Background. The first aim of our long-term study was to describe the natura
l history of diabetic nephropathy in 59 normotensive type 1 diabetic patien
ts. Secondly, we evaluated genetic and nongenetic progression promoters.
Methods. The following progression promoters were determined: the insertion
/deletion polymorphism in the angiotensin converting enzyme (ACE) gene, blo
od pressure, albuminuria, hemoglobin A(1c), cholesterol, smoking, height, a
nd gender. We studied the natural history by measuring Cr-51-EDTA plasma cl
earance at yearly intervals at least three times during [median (range)] 5.
5 (2.2 to 18.3) years.
Results. At baseline the three groups (II, N = 11; ID, N = 25, and DD, N =
23) had comparable GFR (103 +/- 16; 99 +/- 19; 113 +/- 22 ml/min/1.73 m(2),
respectively; mean +/- SD). arterial blood pressure, albuminuria, and hemo
globin A(1c). During the follow-up there was a median rate of decline in GF
R in all 59 patients of 1.2 (range 12.9 to -4.4) ml/min/year. During the st
udy period no significant differences were observed in: the rate of decline
in glomerular filtration rate [median (range) 0.9 (10.6 to -1.9). 2.5 (12.
9 to -4.4); 1.4 (10.8 to -1.9 ml/min/ year)], arterial blood pressure, albu
minuria, hemoglobin A(1c) or cholesterol between the three groups (II, ID a
nd DD), respectively. At baseline, multiple linear regression analysis incl
uding the above-mentioned putative risk factors revealed that albuminuria,
short stature: and male gender independently predict an enhanced decline in
GFR [R-2 (adjusted) = 0.33; P < 0.002]. During: the follow-up period, only
albuminuria acted as an independent progression promoter [R-2 (adjusted) =
0.37; P < 0.0001].
Conclusions. Our study revealed a rather slow progression of kidney disease
in normotensive type 1 diabetic patients with diabetic nephropathy. Albumi
nuria, short stature, and male gender act as progression promoters in such
patients.