Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011860 (type 2 diabetes)
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Albumin excretion rate measured by new immunoassays and semiquantitative tests is advocated as a means for early detection of diabetic nephropathy. We determined albumin excretion rate in 276 patients. Albumin excretion rate was normal in 66%, within the microalbuminuric range in 27%, and within the macroproteinuric range in 7%. Significant predictors of albumin excretion rate included presence of hypertension and glycosylated hemoglobin level in type I diabetes mellitus, and years since diagnosis in type II diabetes mellitus. A semiquantitative test was deemed to be of limited diagnostic value. We conclude that testing for early diabetic nephropathy in routine clinical practice gives valuable information and that determination by a quantitative immunoassay based on a single 24-hour urine sample is preferable. The optimal frequency of screening and the levels that determine progressive renal disease have yet to be established.
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PMID:Microalbuminuria in clinical practice. 188 40

For the early diagnosis of diabetic nephropathy, it is best to use the albumin excretion rate (AER). However, it is a complicated test to perform in the outpatient setting, and it is sometimes affected by inaccurate urine collection. Therefore, we have used the albumin/creatinine ratio, which is measured simply with randomly collected urine, for evaluation of microalbuminuria and found it to be of equal diagnostic value to the AER. The AER, albumin/creatinine ratio, and creatinine excretion rate were measured in 86 patients with NIDDN who were negative for proteinuria. Urine was obtained after bed rest and in the outpatients department (without rest). 1) The reproducibility of time-restricted urine sampling was investigated using the rate of creatinine excretion. The mean coefficient of variation was found to be 42%, and inaccurate urine sampling appeared to cause variation in the AER. 2) The AER and albumin/creatinine ratio obtained in the outpatient setting were higher than those after bed rest, and urine collection at the time of outpatient examination was considered to be more useful than that after bed rest. To check variations in urine collection at the time of outpatient examination, the albumin/creatinine ratio in random urine samples was superior on the basis of the correlation coefficients to urine obtained after bed rest. 3) The urinary creatinine excretion rate showed a significant sex difference (males: 0.823 +/- 0.152 mg/g. creat., females: 0.577 +/- 0.194 mg/g. creat) (p less than 0.001), but there was no significant difference for BMI and age. The relationship between each level of microalbuminuria and the creatinine excretion rate did not change significantly. 4) The following formula was used to calculate the albumin/creatinine ratio corresponding to the AER. Albumin/creatinine ratio formula; (see text) An AER of 30 micrograms/min thus corresponds to an albumin/creatinine ratio of 36 mg/g. creat. for males and 51 mg/g. creat. for females. 5) The percentage of positive results for microalbuminuria in patients with NIDDM showed that the albumin/creatinine ratio and the AER were equal as diagnostic criteria, when the sex difference was taken into consideration. Thus, the albumin/creatinine ratio is equal to the AER for evaluation of microalbuminuria, and it is a simple and convenient test to use in daily clinical practice.
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PMID:[Clinical evaluation of the albumin/creatinine ratio in outpatients with diabetes]. 206 14

Familial clustering of diabetic nephropathy points to genetic susceptibility. The observation that in non-diabetic subjects microalbuminuria occurs more frequently in the presence of a parental history of diabetes supports this hypothesis. However, the role of inherited factors in poorly understood in non-insulin dependent diabetes mellitus (NIDDM). This study investigated the albumin excretion rate in non-diabetic offspring of NIDDM patients with increased albumin excretion rate (> 20 micrograms/min) or normal albumin excretion rate (< 20 micrograms/min). We recruited 20 offspring of NIDDM patients with increased albumin excretion rate (A-off) and 20 offspring rate (N-off), matched for age, sex, body mass index, blood pressure and estimated protein intake. All offspring were normotensive, had normal creatinine clearance, normal glucose tolerance and sterile urine collection. Albumin excretion rate was measured on three sterile overnight urine collections and median values were used for calculations. Albumin excretion rate was significantly higher in A-off than in N-off (7.7 +/- 1.2 vs 3.4 +/- 0.6 micrograms/min p<0.01) and significantly related to parents' albumin excretion rate (p<0.01, r=0.53). These results suggest that an increased glomerular permeability is present in non-diabetic offspring of NIDDM patients with increased albumin excretion rate.
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PMID:Albumin excretion rate levels in non-diabetic offspring of NIDDM patients with and without nephropathy. 869 Jan 75

Proteinuria and nephropathy have been found to cluster in families of non-insulin-dependent diabetic (NIDDM) Pima Indian, and in Caucasian insulin-dependent diabetic (IDDM) patients. No information is at present available for Caucasian NIDDM patients. The aim of the present study was to determine whether micro-macroalbuminuria (AER+) is associated with albumin excretion rate abnormalities in diabetic and non-diabetic siblings of probands with NIDDM and AER+. We identified 169 Caucasian families with one NIDDM proband (the patient with longest known NIDDM duration) (101 families with only NIDDM siblings, 33 families with both NIDDM and non-NIDDM siblings and 35 families with only non-NIDDM siblings). Of the probands 56 had AER+ [Prob-NIDDM-(AER+)], 78 had AER-[Prob-NIDDM-(AER-)], 74 siblings of Prob-NIDDM-(AER+), and 113 siblings of Prob-NIDDM-(AER-) also had NIDDM. Data on albuminuria and retinopathy from multiple sibling pairs when the size of the sibship was more than two was adjusted according to a weighting factor. The odds ratio for AER+, in siblings of Prob-NIDDM-(AER+) adjusted for age, hypertension, glycated haemoglobin A1c and other confounding variables was 3.94 (95% confidence intervals: 1.93-9.01) as compared to siblings of Prob-NIDDM-(AER-). The 74 siblings of Prob-NIDDM-(AER+) had higher prevalence of proliferative retinopathy than siblings of Prob-NIDDM-(AER-) (14 vs 2%; p < 0.01). We also identified 66 non-diabetic siblings of 41 NIDDM probands with AER+ and 36 non-diabetic siblings of 27 NIDDM probands with AER-. Albumin excretion was two times higher, although still within the normal range, in the non-diabetic siblings of Prob-NIDDM-(AER+) than in siblings of Prob-NIDDM-(AER-) [median = 13.5 (range 0.5-148) vs 6.6 (range 1-17) micrograms/min (p < 0.05)]. In conclusion higher rates of albumin excretion aggregate in Caucasian families with NIDDM. Proliferative retinopathy is more frequently observed in families showing a clustering of AER+ and NIDDM. These findings suggest that familial factors play a role in the pathogenesis of renal and retinal complications in NIDDM.
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PMID:Clustering of albumin excretion rate abnormalities in Caucasian patients with NIDDM. The Italian NIDDM Nephropathy Study Group. 924 3

The pathogenetic process of diabetic retinopathy and the role of different systemic risk factors in IDDM and NIDDM is not completely understood. The aim of the present cross-sectional clinical study was (1) to compare the prevalence of systemic risk factors for diabetic retinopathy in IDDM and NIDDM patients, (2) to determine relations between these risk factors and the degree of retinopathy and (3) to evaluate the relationship between retinopathy and neuropathy. The study included 1,218 IDDM and 784 NIDDM patients attending our hospital during 1994. The mean diabetes duration was 15.4 and 13.2 years, respectively. IDDM patients with proliferative retinopathy were characterized by higher mean age of 46.4 +/- 1.08 vs. 21.8 +/- 0.42 years and longer diabetes duration of 30.0 +/- 0.79 vs. 7.7 +/- 0.26 years. Among the NIDDM patients, those ones with proliferative retinopathy had the lowest mean age of 40.5 +/- 1.42 vs. 49.7 +/- 0.61 years (p < 0.01) at diabetes manifestation. There was no statistical difference between mean HbA1c concentrations in relation to retinopathy stages. Albumin excretion was increased in both IDDM and NIDDM patients with proliferative retinopathy (p < 0.01) along with increased BMI of IDDM and increased insulin requirement of NIDDM patients (p < 0.01). Multiple regression analysis showed that proliferative retinopathy with the inclusion of non-proliferative retinopathy of IDDM and NIDDM patients was significantly correlated with diabetes duration, albumin excretion, somatic and autonomic neuropathy (p < 0.01). In NIDDM patients proliferative retinopathy with the inclusion of non-proliferative retinopathy was correlated with the age at diabetes manifestation and with cholesterol levels (p < 0.05). In IDDM and NIDDM patients proliferative retinopathy was found to be correlated with somatic and autonomic neuropathy, albumin excretion (p < 0.01) and hypertension (p < 0.05). The importance of the significant correlation of autonomic neuropathy both with background and proliferative retinopathy in IDDM and NIDDM patients needs to be prospectively investigated.
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PMID:Relations between diabetic retinopathy and cardiovascular neuropathy--a cross-sectional study in IDDM and NIDDM patients. 943 26

Regulation of mesangial matrix deposition is a dynamic phenomenon involving synthetic and degradative processes. The latter involve a number of matrix metalloproteinases (MMP) and tissue inhibitors of matrix metalloproteinases (TIMP). Experimental studies suggest that mesangial matrix degradation is inhibited in diabetic nephropathy, and that this phenomenon has a pathogenic role. The expression of genes for MMP2 and TIMP2 in human diabetic nephropathy was investigated. Reverse transcription polymerase chain reaction was carried out in microdissected glomeruli and tubulo-interstitium obtained from kidney biopsies. We studied 16 NIDDM patients, 5 patients with glomerulonephritis or chronic kidney transplant rejection, and 5 normal control subjects. Albumin excretion rate and renal histology for NIDDM patients were available. Contrary to TIMP2 which was expressed both in tubulo-interstitium and glomeruli in almost all renal biopsies, MMP2 gene down-regulation was observed in glomeruli from all NIDDM patients, irrespective of the albumin excretion rate, and of renal histology. In contrast, this gene was expressed in biopsies from other subjects (chi(2) = 20.6; p = 0.000). In conclusion, this study demonstrates that: 1) in glomeruli of NIDDM patients the MMP2 gene is down-regulated; 2) in biopsies of NIDDM patients the MMP2/TIMP2 pattern is peculiar for NIDDM; 3) the MMP2 gene down-regulation is observed in all NIDDM patients, irrespective of the level of albuminuria and of renal histology. MMP2 gene down-regulation seems to be a molecular epiphenomenon of diabetes, rather than a marker of diabetic nephropathy.
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PMID:Down-regulation of glomerular matrix metalloproteinase-2 gene in human NIDDM. 944 53

In a randomized, double-blind, placebo-controlled study, we investigated in normotensive type 2 diabetics with microalbuminuria the effect of ramipril, an ACE inhibitor, on urine albumin excretion and serum lipids. A total of 1,882 patients were screened for urine microalbumin consecutively by dipstick test, Rapi Tex-Albumin test and RIA. The final 28 normotensive and microalbuminuric patients were assigned to receive either ramipril (1.25 mg/d, n = 16) or placebo (n = 12) for 12 weeks. Throughout the study, both groups had no changes in blood pressure, fasting plasma glucose, HbA1C, serum creatinine and electrolytes and no difference in creatinine clearance. At week 12 only the placebo group showed the significant increment of urine albumin excretion and triacylglycerol (30.6 +/- 38.3 to 39.0 +/- 19.7 and 167 +/- 64 to 208 +/- 77 mg/dl, respectively) but the decrement of HDL-cholesterol (46 +/- 16 to 35 +/- 6 mg/dl). During a 3 month period, increased urine albumin excretion was observed in normotensive type 2 diabetes with microalbuminuria who received only placebo. We conclude that ramipril may arrest the progression of albumin excretion and had favorable effects on serum lipids. Ramipril was safe and well-tolerated without untoward side effects during the study period.
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PMID:Impediment of the progressions of microalbuminuria and hyperlipidemia in normotensive type 2 diabetes by low-dose ramipril. 973 24

The American Diabetes Association emphasizes fasting plasma glucose (FPG) levels, rather than the oral glucose tolerance test (OGTT), to diagnose diabetes mellitus. The diagnostic cutoff for FPG is 126 mg/dL (7.0 mmol/L). A 2-hour plasma glucose level of 200 mg/dL (11.1 mmol/L) or more during an OGTT or a random plasma glucose level of 200 mg/dL (11.1 mmol/L) or more also is diagnostic of diabetes. The 100-g, 3-hour OGTT remains the "gold standard" for gestational diabetes mellitus (GDM). Two of 4 samples exceeding cutoffs (fasting, > or = 105 mg/dL [5.8 mmol/L]; 1 hour, > or = 190 mg/dL [10.5 mmol/L]; 2 hours, > or = 165 mg/dL [9.2 mmol/L]; 3 hours, > or = 145 mg/dL [8.0 mmol/L]) indicate GDM. An effective GDM screening test is plasma glucose 1 hour after a 50-g oral glucose load. Tight control, which requires self-monitoring of blood glucose, reduces microvascular complications for patients with type 1 or type 2 diabetes. Patients with well-controlled diabetes have glycohemoglobin concentrations of 7% AIc (0.07 AIc/A) or less. Microalbuminuria indicates early, reversible, diabetic nephropathy. The random urine albumin-creatinine ratio is a convenient effective screening test. Albumin-creatinine ratios in the 0.03 to 0.30 (g/g) range indicate microalbuminuria.
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PMID:Laboratory diagnosis and monitoring of diabetes mellitus. 1054 54

The aim of the study was to test the hypothesis that in diabetic patients without overt nephropathy there may be a correlation between the activity of natural anticoagulant proteins and glomerular dysfunction. Assays for functional activity of proteins S and C, measurements of urinary albumin excretion, lipid parameters and haemoglobin A1c were performed in 91 patients with type 1 diabetes mellitus and 85 patients with type 2. Patients with type 1 diabetes and microalbuminuria had significantly higher mean age (44.1 +/- 10.9 vs. 37.9 +/- 12.7 years; p<0.05), fibrinogen level (3.75 +/- 1.0 vs. 3.21 +/- 0.8 g/l; p<0.01), protein S activity (92.3 +/- 17.6 vs. 84.5 +/- 15.5%; p<0.05) and higher prevalence of retinopathy (p<0.01) and macrovascular disease (p<0.01) than those with normoalbuminuria. Albumin excretion was significantly correlated to age (r=0.25, p<0.05), fibrinogen level (r=0.39, p<0.01), protein S activity (r=0.27; p<0.05), total cholesterol (r=0.23; p<0.05), apoprotein B (r=0.22; p<0.05), retinopathy (r=0.33; p<0.01) and macrovascular disease (r=0.33; p<0.01). Patients with type 2 diabetes mellitus and microalbuminuria had significantly higher apoprotein B levels (1.17 +/- 0.3 vs. 1.06 +/- 1.2 mg/dl; p<0.05) than those with normoalbuminuria, and apoprotein B was significantly correlated to albumin excretion (r=0.22; p<0.05). In a multivariate model of type 1 diabetes mellitus with fibrinogen, protein S and C activity, cholesterol, triglycerides, haemoglobin A1c, retinopathy, and macrovascular disease as independent parameters (r=0.53; p<0.003), there was significant independent correlation of fibrinogen (beta=0.28; p<0.01), protein S activity (beta=0.27; p<0.05) and retinopathy (beta=0.21; p<0.01) with albumin excretion. We conclude that in type 1 diabetes, relative elevation of fibrinogen level and protein S activity appear in the early stages of development of diabetic nephropathy, and may be related to the pathogenesis of diabetic kidney disease.
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PMID:Urinary albumin excretion is correlated to fibrinogen levels and protein S activity in patients with type 1 diabetes mellitus without overt diabetic nephropathy. 1514 63

Valsartan as angiotensin-II receptor antagonist in normotensive diabetic may provide kidney and heart protection. It also increases insulin receptor sensitivity. The aim of this study was to investigate the effect of valsartan on lipid profile in normotensive type 2 diabetic patients. Fifteen normotensive patients with type 2 diabetes mellitus, mean age 58.6+/-5.6 years, with mean BMI 28.6+/-2.5 kg/m2, were treated with valsartan in doses 20-80 mg per day. After a year of treatment with valsartan we witnessed significant decrease in total cholesterol level (6.8+/-1.4 to 5.4+/-0.9 mmol/l, p<0.05) and low density lipoprotein (LDL) from 4.5 to 2.7 mmol/l. Triglycerides were not affected significantly. Albumin excretion in urine significantly decreased. Level of basal insulin (from 256 to 78 pmol/l) has, also, decreased. In type 2 diabetes mellitus, the use of angiotensin-II receptor antagonists reduces the progression from micro to macro albuminuria. These results suggest that the angiotensin-II receptor antagonist decreases lipid serum levels in normotensive diabetes mellitus type 2 patients.
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PMID:The effects of valsartan on lipid profile in normotensive type 2 diabetic patients. 1613 56


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