To determine the influence of residual beta-cell function on retinopathy an
d microalbuminuria we measured basal C-peptide in 50 type 1 diabetic outpat
ients aged 24.96 +/- 7.14 years, with a duration of diabetes of 9.1 +/- 6.2
years. Forty-three patients (86%) with low C-peptide (<0.74 ng/ml) had lon
ger duration of diabetes than 7 patients (14%) with high C-peptide (greater
than or equal to 0.74 ng/ml) (9 (2-34) vs 3 (1-10) years, P = 0.01) and a
tendency to high glycated hemoglobin (HBA(1)) (8.8 (6-17.9) vs 7.7 (6.9-8.7
)%, P = 0.08). Nine patients (18%) had microalbuminuria (two out of three o
vernight urine samples with an albumin excretion rate (AER) greater than or
equal to 20 and <200 mu g/min) and 13 (26%) had background retinopathy. No
association was found between low C-peptide, microalbuminuria and retinopa
thy and no difference in basal C-peptide was observed between microalbuminu
ric and normoalbuminuric patients (0.4 +/- 0.5 vs 0.19 +/- 0.22 ng/ml, P =
0.61) and between patients with or without retinopathy (0.4 +/- 0.6 vs 0.2
+/- 0.3 ng/ml, P = 0.43). Multiple regression analysis showed that duration
of diabetes (r = 0.30, r(2) = 0.09, P = 0.031) followed by HBA(1) (r = 0.4
1, r(2) = 0.17, P = 0.01) influenced basal C-peptide, and this duration of
diabetes was the only variable affecting AER (r = 0.40, r(2) = 0.16, P = 0.
004). In our sample of type 1 diabetic patients residual beta-cell function
was not associated with microalbuminuria or retinopathy.