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BMJ 2008;336:697-701 (29 March), doi:10.1136/bmj.39478.378241.BE (published 18 March 2008)
Rakesh Amin, consultant paediatric endocrinologist1, Barry Widmer, clinical resource coordinator1, A Toby Prevost, medical statistician2, Phillip Schwarze, clinical research fellow1, Jason Cooper, medical statistician3, Julie Edge, consultant paediatric endocrinologist4, Loredana Marcovecchio, clinical research fellow1, Andrew Neil, consultant diabetologist5, R Neil Dalton, consultant biochemist6, David B Dunger, professor of paediatrics and consultant paediatric epidemiologist1
1 University Department of Paediatrics, Addenbrookes Hospital, Cambridge CB2 0QQ, 2 Department of Public Health and Primary Care, University of Cambridge, Cambridge CB2 0SR, 3 JDRF/Wellcome Trust Diabetes Inflammation Laboratory, Cambridge Institute for Medical Research, Cambridge CB2 0XY, 4 Department of Paediatrics, John Radcliffe Hospital, Oxford OX3 9DU, 5 Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Oxford OX3 7LJ, 6 WellChild Laboratory, Kings College London, Guys Hospital, London WC2R 2LS
Correspondence to: D B Dunger dbd25{at}cam.ac.uk
Design Prospective observational study with follow-up for 9.8 (SD 3.8) years.
Setting Oxford regional prospective study.
Participants 527 participants with a diagnosis of type 1 diabetes at mean age 8.8 (SD 4.0) years.
Main outcome measures Annual measurement of glycated haemoglobin (HbA1c) and assessment of urinary albumin:creatinine ratio.
Results Cumulative prevalence of microalbuminuria was 25.7% (95% confidence interval 21.3% to 30.1%) after 10 years of diabetes and 50.7% (40.5% to 60.9%) after 19 years of diabetes and 5182 patient years of follow-up. The only modifiable adjusted predictor for microalbuminuria was high HbA1c concentrations (hazard ratio per 1% rise in HbA1c 1.39, 1.27 to 1.52). Blood pressure and history of smoking were not predictors. Microalbuminuria was persistent in 48% of patients. Cumulative prevalence of progression from microalbuminuria to macroalbuminuria was 13.9% (12.9% to 14.9%); progression occurred at a mean age of 18.5 (5.8) years. Although the sample size was small, modifiable predictors of macroalbuminuria were higher HbA1c levels and both persistent and intermittent microalbuminuria (hazard ratios 1.42 (1.22 to 1.78), 27.72 (7.99 to 96.12), and 8.76 (2.44 to 31.44), respectively).
Conclusion In childhood onset type 1 diabetes, the only modifiable predictors were poor glycaemic control for the development of microalbuminuria and poor control and microalbuminuria (both persistent and intermittent) for progression to macroalbuminuria. Risk for macroalbuminuria is similar to that observed in cohorts with adult onset disease but as it occurs in young adult life early intervention in normotensive adolescents might be needed to improve prognosis.
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