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SummaryAtherosclerotic changes have not been demonstrated directly in asymptomatic hyperglycaemic non-diabetic subjects, although high mortality due to coronary heart disease has been reported. We measured arterial wall thickness non-invasively, in order to directly demonstrate atherosclerosis of the carotid arteries of hyperglycaemic non-diabetic subjects and to evaluate its risk factors.The thicknesses of the intimal plus medial complex (IMT) of the carotid arteries of 112 asymptomatic hyperglycaemic non-diabetic subjects (aged 22-81, 95 males and 17 females) were compared with those of 55 healthy male subjects and 211 non-insulin-dependent NIDDM male diabetic patients. The subjects were subgrouped into impaired glucose-tolerant (IGT) subjects who had a 2-h glycaemic level of more than 7.8 mmol/1, and non-IGT subjects whose 2-h glycaemic levels were within 6.7-7.7 mmol/1.Non-IGT and IGT subjects showed significantly greater IMTs than age-matched healthy males and showed no significant differences compared to agematched NIDDM patients. Multivariate analysis demonstrated that the risk factors for IMT of non-IGT and IGT subjects were age and systolic blood pressure. According to data on the accumulation of atherogenic risks (hypertension, dyslipidaemia, and smoking), IMT increased linearly in non-IGT and IGT subjects. However, non-IGT and IGT subjects without hyperlipidaemia, hypertension, or smoking risk still had significantly greater IMT than agematched normal males (1.019+0.063 vs 0.770+ 0.111 mm, p < 0.05). Prevalence of ECG-indicated coronary heart disease was significantly higher in hyperglycaemic non-diabetic subjects and NIDDM with increased carotid arterial wall thickness (IMT _> 1.1 mm) than in those without increased thickness (IMT < 1.1 ram). Asymptomatic hyperglycaemic non-diabetic subjects have increased thickness of their carotid arteries compared to age-matched male NIDDM patients. As one of several independent risk factors, mild hyperglycaemia advances atherosclerosis, which leads to coronary heart disease. [Diabetologia (1995) 38: 585-591] Key words Atherosclerosis, borderline diabetes, im-" paired glucose tolerance, non-insulin-dependent diabetes mellitus, B-mode, ultrasound, carotid artery, coronary heart disease, ECG. Received: 5 August 1994 and in revised form: 12 October 1994Corresponding author: Dr. Y. Yamasaki, First Department of Medicine, Osaka University School of Medicine, Yamadaoka 2-2, Suita City, Osaka 565, Japan Abbreviations: IMT, Intimal plus medial complex; NIDDM, non-insulin-dependent diabetes mellitus; IGT, impaired glucose tolerance; CHD, coronary heart disease; T-Chol, serum total cholesterol; HDL-C, high-density lipoprotein cholesterol; TG, serum triglycerides.Several prospective studies [1][2][3][4][5][6][7][8][9][10][11][12] have suggested the occurrence of advanced atherosclerosis in coronary arteries and cerebral arteries in subjects with elevated blood glucose concentrations. In the Whitehall study [1,2], stroke mortality and coronary heart disease (CHD) mortality...

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The concentrations of urea, creatinine, and uric acid were measured in edema fluid and plasma during hemodialysis and 18 h after hemodialysis. The concentrations of these solutes in plasma were 15-17% lower than in the edema fluid after hemodialysis. Eighteen hours after hemodialysis, however, the concentrations in plasma were almost the same as those in edema fluid. These data suggest that the removal of these solutes from the extracellular space is delayed during hemodialysis. The plasma concentrations obtained at 18 h after hemodialysis are better indicators of hemodialysis efficiency.

Summary: The renin‐angiotension system (RAS) component gene polymorphisms was examined in 216 patients undergoing maintenance haemodialysis (HD) therapy and in 208 control subjects. the RAS polymorphisms selected for analysis were angiotensin I converting enzyme (ACE) I/D, angiotensinogen (Agt) T235/M235, angiotensin II type 1 receptor (AGT1R) A1166/C1166. the control allelic frequencies was ACE I/D (0.63/0.37), Agt T235/M235 (0.16/0.84), and AGT1R A1166/C1166 (0.94/0.06). Recently, relationships between ACE I/D and the progression of renal disease attract great attention in Japanese and Caucasian populations. ACE D allele was expected to be more frequent in HD population. However, no accumulation of ACE D allele or Agt T235 allele, AFT1R C1166 allele in Japanese end‐stage renal disease (ESRD) subjects was detected. to explain the paradoxical result of positive association of ACE D allele with progression of renal disease and no bias of ACE genotype in ESRD subjects, further investigation with systematic prospective study regarding the change of ACE genotype distribution around the period of entering dialysis therapy is required.

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