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)

Although increased plasma fibronectin (PF) levels have been found in diabetic patients with microalbuminuria, there is still controversy about its clinical implication for detecting early diabetic nephropathy. To evaluate the PF concentration as a possible marker for early diabetic nephropathy, three groups of sex-and age-matched patients were studied I) 22 insulin dependent diabetic (IDDM) patients with microalbuminuria (mean age +/- SEM: 23.3 +/- 3.6 years, mean urinary albumin excretion rate (AER) +/- SEM: 47.1 +/- 39.5 micrograms/min); II) 17 IDDM patients with normoalbuminuria (mean age: 23.4 +/- 4.4 years, mean AER: 7.8 +/- 2.1 micrograms/min) and III) 20 healthy control subjects (mean age: 22.6 +/- 4.1 years, mean AER: 6.7 +/- 2.1 micrograms/min). PF and urinary excretion of albumin were measured by an immunoturbidimetric method using commercially available kits (Boehringer Mannheim GMBH FRG, and Miles Lab., UK). The mean PF was significantly higher in the group with microalbuminuria (406.5 +/- 122.9 micrograms/ml) than in the group with normoalbuminuria (295.6 +/- 96.9 micrograms/ml, P < 0.01) or in the control group (299.54 +/- 105.5 micrograms/ml, P < 0.01). A weak positive correlation was found between PF and urinary albumin values (r = 0.35, P < 0.05). There were no significant correlations between PF and the other variables such as age, duration of diabetes, body mass index, arterial blood pressure, fasting blood glucose, fructosamine and HbA1 in the diabetic patients or in the control group. Our results suggest that the PF concentration could be a weak marker for early diabetic nephropathy. We cannot therefore use PF instead of microalbuminuria because there is only a weak correlation between PF and microalbuminuria.
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PMID:Can we use plasma fibronectin levels as a marker for early diabetic nephropathy. 762 76

The Fanconi-Bickel syndrome is a rare inherited disorder of metabolism characterized by hepatic glyconeogenesis, galactose intolerance, renal Fanconi syndrome with nephromegaly, and glycogen accumulation in proximal renal tubular cells. An 8-year-old patient with this disease and severe rickets due to medically resistant hypophosphatemia was found to have the previously unrecognized complication of renal glomerular hyperfiltration, microalbuminuria, and diffuse glomerular mesangial expansion. Similar to patients with glucose-6-phosphatase deficiency, the glomerular disease in this patient resembles incipient diabetic nephropathy. The Fanconi syndrome may be due to the defective transport of glucose at the proximal tubular basolateral membrane, which results in accumulation of glucose and secondarily glycogen within tubular cells. Since the metabolic defect, as evidenced by glycogen accumulation, selectively involves proximal renal tubular cells in the kidney of patients with Fanconi-Bickel syndrome and glucose-6-phosphatase deficiency, the abnormalities in renal glomerular hemodynamics and mesangial construct in these rare diseases are likely due to renal tubular factors, if the mechanism originates in the kidney. A delineation of these phenomena may further our understanding of the pathogenesis of diabetic nephropathy.
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PMID:Diabetes-like renal glomerular disease in Fanconi-Bickel syndrome. 763 12

1. In epidemiological studies microalbuminuria, i.e. slightly elevated urinary albumin excretion rate, predicts increased atherosclerotic vascular morbidity and mortality. This study aimed to test the hypothesis that microalbuminuria in clinically healthy subjects is associated with a systemic transvascular albumin leakiness. In animal experiments the outflux of albumin and lipids to the arterial wall are highly correlated, and both are elevated in atherosclerosis. 2. All participants were recruited at random from a population-based epidemiological study, where the upper decile of urinary albumin excretion rate was 6.6 micrograms/min. Twenty-seven patients with persistent microalbuminuria (urinary albumin excretion rate 6.6-150 micrograms/min), and 56 age- and sex-matched control subjects with persistent normoalbuminuria (UAER < or = 6.6 micrograms/min) were studied. 3. The systemic transvascular albumin leakage was measured as the fractional disappearance rate of 125I-labelled albumin from the total plasma compartment in 1 h after intravenous injection. 4. The fractional disappearance rate of albumin from the plasma compartment was higher in the microalbuminuric than in the normoalbuminuric group [5.8 (95% confidence interval 5.3-6.2; n = 27) versus 5.0 (4.6-5.5; n = 56)%/h, P < 0.05]. The positive correlation between urinary albumin excretion rate on continuous scale (logarithmically transformed) and the fractional disappearance rate of albumin from the plasma compartment [slope 0.4 (95% confidence interval 0.1-0.7; n = 83), r = 0.29, P < 0.005] was independent of age, sex, smoking status, blood pressure, body size, plasma volume, plasma albumin concentration and concentrations of blood glucose, serum insulin and serum lipids. 5. In conclusion, microalbuminuria is an independent marker of systemic transvascular albumin leakiness in clinically healthy subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Microalbuminuria reflects a generalized transvascular albumin leakiness in clinically healthy subjects. 763 45

We have evaluated the feasibility of monitoring the 24-hour urinary excretion rate of C-peptide (U-CPR) as a measure of integrated beta-cell function in patients with non-insulin-dependent diabetes mellitus (NIDDM). In 37 normoalbuminuric patients, U-CPR of 117.9 +/- 9.1 micrograms/d (mean +/- SEM) during the poorly controlled glycemic phase (fasting plasma glucose [FPG], 171 +/- 7 mg/dL; hemoglobin A1C [HbA1c], 8.8% +/- 0.4%) was significantly higher than the value of 83.3 +/- 13.7 micrograms/d (P < .001) during the well-controlled phase (FPG, 135 +/- 6 mg/dL; HbA1c, 7.0% +/- 0.2%), although the plasma insulin response to meals was lower during the former phase (53.3 +/- 6.3 microU/mL) versus the latter phase (65.7 +/- 6.6, P < .005). Endogenous creatinine clearance (Ccr) was significantly elevated during the poorly controlled phase (105.4 +/- 7.3 v 88.7 +/- 4.7 mL/min, P < .005). In 26 microalbuminuric patients, the plasma insulin response was greater during good glycemic control, but U-CPR did not differ between the two phases. Ccr was comparable at two phases in this group (92.7 +/- 7.4 v 91.1 +/- 5.9 mL/min, NS). U-CPR correlated positively with Ccr in both groups (r = .593, P < .001 in normoalbuminuria; r = .585, P < .001 in microalbuminuria). In addition, when biosynthetic human C-peptide was infused intravenously at an identical rate in two healthy subjects, resulting steady-state plasma levels of CPR were lower, and fractional U-CPR was higher during the moderately hyperglycemic phase versus the euglycemic phase.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hyperglycemia facilitates urinary excretion of C-peptide by increasing glomerular filtration rate in non-insulin-dependent diabetes mellitus. 766 95

Plasma glucose, glycated hemoglobin lc (HbAlc), urinary albumin excretion rate (AER) and urinary N-acetyl-glucosaminidase (NAG): creatinine ratio were studied in 100 normotensive diabetic patients with no evidence of overt renal disease and in 45 controls, to find out whether the glycaemic control and incipient nephropathy may influence the urinary excretion of NAG. Twenty-three of the diabetics had microalbuminuria (group II). Group I comprised the 77 diabetics without microalbuminuria. The groups I and II of diabetics were divided into two according to plasma glucose were greater o smaller to 140 mg/dl. The group I of diabetics had greater NAG: creatinine ratio than controls, too (0.41 +/- 0.24 and 0.16 +/- 0.08 mu/mmol creatinine, p < 0.0005); in this group urinary NAG was found to positively correlate with plasma glucose and creatinine (p < 0.0005, r = 0.45). Multiple regression analysis was performed in the whole of diabetics and significant association were identified between urinary NAG excretion and plasma glucose, AER and plasma creatinine (p < 0.0005, r = 0.42). The diabetics with plasma glucose lower to 140 mg/dl had more important correlation NAG: creatinine ratio-AER (p < 0.0001, r = 0.70). It is concluded that measurement of urinary NAG may be of value in the detection of diabetic nephropathy at a potentially reversible stage if the plasma glucose is take into account.
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PMID:[Influence of glycemic blood glucose control and incipient diabetic nephropathy on the urinary excretion of N-acetyl-glucosaminidase (NAG) in diabetes mellitus]. 766 72

Microalbuminuria in diabetic patients is associated with ischemic heart disease and insulin resistance. We previously found a 9% prevalence of microalbuminuria in a nondiabetic population that we have reassessed, investigating associations of microalbuminuria with hypertension, dyslipidemia, hyperinsulinemia, and sodium-lithium countertransport. Of 125 subjects reexamined, 42 had been microalbuminuric 3 years previously. Twelve of these (29%) were microalbuminuric on at least one sample at follow-up, and 30 (76%) were normoalbuminuric on two. Of the 79 previously normoalbuminuric subjects, 12 (15%) became microalbuminuric on one sample, while 67 (85%) remained normoalbuminuric. Subjects who were microalbuminuric at both screening and recall were older (mean +/- SD, 65.9 +/- 11 versus 59.1 +/- 10.2 years, P = .04), with a higher waist-to-hip ratio (0.93 +/- 0.09 versus 0.86 +/- 0.08, P = .008) and at recall, on univariate analysis, had higher specific insulin (44.2 [range, 16.9 to 157.0] versus 28.4 [7.4 to 129.0] pmol/L, P = .005), intact proinsulin (5.1 [1.5 to 11.0] versus 3.0 [0.8 to 14.6] pmol/L, P = .003), and des-31,32-proinsulin (5.0 [0.5 to 9.8] versus 1.0 [0.5 to 12.2] pmol/L, P = .004) concentrations. There was also a significant difference in des-31,32-proinsulin concentration, after adjustment for covariates (P = .013), between subjects classified either as microalbuminuric or as normoalbuminuric at screening. There was no difference in body mass index; fasting blood glucose; systolic or diastolic blood pressure; total, HDL, or LDL cholesterol; triglycerides; plasminogen activator inhibitor-1; or sodium-lithium countertransport activity between consistently normoalbuminuric and persistently microalbuminuric subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Longitudinal study of associations of microalbuminuria with the insulin resistance syndrome and sodium-lithium countertransport in nondiabetic subjects. 767 Sep 46

The prevalence of diabetic microangiopathy (retinopathy, microalbuminuria, and neuropathy) and macroangiopathy (ischemic changes in EKG) in patients with diabetes mellitus was compared between patients newly found on occasion of mass-screening without any symptoms and signs in Funagata, Japan, and patients who visited the outpatient clinic of our university hospital. The mean fasting blood glucose level in the Funagata group was lower, and the mean duration of diabetes was shorter. The prevalence of every microangiopathic complication was significantly lower in the Funagata group than in the outpatient clinic group. However, the prevalence of ischemic changes in EKG was not different between the two groups. The conclusion that prevalence of diabetic microangiopathic complications was primarily related to the degree and duration of hyperglycemia seemed to be in accordance with the results of the Diabetes Control and Complications Trial (DCCT). The role of hyperglycemia for pathogenesis of macroangiopathy and atherosclerosis has been controversial. Not only hyperglycemia but also hypertension, dyslipoproteinemia, and other factors due to insulin resistance resulting from visceral fat syndrome, might be responsible for the occurrence of atherosclerosis.
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PMID:[Risk factor: diabetes mellitus]. 769 23

Prevalence of diabetic nephropathy varies in different racial groups, being especially high in communities that have abandoned an active traditional living and embraced a modern but sedentary life-style. As a new and rapidly developing country, Saudi Arabia has witnessed impressive changes in socio-economic growth and development and concurrently, a disturbing trend in non-insulin-dependent diabetes mellitus (NIDDM). These observations therefore prompted us to investigate the prevalence of microalbuminuria among Saudi Arabians with NIDDM. Two hundred and eleven patients attending a large Diabetic Clinic in Riyadh were screened for microalbuminuria (30-300 mg/24 h). Twenty-seven subjects had clinical proteinuria (dipstick-positive) and were excluded, leaving 184 cases for analysis. Seventy-six subjects (76/184, 41.3%) had microalbuminuria. These subjects had higher fasting plasma glucose concentrations (P = 0.002) and greater body mass index (P = 0.049) than subjects with normal albumin excretion rate (< 30 mg/24 h). There were no significant differences between subjects with and without microalbuminuria with regards to fasting total plasma cholesterol and triglycerides concentrations, frequency of hypertension, duration of diabetes or type of therapy for diabetes. In multivariate analysis, glycaemia (P < 0.005) and years since diagnosis of diabetes (P = 0.05) remained independently associated with albumin excretion rate. We conclude that microalbuminuria is exceedingly common in a clinic-based population of Saudi Arabians with NIDDM and its presence is closely related to glycaemic control. Whether the prevalence of microalbuminuria is truly increased in the diabetic population at large in Saudi Arabia must now await further population-based studies.
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PMID:Prevalence of microalbuminuria in Saudi Arabians with non-insulin-dependent diabetes mellitus: a clinic-based study. 770 92

The clinical characteristics of subjects with a missense glucokinase mutation, gly299-->arg, were studied in a large pedigree, BX, initially characterized by some members having Maturity Onset Diabetes of the Young (MODY). Glucose tolerance, beta cell function and insulin sensitivity were measured with Homeostasis Model Assessment (HOMA) and with a 'Continuous Infusion of Glucose with Model Assessment' (CIGMA) test. Diabetic complications were clinically assessed. Subjects with glucokinase gly299-->arg were the same age, height, and obesity as the subjects without the mutation. Diabetes was usually asymptomatic at diagnosis and was treated with diet alone in 15 of the 18 subjects. Five of the 11 adult females had been diagnosed when they developed gestational diabetes. The fasting plasma glucose concentrations at the time of study were 4.3-12.6 mmol l-1, with the higher levels being in the more obese (p < 0.05) and in the older subjects (p < 0.05). In subjects with the mutation, beta cell function was impaired, being geometric mean 63% (normal-100%) compared with 126% in the subjects without the mutation (p < 0.001) measured by HOMA and in a subset assessed by CIGMA 59% and 127% (p < 0.01), respectively. There was no difference in fasting insulin concentrations, insulin sensitivity, lipid concentrations or blood pressure between the groups. The haemoglobin A1c was raised (mean 6.5% compared with 5.5% in the subjects without the mutation), but microvascular and macrovascular complications were uncommon. The subjects with the mutation did not have microalbuminuria but had an impaired vibration perception threshold compared with subjects without the mutation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical characteristics of subjects with a missense mutation in glucokinase. 775 56

Increased fracture frequency and low bone mass have each been reported in patients with diabetes. To see if these were related to increased bone resorption we have measured the urinary excretion of hydroxyproline in 73 patients with Type 1 (insulin-dependent) diabetes, 67 patients with Type 2 (non-insulin-dependent) diabetes, and 75 control subjects. Hydroxyproline excretion was increased in both types of diabetes: Type 1: 21 (10-36) (median (IQR) mumol mmol creatinine-1; Type 2: 25 (13-43) mumol mmol creatinine-1; control: 10 (6-22) mumol mmol creatinine-1 (p < 0.0001 and < 0.0002, respectively). Hydroxyproline excretion was not related to age, duration of diabetes or blood glucose control. Neither was it different in patients with or without retinopathy, neuropathy and macrovascular disease. However it was higher in patients with microalbuminuria at 35 (20-53) mumol mmol creatinine-1 than in those with normal protein excretion (25(13-37) mumol mmol creatinine-1 p = 0.03) or those with established proteinuria (18(8-26) mumol mmol creatinine-1 p = 0.001). We conclude that there is evidence of increased bone resorption in diabetes and that this is related to alterations in renal function.
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PMID:Hydroxyproline excretion is increased in diabetes mellitus and related to the presence of microalbuminuria. 868 52


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