Prepubertal duration of diabetes and prepubertal hyperglycemia contribute to the risk of postpubertal MA. The differences in rates of development of MA relating to HbAlc, sex, and age at diagnosis relative to puberty may have long-term consequences for the risk of subsequent nephropathy and for cardiovascular risk.

We conclude that both glycaemic control and familial factors may be important determinants of lipid levels in young people with diabetes. Both may contribute to the subsequent risk of cardiovascular disease and possibly the development of incipient diabetic nephropathy.

Macroalbuminuria represents an advanced stage of diabetic renal injury [1]. Microalbuminuria, defined as an albumin excretion rate between 20±200 mg/ min could predict the development of overt nephropathy in adults with Type I (insulin-dependent) diabetes mellitus [2]. Substantial renal injury, as indicated by changes in renal morphology [3] and incremental rises in blood pressure [4] could, however, already be detectable in subjects with microalbuminuria. Diabetologia (2001) Abstract Aims/hypothesis. Early detection of risk of microalbuminuria could prevent early renal damage. We investigated whether urine retinol binding protein and N-acetyl-glucosaminidase could predict the risk of microalbuminuria in a large cohort of children followed from diagnosis of Type I (insulin-dependent) diabetes mellitus. Methods. Subjects under 16 years of age within a georaphically defined region were recruited at diagnosis of Type I (insulin-dependent) diabetes mellitus. Annually, albumin-, retinol binding protein-and N-acetyl-glucosaminidase-to creatinine ratios were each measured in 3 urine samples. Results. A total of 511 subjects were followed for a median of 6 years (range: 1±14). Microalbuminuria (males: ³ 3.5 mg/mmol; females: ³ 4.0 mg/mmol, in 2 out of 3 urines) developed in 78 subjects (36 male). The cumulative probability of microalbuminuria was 40 % after 12 years duration of diabetes. Retinolbinding-proteinuria (men: ³ 21 mg/mmol; women ³ 33 mg/mmol) developed in 217 subjects (152 men). The cumulative probability of retinol-binding-proteinuria was 67 % after 12 years duration of diabetes.The cumulative probability of retinol-binding-proteinuria was 40 % before the onset of microalbuminuria and 59 % in subjects who did not subsequently develop microalbuminuria. Retinol-binding-proteinuria developed at a higher rate with increasing HbA 1 c than microalbuminuria. N-acetyl-glucosaminidase-uria (males: ³ 56 mmol-pnp´h ±1´m mol ±1; females: ³ 46 mmol-pnp´h ±1´m mol ±1 ) developed in 477 subjects. The cumulative probability of N-acetylglucosaminidase-uria was 98 % after 10 years of diabetes duration. The cumulative probability of N-acetyl-glucosaminidase-uria was 73 % in the years before the onset of microalbuminuria and 97 % in subjects without microalbuminuria. The probability of Nacetyl-glucosaminidase-uria was 99 % with an HbA 1 c greater than or equal to 14.5 %. Conclusions/interpretation. Raised amounts of urine retinol binding protein and N-acetyl-glycosaminidase are related to HbA 1 c and the duration of diabetes. They occur in the majority of subjects and are not early markers for the risk of microalbuminuria. [Diabetologia (2001)