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Keywords:

  • insulin dependent diabetes mellitus;
  • adolescents;
  • microalbuminura;
  • diabetic nephropathy

Abstract

We aimed to determine the natural history of borderline increases in albuminuria in adolescents with insulin-dependent (Type 1) diabetes mellitus (IDDM) and factors which are associated with progression to persistent microalbuminura. Fifty-five normotensive adolescents with IDDM and intermittent microalbuminura (overnight albumin excretion ratte of 20–200 μg min−1 on one of three consecutive timed collections, n  = 29) or borderline albuminura (mean overnight albumin excretion rate of 7.2–20 μg min−1 on one of three consecutive timed collections, n  = 30) were followed prospectively at 3 monthly intervals. The endpoint was persistent microalbuminuria defined as a minimum of three of four consecutive overnight albumin excretion rates of greater than 20 μg min−1 . One hundred and forty-two adolescents with IDDM and normoalbuminura were also followed prospectively. Fifteen of the 59 patients (25.4 %) with intermittent (9/29) or borderline (6/30) albuminura progressed to persistent microalbuminura (progressors) over 28 (15–50) months [median (range)] in comparison with two of the 142 patients with normoalbuminuria at entry (relative risk =12.6; p  =0.001). Progressors to persistent microalbuminura were pubertal and had higher systolic (p  = 0.02) and diastolic (p  = 0.02) blood pressure, and HbAlc (p  = 0.004) than non-progressors. All patients remained normotensive. Glomerular filtration rate, apolipoproteins, dietary phosphorus, protein and sodium intakes, and prevalence of smoking did not differ between progressors and non-progressors. Total renin was higher in the diabetic patients without a difference between progressors and non-progressors. In conclusion there is a relatively high rate of progression to persistent microalbuminuria in pubertal adolescents with borderline increases in albuminura and duration greater than 3 years. These patients require attention to minimize associated factors of poor metabolic control and higher blood pressure in the development of incipient nephropathy. © 1997 John Wiley & Sons, Ltd.