Bi. Freedman et al., FAMILIAL PREDISPOSITION TO NEPHROPATHY IN AFRICAN-AMERICANS WITH NON-INSULIN-DEPENDENT DIABETES-MELLITUS, American journal of kidney diseases, 25(5), 1995, pp. 710-713
Nephropathy clusters in Pima Indian families with non-insulin-dependen
t diabetes mellitus (NIDDM), suggesting that susceptibility to nephrop
athy is distinct from NIDDM per se. The authors compared the family hi
story of endstage renal disease (ESRD) from 52 African-American patien
ts with NIDDM-induced ESRD (cases) with 45 age-, sex-, and race-matche
d non-insulin-dependent diabetics without nephropathy (controls) to as
sess whether the risk of renal disease was independent from NIDDM in A
frican-Americans as well. Thirty-seven percent (19 of 52) of NIDDM-ind
uced ESRD patients had either a first-, second-, or third-degree relat
ive with ESRD, in contrast to only 7% (3 of 45) of diabetic controls.
African-American individuals with NIDDM were at eightfold increased ri
sk for developing subsequent ESRD in the presence of a close relative
with ESRD (odds ratio = 8.06; 95% confidence interval, 2.2 to 29.6; P
less than or equal to 0.0005). No significant differences were observe
d in yearly income, years of formal education, total serum cholesterol
level, prevalence of smoking, or hypertension between the groups. Dia
betic control (assessed by glycosylated hemoglobin and random glucose
levels) was suboptimal in nonrenal disease controls, suggesting that h
yperglycemia alone fails to cause nephropathy in patients with NIDDM.
Family size was unlikely to have influenced the results because diabet
ic cases had significantly fewer first-degree relatives than did diabe
tic controls. Familial clustering of ESRD is present in certain Africa
n-American families with NIDDM. Differences in family size and degree
of diabetic control are unlikely to account for the differences observ
ed between families. As in the Pima Indians, susceptibility to ESRD in
African-Americans appears to be independent of the presence of NIDDM.
These data strongly suggest that a genetic predisposition to renal di
sease is present in these families, although shared environment cannot
be excluded from contributing to this risk. (C) 1995 by the National
Kidney Foundation, Inc.