We prospectively followed a cohort of 278 non-insulin-dependent (NIDDM
) patients for a 6-year period, intending to estimate the rate of incr
ease of albuminuria and to identify clinical variables that influence
this increase. At baseline, normoalbuminuria (N) was seen in 74 %, mic
roalbuminuria (M) in 19 % and 7 % presented with proteinuria (P). A to
tal of 80 patients died; they were older (p < 0.001) and had higher al
bumin excretion both at baseline and as an average during follow-up (p
< 0.01). At baseline, patients with proteinuria had higher blood pres
sures (systolic and diastolic), where as there was no difference betwe
en patients with normo- and microalbuminuria. Glycaemic control was in
creasingly poor throughout the three groups. At follow-up, an average
relative rate of increase of albuminuria (slope) of 17 % per year was
seen both for patients with complete 6-years, follow-up (n = 135) and
patients with at least 4 years follow-up (n = 178). Slope correlated s
ignificantly with systolic blood pressure (r = 0.26 and 0.29) in both
groups, diastolic blood pressure only in the 4-year group (r = 0.22) a
nd average albuminuria in both (r = 0.31 and 0.24). By multiple regres
sion analyses systolic blood pressure and average albuminuria remained
with significant influence on slope. Progression was defined as an in
crease in the category (e.g. normoto microalbuminuria) as well as an i
ncrease of more than 20 % in albumin excretion, and was seen in 46 pat
ients with at least 4 years' follow-up. Progressors (patients demonstr
ating progression) had higher systolic blood pressure (165 mm Hg +/- 2
0 vs 156 +/- 17) and poorer glycaemic control (HbA(1c): 8.2 % +/- 1.5
vs 7.7 +/- 1.3) p < 0.05, as well as a higher level of albuminuria at
baseline. The present study points to systolic blood pressure and gene
ral level of albuminuria as factors determining the rate of progressio
n of albuminuria. However, only a modest fraction of the variation bet
ween subjects was explained by these variables.