PROGRESSION OF BORDERLINE INCREASES IN ALBUMINURIA IN ADOLESCENTS WITH INSULIN-DEPENDENT DIABETES-MELLITUS

We aimed to determine the natural history of borderline increases in a lbuminuria in adolescents with insulin-dependent (Type 1) diabetes mel litus (IDDM) and factors which are associated With progression to pers istent microalbuminura. Fifty-five normotensive adolescents with IDDM and intermittent microalbuminura (overnight albumin excretion ratte of 20-200 mu g min(-1) on one of three consecutive timed collections, n= 29) or borderline albuminura (mean overnight albumin excretion rate of 7.2-20 mu g min(-1) on one of three consecutive timed collections, n= 30) were followed prospectively at 3 monthly intervals. The endpoint w as persistent microalbuminuria defined as a minimum of three of four c onsecutive overnight albumin excretion rates of greater than 20 mu g m in(-1). One hundred and forty-two adolescents with IDDM and normoalbum inura were also followed prospectively. Fifteen of the 59 patients (25 .4 %) with intermittent (9/29) or borderline (6/30) albuminura progres sed to persistent microalbuminura (progressors) over 28 (15-50) months [median (range)] in comparison with two of the 142 patients with norm oalbuminuria 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 HbA(lc) (p=0.004) than non-progressors. All patients remained normotensive. Glomerular filtra tion rate, apolipoproteins, dietary phosphorus, protein and sodium int akes, and prevalence of smoking did not differ between progressors and non-progressors. Total renin was higher in the diabetic patients With out a difference between progressors and non-progressors. In conclusio n there is a relatively high rate of progression to persistent microal buminuria in pubertal adolescents with borderline increases in albumin ura and duration greater than 3 years. These patients require attentio n to minimize associated factors of poor metabolic control and higher blood pressure in the development of incipient nephropathy. (C) 1997 b y John Wiley & Sons, Ltd.