O. Hanyu et al., POLYMORPHISM OF THE ANGIOTENSIN-I-CONVERTING-ENZYME GENE IN DIABETIC NEPHROPATHY IN TYPE-II DIABETIC-PATIENTS WITH PROLIFERATIVE RETINOPATHY, Renal failure, 20(1), 1998, pp. 125-133
Recently, deletion (D)/insertion (i) polymorphism in the Angiotensin I
-converting enzyme (ACE) gene has been suggested to be related to the
development of diabetic nephropathy in type I diabetes mellitus. This
hypothesis, however, remains controversial. Differences in clinical st
ates between patients, especially in glycemic control or duration of d
iabetes, could be responsible for these contradictory results. In this
study we examined the relationship between D/I polymorphism of the AC
E gene and diabetic nephropathy in type II diabetic patients who had a
lready developed proliferative retinopathy (n = 45), and were thought
to have been in a hyperglycemic state for long enough to develop micro
angiopathy. The patients were divided into two subgroups: 24 with neph
ropathy (albumin excretion rate:AER greater than or equal to 20 mu g/m
in) and 21 without (AER < 20 mu g/min). There was no difference in the
duration of diabetes, HbAlc levels or average blood pressure over the
previous year between these subgroups and other clinical characterist
ics were comparable. Patients without nephropathy exhibited allele I m
ore often than those with nephropathy (p = .025). AER was lowest in ge
notype II and highest in genotype DD patients but the difference was n
ot statistically significant (p = .07). From these findings, it was co
ncluded that genotype II for the ACE gene could be a marker for reduce
d risk of diabetic nephropathy.