Aims To determine the occurrence of microalbuminuria in young people with Type 1 diabetes mellitus followed prospectively for 2 years and to relate the presence of persistent elevations in urinary albumin excretion (UAE) to age, diabetes duration, puberty and other factors. Methods During a 2 year period, random urine samples were obtained from 471 patients, aged 8–18 years (mean ± SD 12.9 ± 2.3 years) with Type 1 diabetes duration 5.6 ± 3.0 years, as part of routine clinical care. Urine albumin and creatinine concentrations were measured in 1310 samples (median, 3 samples per patient) and the albumin:creatinine ratio was calculated (in micrograms albumin per milligram creatinine). Height, weight, blood pressure (BP), glycated haemoglobin (HbA1c), blood glucose monitoring frequency and Tanner staging were collected from patients’ medical records. Results Twenty-three per cent of patients had one or more sample with elevated UAE (≥20 μg/mg) and 9.3% had persistent elevations (≥2 samples ≥20 μg/mg). Those with and without persistent microalbuminuria did not differ significantly in age, diabetes duration, z–score for body mass index, pubertal status or BP percentile. Ten per cent of children <13 years old and 9% of children ≥13 years old had persistent microalbuminuria. Persistent microalbuminuria was significantly associated with diabetes duration only in older children (duration 0.5–3 years, 4%; 4–6 years, 8%; ≥7 years, 14%; P = 0.02, trend test). Mean HbA1c over the 2 years was 8.7 ± 1.2%. In a logistic regression model, mean HbA1c was the only significant predictor of persistent microalbuminuria (odds ratio 1.3, 95% confidence interval 1.0–1.6, P = 0.05). Conclusions Microalbuminuria in older children with Type 1 diabetes is likely to be clinically significant. In younger children, it may reflect functional, reversible renal changes. Longitudinal analysis is needed to confirm the probable transient nature of microalbuminuria in young patients with Type 1 diabetes.

Context The management of youth with delayed puberty is hampered by difficulty in predicting who will eventually progress through puberty and who will fail to attain adult reproductive endocrine function. The neuropeptide kisspeptin, which stimulates gonadotropin-releasing hormone (GnRH) release, can be used to probe the integrity of the reproductive endocrine axis. Objective We sought to determine whether responses to kisspeptin can predict outcomes for individuals with pubertal delay. Design, Setting, and Participants We conducted a longitudinal cohort study in an academic medical center of 16 children (3 girls and 13 boys) with delayed or stalled puberty. Intervention and Outcome Measures Children who had undergone kisspeptin- and GnRH-stimulation tests were followed every 6 months for clinical evidence of progression through puberty. Inhibin B was measured in boys. A subset of participants underwent exome sequencing. Results All participants who had responded to kisspeptin with a rise in luteinizing hormone (LH) of 0.8 mIU/mL or greater subsequently progressed through puberty (n = 8). In contrast, all participants who had exhibited LH responses to kisspeptin ≤ 0.4 mIU/mL reached age 18 years without developing physical signs of puberty (n = 8). Thus, responses to kisspeptin accurately predicted later pubertal outcomes (P = .0002). Moreover, the kisspeptin-stimulation test outperformed GnRH-stimulated LH, inhibin B, and genetic testing in predicting pubertal outcomes. Conclusion The kisspeptin-stimulation can assess future reproductive endocrine potential in prepubertal children and is a promising novel tool for predicting pubertal outcomes for children with delayed puberty.

Risk of type 1 diabetes at 3 years is high for initially multiple and single Ab+ IT and multiple Ab+ NT. Genetic predisposition, age, and male sex are significant risk factors for development of Ab+ in twins.

Aims Point-of-care HbA1c is routine in clinical practice. Comparison of point-of-care HbA1c against laboratory measurements across sites and over time is warranted. Methods One hundred and twenty-one young persons with Type 1 diabetes from four centres provided 450 paired samples collected over 10 months for point-of-care HbA1c and central laboratory-based high-performance liquid chromatography (HPLC) HbA1c determinations. Change in HbA1c over time was assessed by difference from initial to final HbA1c and by growth modelling with annualized slope calculation. Change in HbA1c was categorized as improved (decrease of ≥ 0.5% or negative slope), no change (± 0.4% of initial HbA1c or slope = 0) or worsened (increase of ≥ 0.5% or positive slope). Results The 450 paired samples (median of four pairs/patient) were highly correlated (r = 0.97, P < 0.0001), as were time-specific and site-specific pairs (r = 0.94 to 0.98, P < 0.0001). Initial-to-final point-of-care HbA1c and HPLC HbA1c changes were 0.3 ± 1.1% (range −2.7 to 4.1) and 0.4 ± 1.2% (–3.9 to 4.5), respectively, with 21% of patients (n = 26) discordant for change categories. ΔHbA1c by point-of-care HbA1c vs. HPLC HbA1c differed across the HbA1c range and by ≥ 0.5% absolute difference in ΔHbA1c in 14 (54%) of the 26 patients discordant for HbA1c change categories. Mean annual HbA1c slope was 0.4 ± 1.5% (−5.4 to 4.8) for point-of-care HbA1c and 0.4 ± 1.6% (−6.9 to 5.2) for HPLC HbA1c, with 18% (n = 22 pairs) discordant for change categories. Conclusions Assessment of absolute HbA1c change may not be different for point-of-care HbA1c compared with HPLC HbA1c; however, misclassification of patients by discrete cut-off values may occur with point-of-care HbA1c compared with HPLC HbA1c determinations.