Progression of borderline increases in albuminuria in adolescents with insulin-dependent diabetes mellitus.
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 micrograms min-1 on one of three consecutive timed collections, n = 29) or borderline albuminura (mean overnight albumin excretion rate of 7.2-20 micrograms 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 micrograms 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 HbA1c (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.
Couper
J J
JJ
Department of Endocrinology, Women's and Children's Hospital, Adelaide, Australia.
Clarke
C F
CF
Byrne
G C
GC
Jones
T W
TW
Donaghue
K C
KC
Nairn
J
J
Boyce
D
D
Russell
M
M
Stephens
M
M
Raymond
J
J
Bates
D J
DJ
McCaul
K
K
D000293:Adolescent; D000419:Albuminuria / Q000175:diagnosis / Q000209:etiology* / Q000503:physiopathology; D001794:Blood Pressure / Q000502:physiology*; D002648:Child; D003922:Diabetes Mellitus, Type 1 / Q000150:complications* / Q000503:physiopathology; D003928:Diabetic Nephropathies / Q000175:diagnosis / Q000209:etiology* / Q000503:physiopathology; D018450:Disease Progression; D005260:Female; D005500:Follow-Up Studies; D006442:Glycated Hemoglobin / Q000032:analysis* / Q000378:metabolism; D006801:Humans; D008297:Male; D011446:Prospective Studies; D012709:Serum Albumin / Q000378:metabolism*; D013997:Time Factors
D006442:Glycated Hemoglobin; D012709:Serum Albumin