Aims/hypothesis: We examined long-term total and cause-specific mortality in a nationwide, populationbased Norwegian cohort of patients with childhood-onset type 1 diabetes. Materials and methods: All Norwegian type 1 diabetic patients who were diagnosed between 1973 and 1982 and were under 15 years of age at diagnosis were included (n=1,906). Mortality was recorded from diabetes onset until 31 December 2002 and represented 46,147 person-years. The greatest age attained among deceased subjects was 40 years and the maximum diabetes duration was 30 years. Cause of death was ascertained by reviews of death certificates, autopsy protocols and medical records. The standardised mortality ratio (SMR) was based on national background statistics. Results: During follow-up 103 individuals died. The mortality rate was 2.2/1000 person-years. The overall SMR was 4.0 (95% CI 3.2-4.8) and was similar for males and females. For ischaemic heart disease the SMR was 20.2 (7.3-39.8) for men and 20.6 (1.8-54.1) for women. Acute metabolic complications of diabetes were the most common cause of death under 30 years of age (32%). Cardiovascular disease was responsible for the largest proportion of deaths from the age of 30 years onwards (30%). Violent death accounted for 28% of the deaths in the total cohort (35% among men and 11% among women). Conclusions/interpretation: Childhood-onset type 1 diabetes still carries an increased mortality risk when compared with the general population, particularly for cardiovascular disease. To reduce these deaths, attention should be directed to the prevention of acute metabolic complications, the identification of psychiatric vulnerability and the early detection and treatment of cardiovascular disease and associated risk factors.
SummaryWe investigated in a randomized, prospective study the influence of improved blood glucose control during 2-3 years in young insulin-dependent diabetic (IDDM) patients with microalbuminuria, which is indicative of early nephropathy. Patients were randomized either to intensive treatment by continuous subcutaneous insulin infusion (CSII) (n = 9) or CT (n = 9). Kidney biopsies were taken at baseline and after 26-34months. End points were structural changes in the glomeruli. Sensitive, quantitative, morphometric methods were used. The blood glucose control improved significantly (p ---0.01) during the study in the CSII-group as glycated haemoglobin (HbAlc) fell from 10.1% ([95 % CI] 8.9-11.3) to 8.6 % (7.9-9.2), but not in the . Mean HbAIr during the study period was significantly lower in the CSII-group than in the CTgroup, 8.7% (8.1-9.3) vs 9.9% (8.5-11.3), p =0.04. Basement membrane thickness (BMT) increased in both groups, most (CT vs CSII, p = 0.03) in the CTgroup: 140 nm (50-230) vs CSII: 56 nm (27-86). In the CT-group only an increase was seen in matrix/mesangial volume fraction (p = 0.006) and matrix star volume (p =0.04). Furthermore, a positive correlation between mean HbAlc during the study and change from baseline in BMT (r=0.70, p =0.001) and matrix/glomerular volume fraction (r --0.33,p = 0.09, NS) was demonstrated. Albumin excretion rate correlated significantly to BMT and most of the matrix parameters. The present study shows that during a period of only 2.5 years, a close relationship between the level of mean blood glucose and progression of glomerular morphological changes in early diabetic nephropathy can be demonstrated. [Diabetologia (1994) 37: 483-490] Key words Diabetic glomerulopathy, microalbuminuria, basement membrane thickness, mesangial expansion, mesangial matrix, stereology, hyperglycaemia.Even though hyperglycaemia is a prerequisite for the development of diabetic nephropathy, the impact of long-term hyperglycaemia on the progression of early diabetic nephropathy is not well understood. Abbreviations: IDDM, insulin-dependent diabetes mellitus; CSII, continuous subcutaneous insulin infusion; CT, conventional treatment (2, 3 or multiple injections daily); BMT, basement membrane thickness; AER, urinary albumin excretion rate; CI, confidence interval.Pirart [1] showed in a study comprising both IDDM and NIDDM patients, that the risk of development of serious complications including nephropathy, is associated with more severe hyperglycaemia. In cross-sectional [2--6] and long-term retrospective studies [7,8] an association between the level of glycated haemoglobin and microalbuminuria, which is an early sign of diabetic nephropathy [9,10], has been found. Improved blood glucose control obtained in prospective randomized studies has retarded the progression of AER [11] and the risk of developing clinical nephropathy [12,13]. However, it is not known if reducing mean blood glucose affects the progression of morphological changes at a very early stage of diabetic nephropathy. There...
Increased urinary albumin excretion, microalbuminuria, may be the first sign of early diabetic nephropathy. We examined glomeruli by morphometric methods in 17 patients with Type 1 (insulin-dependent) diabetes mellitus and microalbuminuria. The median age was 19 (range 18-29) years, duration of diabetes 12 (8-15) years, mean blood pressure 93 (87-115) mm Hg, glomerular filtration rate 132 (101-209) ml.min-1.1.73 m2 -2, albumin excretion rate (mean over 1 year) 32 (15-194) micrograms/min. Reference data were obtained from 11 healthy kidney donors. Mesangial volume estimates were obtained by serial sectioning in three total profiles in each of three glomeruli in diabetic patients. Basement membrane thickness and matrix volume fraction were estimated from one level per glomerulus. Two matrix parameters, matrix star volume and matrix thickness, were estimated. Interstitial volume fraction in cortex was measured by light microscopy. The morphological parameters were significantly increased in the diabetic group compared to the control group, basement membrane thickness (mean with 95% confidence intervals) was 595 nm (549-641 nm) vs 305 nm (287-325 nm), p = 0.0001; mesangial volume fraction 0.22 (0.21-0.23) vs 0.19 (0.18-0.21), p = 0.04, and matrix volume fraction 0.13 (0.12-0.13 vs 0.09 (0.08-0.10), p = 0.001. Also matrix star volume and thickness, interstitial volume fraction and mean capillary diameter were significantly increased. The intra-individual variation among glomeruli expressed as coefficient of variation was 7.4% vs 9% (basement membrane thickness) and 11.7% vs 25% (mesangial volume fraction) in the diabetic and the control group, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
Long-term treatment with angiotensin converting enzyme inhibitors (ACEI) has a beneficial effect on the progression of microalbuminuria in patients with Type I (insulin-dependent) diabetes mellitus [1,2]. In addition, some clinical studies but not all [3±5] have suggested a superior effect of ACE-inhibitors over beta-blockers on the progressive decline in glomerular filtration rate (GFR) in Type I diabetic patients with nephropathy.Microalbuminuria predicts overt diabetic renal disease [6]. Still around 30 % of patients with low- Diabetologia (1999) Abstract Aims/hypothesis. To investigate the influence of angiotensin converting enzyme inhibitors and beta blockers on the progression of early diabetic glomerulopathy.Methods. Thirteen patients with Type I (insulin-dependent) diabetes mellitus (mean age 18.8 years) with microalbuminuria 31 (19±160) mg/min were randomised to treatment with enalapril (group 1, n = 7) or metoprolol (group 2, n = 6). Renal biopsies were taken before and after 38 (36±48) months of treatment. Albumin excretion rate, blood pressure and HbA 1 c were measured every third month. A reference group without antihypertensive treatment (group 3, n = 9), with similar age, diabetes duration and degree of microalbuminuria as group 1 and 2, had baseline and follow-up renal biopsies taken previously with an interval of 26±34 months, analysed at the same laboratory. Glomerular structures were measured by stereological methods.
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