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 effect of simvastatin (10-20 mg/day) on kidney function, urinary albumin excretion rate and insulin sensitivity was evaluated in 18 Type 2 (non-insulin-dependent) diabetic patients with microalbuminuria and moderate hypercholesterolaemia (total cholesterol > or = 5.5 mmol.l-1). In a double-blind, randomized and placebo-controlled design treatment with simvastatin (n = 8) for 36 weeks significantly reduced total cholesterol (6.7 +/- 0.3 vs 5.1 mmol.l-1 (p < 0.01)), LDL-cholesterol (4.4 +/- 0.3 vs 2.9 +/- 0.2 mmol.l-1 (p < 0.01)) and apolipoprotein B (1.05 +/- 0.04 vs 0.77 +/- 0.02 mmol.l-1 (p < 0.01)) levels as compared to placebo (n = 10). Both glomerular filtration rate (mean +/- SEM) (simvastatin: 96.6 +/- 8.0 vs 96.0 +/- 5.7 ml.min-1 x 1.73 m-2, placebo: 97.1 +/- 6.7 vs 88.8 +/- 6.0 ml.min-1 x 1.73 m-2)(NS) and urinary albumin excretion rate (geometric mean x/divided by antilog SEM) (simvastatin: 18.4 x/divided by 1.3 vs 16.2 x/divided by 1.2 microgram.min-1, placebo 33.1 x/divided by 1.3 vs 42.7 x/divided by 1.3 micrograms.min-1)(NS) were unchanged during the study. A euglycaemic hyperinsulinaemic clamp was performed at baseline and after 18 weeks in seven simvastatin- and nine placebo-treated patients. Isotopically determined basal and insulin-stimulated glucose disposal was similarly reduced before and during therapy in both the simvastatin (2.0 +/- 0.1 vs 1.9 +/- 0.1 (NS) and 3.1 +/- 0.6 vs 3.1 +/- 0.7 mg.kg-1 x min-1 (NS)) and the placebo group (1.9 +/- 0.1 vs 1.8 +/- 0.1 (NS) and 4.1 +/- 0.6 vs 3.8 +/- 0.2 mg.kg-1 x min-1 (NS)).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal function and insulin sensitivity during simvastatin treatment in type 2 (non-insulin-dependent) diabetic patients with microalbuminuria. 824 58

Previous cross-sectional studies have shown a significant correlation between limited joint mobility (LJM) and the microvascular complications of Type 1 diabetes, but whether LJM precedes and, therefore, may be regarded as an early marker for complications is unknown. Twenty-two Type 1 diabetic patients (10 male/12 female; diabetes duration at follow-up 20.1 +/- 1.3 (SEM) years) with LJM, and 22 subjects matched for age, sex, and duration of diabetes, without LJM were observed over a 10-year period. Both groups were free of retinopathy and negative for 'dipstick' proteinuria at baseline. After 10 years, of 22 patients with LJM, 10 had developed background and 3 proliferative retinopathy compared with 9 and 1 control subjects, respectively. Microalbuminuria (20 < or = albumin excretion rate < 200 micrograms min-1) was present in 3 and macroalbuminuria (albumin excretion rate > or = 200 micrograms min-1) in 2 of LJM patients compared with 6 and 1 control subjects, respectively. Ankle and toe vibration perception thresholds, HbA1, mean HbA1 (a mean of serial HbA1 measurements obtained during the 10-year follow-up period), and arterial blood pressure did not differ between the two groups (p > 0.05). At 10-year review, 9 of the control subjects had developed LJM of whom 4 had retinopathy and 4 microalbuminuria. Thus, while LJM may be another 'chronic complication' of diabetes, its presence does not appear to predict those at increased risk of developing microvascular complications.
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PMID:Incidence of microvascular complications in type 1 diabetic subjects with limited joint mobility: a 10-year prospective study. 828 23

1. Microalbuminuria is a risk factor for cardiovascular disease in patients with insulin-dependent diabetes mellitus, and may be a marker of microvascular dysfunction including endothelial damage. The purpose of this study was to determine whether vasoconstrictor responses to NG-monomethyl-L-arginine, an inhibitor of endothelium-derived relaxing factor/nitric oxide biosynthesis, differ between healthy subjects and insulin-dependent patients with or without microalbuminuria. 2. Twenty-eight insulin-dependent diabetic patients (14 with normal albumin excretion, 14 with microalbuminuria) were studied under euglycaemic conditions, together with 14 healthy control subjects. Forearm vascular responses to brachial artery infusions of NG-monomethyl-L-arginine, sodium nitroprusside (an endothelium-independent nitrovasodilator) and carbachol (an endothelium-dependent vasodilator) were determined by strain gauge plethysmography. 3. Basal blood flow and vasodilator responses were similar in each group. NG-Monomethyl-L-arginine reduced blood flow by 41.3 +/- 2.3% (mean +/- SEM) in healthy control subjects, 34.0 +/- 3.4% in diabetic patients without microalbuminuria and 29.2 +/- 2.0% in diabetic patients with microalbuminuria. Diabetic patients differed from healthy subjects (P = 0.005), due to a difference between control subjects and microalbuminuric diabetic patients (P < 0.001). NG-Monomethyl-L-arginine did not influence nitroprusside responses but reduced carbachol responses in control subjects and normoalbuminuric diabetic patients but not in microalbuminuric diabetic patients. 4. These results provide evidence of abnormal endothelium-derived relaxing factor/nitric oxide biosynthesis in insulin-dependent diabetic patients with microalbuminuria.
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PMID:Inhibition of nitric oxide synthesis in forearm vasculature of insulin-dependent diabetic patients: blunted vasoconstriction in patients with microalbuminuria. 828 60

In order to evaluate the influence of regular non-strenuous physical exercise on the appearance of microalbuminuria in Type 2 (non-insulin-dependent) diabetic patients, we have studied a cohort of 372 Type 2 diabetic patients (152 males and 220 females, mean age: 63.59 +/- 0.70 years, evolution time: 10.31 +/- 0.4 years, M +/- SEM). One hundred and ninety seven (52.9%) presented normo-albuminuria, 124 (33.3%) microalbuminuria and 51 (13.7%) proteinuria. These three groups were different with regard to evolution time, weight, BMI, waist-hip ratio, Hb1Ac value, prevalence of hypertension and physical activity level. 132 (35.4%) patients had a regular exercise-induced caloric expenditure under 500 kcal/wk whereas 122 (32.7%) were between 500 and 1.000 kcal/wk and 118 (31.7%) over 1.000 kcal/wk. Prevalence of normo-albuminuric patients was 40.1%, 52.4% and 67.7% respectively (p < 0.01). Prevalence of normo-albuminuric patients remained significatively higher in the patient with the greater physical activity level when adjusted to systolic blood pressure, diastolic blood pressure, evolution time and HbA1c value. Our results stress the fact that regular non-strenuous physical activity may have a protective effect on the appearance of microalbuminuria in Type 2 (non-insulin-dependent) diabetic patients. Whether the cardiovascular protective influence of exercise in these patients depends on such an effect remains unknown. On the basis of this cross-sectional evidence, a longitudinal study is now under way.
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PMID:Regular physical activity and reduced occurrence of microalbuminuria in type 2 diabetic patients. 840 21

The fractional plasma escape rates of glycated and non-glycated albumin have earlier been measured in groups of Type 1 (insulin-dependent) diabetic patients and control subjects. The escape of non-glycated albumin was similar in control subjects and normoalbuminuric patients, but elevated in patients with micro or macroalbuminuria. In all groups the escape rate of glycated albumin was lower than that of non-glycated albumin. Glycation increases the anionic charge of albumin. To assay for charge-dependent alterations of transport a selectivity index (non-glycated albumin/glycated albumin transport ratio) was determined from the disappearance data. The index was high in control subjects (1.021 +/- 0.0057 (SEM)). This reflects a mean difference between the two escape rates of 2.1% per hour (for comparison the mean of the fractional escape rate of non-glycated albumin of the normal control subjects was 4.7% per hour). The index was numerically even higher in normoalbuminuric patients (1.031 +/- 0.0047 (SEM)), but reached significantly lower levels in patients with microalbuminuria (1.013 +/- 0.0030 (SEM), p < 0.02). Patients with clinical nephropathy had very low levels indicating loss of selectivity (1.002 +/- 0.0068 (SEM), p < 0.001). This pattern accords well with measurements of renal clearance selectivity indices, suggesting a general, progressive deterioration of anionic perivascular barrier components in diabetic microangiopathy. The structural target for these changes is likely to be the glycosaminoglycans of the glomerular basal membrane and the interstitial matrix.
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PMID:Plasma disappearance of glycated and non-glycated albumin in type 1 (insulin-dependent) diabetes mellitus: evidence for charge dependent alterations of the plasma to lymph pathway. 847 83

Taking into account both the importance of microalbuminuria (MA) as a predictive parameter of clinical nephropathy in diabetic patients and the efficiency of exertion to show and/or to increase MA in both diabetic patients and normal individuals, we studied 37 type I diabetic patients divided into two groups: group A, with no MA at rest (n = 19), and group B, with MA at rest (n = 18). Group C comprised 10 healthy volunteers as controls. Changes of basal MA during exercise and postexercise were studied in all three groups. Normotensive patients with no metabolic disorders, normal renal function, and no proteinuria underwent an ergometric test up to 600 kg. This test was repeated after the administration of 20 mg enalapril in a single daily dose for 60 days. Body weight, systolic and diastolic arterial pressure, creatinine, and creatinine clearance were determined and showed no significant variations either between groups or with treatment. Microalbuminuria was studied in the three groups with and without administration of enalapril throughout the 2 months of the study. Determinations were performed under conditions of rest, exercise, and postexercise. Mean baseline MA values +/- SEM were as follows: at rest, 5.22 +/- 0.49, 58.36 +/- 13.24, and 4.73 +/- 0.45 micrograms/min for groups A, B, and C, respectively; with exercise, 15.19 +/- 4.43, 74.70 +/- 14.89, and 16.76 +/- 4.62 micrograms/min for groups A, B, and C, respectively; and postexercise, 32.04 +/- 6.64, 253.15 +/- 63.88, and 9.23 +/- 3.25 micrograms/min, respectively. The geometric means of the baseline to posttreatment MA ratio were as follows: at rest, 0.95, 1.59 (P < 0.01), and 1.03 for groups A, B, and C, respectively; with exercise, 1.53 (P < 0.01), 1.91 (P < 0.01), and 1.69 for groups A, B, and C, respectively; and postexercise, 2.94 (P < 0.01), 3.24 (P < 0.01), and 1.03 for groups A, B, and C, respectively. In conclusion, in the early diagnostic suspicion of diabetic nephropathy, the screening of postexercise MA during an ergometric test could be of help. Treatment with enalapril decreased MA in diabetic groups A (no MA at rest) and B (MA at rest) during exercise and postexercise, and also decreased MA in group B while at rest.
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PMID:Decrease of exercise-induced microalbuminuria in patients with type I diabetes by means of an angiotensin-converting enzyme inhibitor. 854 35

Kidney volume was measured during pregnancy in insulin-dependent diabetic women by an ultrasound technique and prognostic value of these measurements evaluated. A prospective study was performed on 87 pregnant women with insulin-dependent diabetes attending the maternity clinic of Aarhus Kommunehospital. Patients with proliferative retinopathy alone, hydronephrosis, or nephrotic syndrome were excluded. The patients were grouped according to onset and duration of diabetes and to vascular lesions; group I (n = 35, White class B+C), group II (n = 11, White class D0), group III (n = 26, White class D+), and group IV (n = 15, White class F+F/R). The patients visited the hospital every 2 weeks during pregnancy for general obstetric and glycaemic control and blood sampling. The volume of both kidneys was measured by a computerized nephrosonograph during the three terms of pregnancy, the puerperium and 4 months postpartum. The kidney volume increased significantly in all four groups from first to third trimester. In the third trimester the kidney volumes were 375 +/- 68 ml (I), 341 +/- 50 ml (II), 362 +/- 63 ml (III), and 343 +/- 54 ml (IV). The kidney volume in the third trimester was positively correlated with creatinine clearance (r = 0.33, P < 0.01) and inversely correlated with creatinine in serum (r = -0.27, P = < 0.02). Total kidney volume decrease (in percent) defined as the difference of maximal volume and value at 4 months postpartum was inversely correlated to albuminuria in the third trimester (r = -0.25, P < 0.05) and vascular lesions of the patients: (mean +/- SEM) 37 +/- 4% (I), 25 +/- 7% (II), 19 +/- 5% (III), and 11 +/- 7% (IV), P < 0.01. In the puerperium, kidney volume decreased significantly from third trimester in groups I, II, and III, whereas we observed no change in group IV. Six of 15 women in groups II and III with kidney volume < 300 ml and normoalbuminuria in the first trimester developed persistent microalbuminuria after pregnancy (P < 0.02). The renal volume in insulin-dependent diabetic women increases significantly during pregnancy and is inversely related to the vascular lesions of the patients. The decrease in renal volume after pregnancy is related to the albuminuria at the end of pregnancy. Women with longstanding diabetes, White class D (= groups II+III), and kidney volume < 300 ml in the first trimester have a high risk of developing permanent microalbuminuria after pregnancy.
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PMID:Renal growth during pregnancy in insulin-dependent diabetic women. A prospective study of renal volume and clinical variables. 875 Jul 60

Fifteen out-patients with type I diabetes mellitus and microalbuminuria (mean +/- SEM: 95.4 +/- 13.9 micrograms/min), were administered the glycosaminoglycan sulodexide, with the aim of investigating its influence on the rate of albumin excretion. Sulodexide was given intramuscularly in a dose of 600 lipoproteinlipase releasing units/day for three weeks. Albumin excretion was measured before dosing, at weekly intervals during dosing and also during the subsequent follow-up period of six weeks. Sulodexide yielded a clear-cut and statistically significant lowering of albumin excretion after the first week of treatment (from 95.4 +/- 13.9 micrograms/min to 53.6 +/- 11.1 micrograms/min; p = 0.0055); albumin excretion was further decreased after three weeks of treatment (26.5 +/- 6.05 micrograms/min; p = 0.0007) and was maintained during the follow-up period, at the end of which the mean value was still significantly lower than at baseline (39.6 +/- 10.3 micrograms/min; p = 0.01). Sulodexide short-term administration did not influence the routine haematological, haematochemical and coagulative tests performed contemporaneously. Patients' compliance with treatment was very good and no adverse events were reported.
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PMID:A pilot study of the effect of the glycosaminoglycan sulodexide on microalbuminuria in type I diabetic patients. 916 56

The importance of glycemic control for the avoidance of micro- and macroalbuminuria after a diabetes duration of 20 years or more was studied in type I (insulin-dependent) diabetic patients diagnosed before an age of 31 years. Glycemic control was assessed as glycated hemoglobin for 5 years or more, on average 9.8 years with 3.2 measurements per year. Of the 197 included patients, 97 men and 100 women, 112 were normoalbuminuric, 45 had microalbuminuria (20-200 mg/L), and 40 had macroalbuminuria (persistent albuminuria > 200 mg/L). Normoalbuminuric patients had a mean HbA1c +/- SEM for the whole measurement period of 6.9 +/- 0.08%, the microalbuminuric patients 7.3 +/- 0.14% (Mann-Whitney test versus normoalbuminuric group, p = 0.025), and macroalbuminuric patients 7.6 +/- 0.13 (p < 0.001). The patients were on average 45 years old, and had an age at onset of 14 years, without significant differences between the groups. Thirteen patients had regressed from macroalbuminuria to normo- (n = 6) or microalbuminuria (n = 7). Of the normoalbuminuric patients, 43% were male, compared to 44% with microalbuminuria and 73% with macroalbuminuria (chi 2, p = 0.026). Logistic regression, with absence of albuminuria as dependent variable, showed a beneficial impact from lower HbA1c and normal blood pressure (blood pressure < 140/90 mm Hg without antihypertensive treatment). In conclusion, these results suggests that absence of albuminuria after 20 years or more of diabetes is associated with lower HbA1c.
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PMID:Glycemic control in patients with type I diabetes and normoalbuminuria after long diabetes duration. 917 95

We analysed a well-characterized group of 83 patients (43 men, 40 women; mean age +/- SEM: 65.5 +/- 0.6 years at the 10-year examination) with non-insulin-dependent (Type 2) diabetes mellitus (NIDDM) and in 123 control subjects (56 men, 67 women; mean age +/- 0.9 years) retrospectively for the relationship of apolipoprotein E (apo E) genotypes (E2/3, E3/3 vs E3/4, E4/4) to the incidence of clinical macrovascular disease and its risk factors and the incidence of microvascular complications of diabetes during the first 10 years of NIDDM, as well as carotid intima-media thickness measured by B-mode ultrasound at the 10-year examination. In patients with NIDDM, apo E4 genotype showed no relationship to clinical events or carotid intima-media thickness. However, in the control subjects with apo E4, the incidence of non-fatal myocardial infarction during the follow-up was increased (apo E4 positivity: 17.1%; apo E4 negativity 5.1%; p = 0.035) and they had higher common carotid intima-media thickness than those with apo E2/3 or apo E3/3 (1.15 +/- 0.05 mm vs 1.01 +/- 0.03 mm, p = 0.008). Apo E genotype groups showed no relationship to microvascular complications of diabetes, although control subjects with apo E4 positivity showed a higher frequency of microalbuminuria than those lacking apo E4. We conclude that apo E4 was a marker of vascular disease and increased atherosclerosis in non-diabetic subjects, whereas in the diabetic patients these relationships were absent. It is likely that NIDDM per se influences the vascular risk so overwhelmingly that the effects of other risk factors are obscured.
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PMID:Divergent association of apolipoprotein E polymorphism with vascular disease in patients with NIDDM and control subjects. 930 Feb 24


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