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      Prevalence of Microalbuminuria and Relationship to the Risk of Cardiovascular Disease in the Japanese Population

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          The prevalence of microalbuminuria and its relationship to cardiovascular disease risk factors were examined in subjects participating in an annual physical and laboratory examination program. The urinary albumin concentration and the urinary albumin/creatinine ratio were determined in morning urine specimens. A turbidimetric immunoassay was used for the measurement of urinary albumin. Of the 731 subjects, 41 (5.6%) who were weakly positive or positive on a routine dipstick test for protein were excluded from the final analysis of data. Microalbuminuria was present in 14.5% of the men, in 12.4% of the women, and in 13.2% of the entire subject population when defined as a urinary albumin concentration of 30–299 μg/ml. The prevalence of microalbuminuria was significantly higher in subjects with a high normal blood pressure (15.0%) or hypertension (26.2%) as compared with normotensive subjects (6.5%). Subjects with impaired glucose tolerance (24.3%) or hyperglycemic subjects (50.0%) had a significantly higher prevalence of microalbuminuria than normoglycemic subjects (11.3%). The prevalence of microalbuminuria was significantly higher in subjects with left ventricular hypertrophy (47.1%) as compared with those with normal electrocardiograms (11.3%). A good correlation was observed between urinary albumin concentration and albumin/creatinine ratio, and both showed a significant positive correlation with age, systolic and diastolic blood pressures, and fasting plasma glucose, total serum protein, albumin, and triglyceride levels, but not with angiotensin-converting enzyme activity. Multiple regression analysis demonstrated that both the urinary albumin concentration and the albumin/creatinine ratio show a significant positive correlation with systolic blood pressure and fasting plasma glucose. The prevalence of microalbuminuria was about 13% in this Japanese cohort, and the systolic blood pressure and the fasting plasma glucose level were demonstrated as independent risk indicators for both urinary microalbumin level and urinary microalbumin/creatinine ratio.

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          Effect of captopril on progression to clinical proteinuria in patients with insulin-dependent diabetes mellitus and microalbuminuria. European Microalbuminuria Captopril Study Group.

          To study the effect of angiotensin converting enzyme inhibition on the rate of progression to clinical proteinuria and the rate of change of albumin excretion rates in patients with insulin-dependent diabetes mellitus and persistent microalbuminuria. Randomized, double-blind, placebo-controlled clinical trial of 2 years' duration at 12 hospital-based diabetes centers. Ninety-two patients with insulin-dependent diabetes mellitus and persistent microalbuminuria but no hypertension. The patients were randomly allocated in blocks of two to receive either captopril, 50 mg, or placebo twice per day. Albumin excretion rate, blood pressure, glycosylated hemoglobin level, and fructosamine level every 3 months; urinary urea nitrogen excretion every 6 months; and glomerular filtration rate every 12 months. Twelve patients receiving placebo and four receiving captopril progressed to clinical proteinuria, defined as an albumin excretion rate persistently greater than 200 micrograms/min and at least a 30% increase from baseline (P = .05). The probability of progression to clinical proteinuria was significantly reduced by captopril therapy (P = .03 by log-rank test). Albumin excretion rate rose from a geometric mean (95% confidence interval) of 52 (39 to 68) to 76 (47 to 122) micrograms/min in the placebo group but fell from 52 (41 to 65) to 41 (28 to 60) micrograms/min in the captopril group, a significant difference (P < .01). Mean blood pressure was similar at baseline in the two groups and remained unchanged in the placebo group but fell significantly, by 3 to 7 mm Hg, in the captopril group. Glycosylated hemoglobin levels and glomerular filtration rate remained stable in the two groups. Captopril therapy significantly impeded progression to clinical proteinuria and prevented the increase in albumin excretion rate in nonhypertensive patients with insulin-dependent diabetes mellitus and persistent microalbuminuria.
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            Randomised placebo-controlled trial of lisinopril in normotensive patients with insulin-dependent diabetes and normoalbuminuria or microalbuminuria

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              Hemodynamic factors in the genesis of diabetic microangiopathy.

              There are many candidate mechanisms to explain the phenomenon of delayed microvascular disease in the diabetic. All may play some part in determining the genesis, the evolution or the ultimate degree and form of the angiopathy. General metabolic and humoral factors may provide the pathogenetic background against which special local conditions, e.g., in the retina or renal cortex, will determine the morphology of the angiopathy and its functional and structural consequences. Some of the processes occurring in the diabetic person may, however, be of major importance in initiating and maintaining conditions for the evolution of microvascular disease. The hemodynamic changes and the vascular responses to them that we have described are, we suggest, very likely to be an important component of this sort. Unlike the later structural changes, these hemodynamic phenomena are to be found very early in the diabetic state. Of most clinical importance, perhaps, is that they appear, with the achievement of adequate metabolic correction, to be reversible.

                Author and article information

                Am J Nephrol
                American Journal of Nephrology
                S. Karger AG
                February 1999
                22 March 1999
                : 19
                : 1
                : 13-20
                aInstitute of Community Medicine, University of Tsukuba, Tsukuba; bCenter of Health Screening and Management, Tsuchiura Kyodo General Hospital, Tsuchiura; cSchool of Allied Health Sciences, Faculty of Medicine, Tokyo Medical and Dental University, Tokyo, Japan
                13419 Am J Nephrol 1999;19:13–20
                © 1999 S. Karger AG, Basel

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                Figures: 1, Tables: 7, References: 37, Pages: 8
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