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Early diabetic nephropathy is associated with glomerular hyperfiltration, whereas the development of persistent microalbuminuria (MA) may herald progressive decline in renal function. We have evaluated endogenous GFR markers in subjects with type 1 diabetes from the Oxford Regional Prospective Study, an inception cohort of 527 children followed for a median of 10.3 y (range 0.9-19.2) with annual assessment of urinary albumin/creatinine ratios. Longitudinal blood samples were available from 417 subjects for measurement of symmetric dimethylarginine (SDMA) and creatinine. In a representative subgroup (n= 130) GFR was also assessed using an inulin infusion method and estimated GFR (eGFR=35*height/plasma creatinine). Formal measurement of GFR by inulin was significantly correlated with SDMA (r=-0.25, p=0.003) but not with creatinine (r=-0.13, p=0.15) or eGFR (r=0.15, p=0.08). Overall SDMA and creatinine were higher in males than in females (0.42±0.07 vs 0.38±0.07 µM/L and 53.87±14.45 vs 47.42±11.08µ M/L respectively, p<0.0001) and SDMA declined whereas creatinine increased with age (B=-0.006±0.001/yr and 0.94±0.19/yr respectively, p<0.0001). Mean levels of SDMA were significantly different in MA positive (MA+ n= 116) vs MA negative (MA- n=301) subjects (0.38±0.07µM/L vs 0.41 ± 0.07 µ M/L, p<0.0001). Change with age in SDMA levels differed between MA+ and MA- subjects (p=0.03 for interaction). Initially SDMA levels were lower in MA+ subjects reflecting greater hyperfiltration but from the age of 18 y there was an increase in SDMA relating to decline in renal function, particularly in those with persistent MA (Fig). In this longitudinal study, measurement of SDMA, in contrast to creatinine, was a reliable marker of GFR and the rise in SDMA in subjects developing MA could provide a useful marker of decline in renal function and cardiovascular risk. [ABSTRACT FROM AUTHOR]

The article presents the discussion on inclusion of continuous glucose monitoring (CGM) targets for children, adolescents, and young adults. Topics include recognition where disparities in the social determinants of health (SDOH) and inequitable access to modern diabetes therapies representing significant barriers in achieving glucose targets; and reducing the risks of acute and chronic complications of diabetes.

Objectives To describe independent predictors for the development of mkroalbuminuria and progression to macroalbuminuria in those with childhood onset type 1 diabetes. Design Prospective observational study with follow-up for 9.8(SD3.8} year. 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 (HbAlc) 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 HbAlc concentrations (hazard ratio per 1% rise in HbAu 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 HbAu 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. [ABSTRACT FROM AUTHOR]