diabetic patients (mean age 15 +/- 3.2 yr). Of the 59 patients, 11 were microalbuminuric while 48 had normal urinary albumin excretion (UAE). Patients were compared with 40 matched healthy subjects. Diabetic patients with microalbuminuria (n = 11) had concomitant renal tubular disorder indicated by high urinary beta-NAG in all (100%) and RBP in 10 (90.9%) of them. Meanwhile, patients without microalbuminuria (n = 48) had both tubular markers excreted in urine in significantly higher amounts than controls (mean beta-NAG = 6.88 vs. 3.76 U/g Cr, p < 0.001; RBP = 386.6 vs. 151.8 microg/dL, p < 0.001). Among those patients, 29 (61%) had raised urinary beta-NAG activity, and 39 (82%) had increased loss of RBP in urine. A significant correlation was found between urinary beta-NAG and RBP in normoalbuminuric patients (r = 0.66, p < 0.001), as well as between each of the two tubular markers and HbA1c (r = 0.83, p < 0.001). At 30 and 36 months of follow-up, two out of 48 (4.2%) diabetic patients developed persistent microalbuminuria. Both had elevated baseline HbA1C, and urinary beta-NAG. In conclusion, proximal tubular dysfunction may occur independent of glomerular alteration. Whether tubular markers precede the development of microalbuminuria needs further study.
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PMID:Urinary excretion of n-acetyl-beta-D-glucosaminidase and retinol binding protein as alternative indicators of nephropathy in patients with type 1 diabetes mellitus. 1501 73


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