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The concept of microalbuminuria is reviewed. Measuring the urinary albumin excretion rate and testing for microalbuminuria is well established in the control and treatment of patients with insulin-dependent diabetes mellitus. Microalbuminuria predicts nephropathy and early cardiovascular death. In the presence of microalbuminuria, frequent examinations are warranted for early detection of retinopathy, hypertension and for optimizing the glycaemic control. In patients with non-insulin dependent diabetes, the independent value of microalbuminuria as a cardiovascular risk factor is not yet clarified. The urinary albumin excretion rate should be measured at diagnosis, because the indications are that presence of microalbuminuria reinforces the urge to intervene against other well-documented cardiovascular risk-factors (hypertension, dyslipidemia, tobacco and obesity). In the non-diabetic population there is accumulating evidence that an elevated urinary albumin excretion rate is associated with early cardiovascular morbidity and mortality. Large scale cross-sectional and prospective studies are needed in order to further clarify the role of microalbuminuria as an independent risk factor in the background population.
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PMID:[Microalbuminuria--a valuable diagnostic parameter]. 827 36

It is not clear whether elevated levels of the fibrinolytic inhibitor, plasminogen activator inhibitor-1 (PAl-1) in Type 2 diabetes mellitus are the result of obesity or coexistent atherosclerosis. Therefore the relationship between PAl-1 and insulin resistance, determined by the homeostasis model assessment (HOMA) was investigated in a group of 26 insulin-resistant, normotensive newly diagnosed Type 2 diabetic patients with a low probability of atherosclerosis. Compared with a normal control group, closely matched for body mass index (BMI), fibrinolytic activity was depressed in the diabetic patients due to elevated levels of the inhibitor PAl-1, 17.6 (11.1-28) vs 8.4 (4.9-14.1) IU ml-1, p < 0.001. PAl-1 was related to BMI, r = 0.59, p < 0.001 plasma insulin, r = 0.66, p < 0.001; insulin resistance, r = 0.54, p < 0.005 and urinary albumin excretion, r = 0.48, p < 0.01, but not HbA1c or fasting glucose. PAl-1 was not related to blood pressure or plasma triglyceride levels. This study suggests that at the time of diagnosis of Type 2 diabetes mellitus, elevated PAl-1 levels are already linked to other risk factors for vascular disease including hyperinsulinaemia, insulin resistance, and urinary albumin excretion, and this is not the result of obesity or coexistent atherosclerosis.
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PMID:The relationship between plasminogen activator inhibitor-1 and insulin resistance in newly diagnosed type 2 diabetes mellitus. 840 25

The aim of the present work was to investigate the impact of disease states and environmental and host factors on the glucuronidation of oxazepam. Glucuronidation represents quantitatively one of the most important metabolic conjugation pathways (phase II) in man for the inactivation and detoxication of xenobiotics and endogenous compounds and the liver is the major site for it to take place. Far less attention has been paid to the conjugation reactions in previous clinical research in this field compared to the immense interest in the oxidative biotransformation pathways (phase I). This fact is mainly due to the latter giving rise to active or reactive metabolites with a toxicological potential. The metabolism of oxazepam expresses exclusively the capacity for glucuronide formation. It was a prerequisite to establish the bioavailability of oxazepam prior to succeeding studies on the oral disposition of the drug. A preparation for intravenous administration was created. Clearance was chosen as measurement of the capacity to glucuronidate oxazepam. Severe decompensated liver disease was associated with a significant decrease in oxazepam clearance, that became even more obvious when corrected for by a diminished binding to plasma proteins. This increase in free fraction of oxazepam was substantial and could mainly be accounted for by low plasma albumin values. The results are in part a settlement with earlier studies on glucuronidation in liver disease and they may undoubtedly be ascribed to the severe degree of liver disease. For the first time it was shown that hypothyroidism led to a decline in the clearance and metabolism of oxazepam and paracetamol that is mainly biotransformed by glucuronidation. It was concluded that the enzymes responsible for glucuronidation in hypothyroidism are under the influence of thyroid hormones as is the case with oxidative enzymes. Further studies focused on the effect of host and environmental factors on glucuronidation. A commercially available very low calorie product for the treatment of obesity resulted in a decrease in oxazepam clearance and a lack of co-factors as a consequence of the low calorie intake was explanatorily proposed. Beta-adrenoceptor antagonists are often prescribed together with other drugs and close knowledge on interactions is mandatory but insufficient in regard of drugs being glucuronidated. Despite the mutual metabolic pathway labetalol exerted no dispositional alterations concerning oxazepam. It was moreover suggested that very elderly subjects between the age of 80 to 94 years had a reduced clearance of oxazepam.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Factors and conditions affecting the glucuronidation of oxazepam. 841 17

In subjects with insulin-dependent diabetes mellitus, microalbuminuria has been associated with increased triglyceride and lipoprotein (a) (Lp[a]) concentrations and increased blood pressure. However, few studies have examined whether this association is present in subjects with non-insulin-dependent diabetes mellitus (NIDDM). We measured lipids, lipoproteins, Lp(a), blood pressure, and albumin excretion in 234 subjects with NIDDM from the San Antonio Heart Study, a population-based study of diabetes and cardiovascular disease. Seventy-two subjects had microalbuminuria (> or = 30 mg/dl). These subjects had increased systolic and diastolic blood pressures and higher fasting glucose concentrations relative to subjects without microalbuminuria. However, there were no significant differences between subjects with and without microalbuminuria with respect to lipids, lipoproteins, Lp(a), self-reported myocardial infarction, obesity, or body fat distribution. Subjects with diabetic retinopathy had increased microalbuminuria. In multivariate analysis both glycemia and blood pressure continued to be significantly related to the presence of microalbuminuria. We conclude that NIDDM subjects with microalbuminuria have elevated blood pressure and more severe glycemia but do not have a significantly more atherogenic pattern of lipids, lipoproteins, or Lp(a) than subjects without microalbuminuria.
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PMID:Cardiovascular risk factors in non-insulin-dependent diabetic subjects with microalbuminuria. 842 56

A total of 412 Hong Kong Chinese diabetic patients were studied on at least two occasions 8-16 weeks apart. Although 28% were insulin-treated, only 3.6% had insulin-dependent diabetes (IDDM). In the remaining 397 patients with non-insulin-dependent diabetes (NIDDM), the mean (s.d.) body mass index (BMI) was 24.4 +/- 3.2 kg/m2 in females and 24.2 +/- 3.2 kg/m2 in males. Obesity was present in 17% of males (BMI > 27 kg/m2) and 40% of females (BMI > 25 kg/m2). Established hypertension was present in 49%. Abnormal albuminuria, defined as a mean urinary albumin/creatinine (UA/Cr) ratio greater than 5.4 mg/mmol based on two random spot urine samples, was present in 47%. On stepwise multiple regression analysis, UA/Cr ratio (R2 = 0.34, F = 65.4, P < 0.001) showed significant associations with systolic blood pressure (standardized regression coefficient beta = 0.40, P < 0.001), plasma creatinine concentration (beta = 0.27, P < 0.001) and glycosylated haemoglobin (beta = 0.20, P < 0.001). While the prevalence of hypertension increased with increasing severity of proteinuria, 40% of normoalbuminuric patients had hypertension. Among patients diagnosed before the age of 35 (n = 67), 52% were insulin-treated although only 10% were insulin-dependent. Among these NIDDM patients of young onset (n = 59), obesity was present in 25% of males and 56% of females. Overall, 18% of these patients had a blood pressure greater than 140/90 mmHg and 27% had abnormal albuminuria. In Hong Kong Chinese, diabetes mellitus is predominantly non-insulin-dependent even in the young. Obesity is more prevalent among females. Abnormal albuminuria is relatively common and is closely associated with hypertension and glycaemic control. In the light of increasing prevalence of diabetes among overseas Chinese, our findings may have important implications in the management of Chinese diabetic patients.
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PMID:Obesity, albuminuria and hypertension among Hong Kong Chinese with non-insulin-dependent diabetes mellitus (NIDDM). 849 35

The prevalence of hypertension in diabetes is significantly higher than in non-diabetics, perhaps twice as common. The excess is related to diabetic nephropathy, mainly in type 1 diabetes, to obesity, mainly in type 2 diabetes, but also to increased sympathetic activity. Furthermore, the increased prevalence of hypertension may relate to insulin resistance and its sequelae. Insulin resistance leads to hyperinsulinemia, relates to increased LDL and reduced HDL levels, causes the development of impaired glucose tolerance and type 2 diabetes and might also be causally related to the onset of hypertension. Syndrome X has relevant therapeutic implications in the management of hypertension. Hypertension is a major risk factor for large vessel disease in diabetics and also a risk factor for microangiopathy, particularly nephropathy. The incidence of atherosclerotic disease is dramatically increased in both type 1 and type 2 diabetics and is the major cause of morbidity and premature death mainly in patients with raised urinary albumin excretion. Thus, diabetics show a two-fold increased risk of coronary heart disease, 2-6 fold increased risk of stroke and a several-fold increased risk of peripheral vessel disease. Some evidence suggests that hypertension may be a risk factor for retinopathy, particularly its progression, but surely hypertension is a significant risk factor for nephropathy, accelerating its progression and perhaps even causing the onset of the glomerulopathy. The mechanisms by which hypertension might contribute to the evolution of both large vessel as well as small vessel disease is still unknown, although increased capillary leakage and vascular endothelium alterations might be important factors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hypertension and diabetes]. 856 58

A total of 359 Wanigelas from Papua New Guinea and 1041 Nauruans had urinary albumin concentrations (UAC), serum insulin, and a number of cardiovascular disease (CVD) risk factors measured during population-based surveys of non-insulin-dependent diabetes mellitus. These data were used to explore the hypothesis that microalbuminuria is closely associated with insulin resistance and the metabolic syndrome. In both Nauruans and Wanigelas, worsening glucose tolerance was associated with increasing prevalence of micro- and macroalbuminuria. Within each category of glucose tolerance, microalbuminuria was associated with general worsening of cardiovascular risk factors including lipid concentrations, blood pressure and obesity, although few of the associations were statistically significant. Correlations between UAC and markers of insulin resistance (fasting insulin, fasting insulin/glucose ratio and HOMAS%, a computer-modelled estimate of insulin sensitivity) were weak and inconsistent irrespective of glucose tolerance status. Relationships between insulin sensitivity and urinary albumin in normoglycaemic Wanigelas and Nauruans, and in diabetic Nauruans, were no longer significant after adjusting for fasting glucose and body mass index. While microalbuminuria in Nauruans and Wanigelas was associated with cardiovascular risk factors irrespective of glucose tolerance, it seems unlikely on the basis of these results that the relationship is mediated through a common association with insulin resistance.
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PMID:Microalbuminuria, cardiovascular risk factors, and insulin resistance in two populations with a high risk of type 2 diabetes mellitus. 873 26

Renal blood flow decreased depending on the increase in exercise intensity. The kidneys may have roles to conserve the electrolytes and body fluid, and maintenance of acid-base balance during and after severe exercise. Increases in plasma hormones involved in the regulation of electrolyte-water balance, and decreases in urine flow, Na, Cl and K excretions into urine were observed following moderate exercise under a warm environment. Inhibition of electrolytes and water excretion into urine following exercise in water was less than that following exercise on land. Exercise in water is good for patients with hypertension, obesity and a mild renal disease who have tendency to conserve sodium and/or water. Increase in urinary albumin excretion, glomerular-type proteinuria was observed after moderate exercise (50 approximately 75%HRmax) in the obese individuals who had higher levels of hematocrit, serum concentrations of triglyceride, total cholesterol, LDL-cho, apoprotein B, CIII, and fasting insulin. The findings suggest that moderate exercise causes a latent abnormality of renal glomerular basement membrane in the obese individuals who had an early disturbance of glucose-fatty metabolism.
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PMID:[Sports and measurement of components in urine--responses of renal blood flow, electrolytes and hormones and of excretion of proteins into urine to exercise]. 874 92

To investigate the role of sodium in obesity induced hypertension, Wistar fatty rats (WFR) were employed. This rat has the following characteristics: (1) hyperglycemia, (2) hyperinsulinemia, and (3) hypertriglycemia. Four percent sodium chloride with constant amount of food intake was administered to these rats from 8 to 16 weeks. During this period, body wt, food intake, water consumption, urine volume, systolic blood pressure, urinary excretion of sodium and potassium, urinary albumin excretion, plasma sodium and potassium, and plasma glucose and immunoreactive insulin (IRI) were measured before, and twice more during eight weeks. No remarkable changes were observed in plasma glucose level during these periods between the two groups. On the other hand, in group 1 IRI significantly increased compared with group 2. Mean blood pressure was increased from 110 +/- 5 to 130 +/- 8 mm Hg (P < 0.01). To ascertain whether this salt sensitivity relates to the abnormalities in pressure-natriuresis responses, the pressure-natriuresis (P-N) was characterized. The P-N curve in WFR was shifted to the right and its slope was flattened compared to its control Wistar lean rats. In conclusion, an excess of dietary sodium intake may contribute to an elevation of blood pressure in Wistar fatty rat with hyperglycemia and hyperinsulinemia. This salt sensitivity may change the abnormal pressure-natriuresis responses.
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PMID:Sodium balance and hypertension in obese and fatty rats. 874 40

To challenge the view that resistance to insulin-mediated glucose uptake in noninsulin-dependent diabetes mellitus (NIDDM) is limited to patients with microalbuminuria, high blood pressure, or obesity, we compared measurements of insulin resistance in 29 normal volunteers and 31 normotensive patients with NIDDM (mean +/- SE fasting plasma glucose, 160 +/- 10 mg/dL). The patients with NIDDM were nonobese (body mass index, < 27 kg/m2), with urinary albumin excretion (UAE) less than 20 micrograms/min on the basis of two overnight urine collections. The two groups were similar in age and body mass index. Although patients with NIDDM had neither high blood pressure nor microalbuminuria; both their blood pressure (125 +/- 2/79 +/- 1 vs, 113 - 2/73 +/- 2 mm Hg) and UAE excretion (4.7 +/- 0.58 vs. 2.12 +/- 0.17 micrograms/min) were somewhat higher than those in the control population. Resistance to insulin-mediated glucose disposal was quantified by measurement of the steady state plasma glucose (SSPG) and insulin (SSPI) concentrations during the last 30 min of an 180-min infusion of somatostatin (5 micrograms/min), insulin (25 mU/min-m2), and glucose (240 mg/min-m2). The results showed that SSPI concentrations were similar in the two groups (64 +/- 3 vs. 62 +/- 3 microU/mL), but SSPG concentrations were approximately twice as high in patients with NIDDM (258 +/- 15 vs. 139 +/- 11 mg/dL;P < 0.001); demonstrating the presence of severe insulin resistance. Furthermore, the magnitude of the differences in the SSPG values of the two groups did not change and remained highly significant when adjusted for small differences in age, body mass index, blood pressure, and UAE. Finally, SSPG did not correlate with age, body mass index, blood pressure, or UAE in either group. These data again demonstrate that insulin resistance exists in patients with NIDDM, and that this defect is present in the absence of obesity, high blood pressure, or microalbuminuria.
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PMID:Resistance to insulin-mediated glucose disposal in patients with noninsulin-dependent diabetes mellitus in the absence of obesity or microalbuminuria--a Clinical Research Center study. 877 92


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