OBJECTIVE—To study the prevalence of microalbuminuria (MA) in African-American women with a history of gestational diabetes (GDM) who are at high risk for insulin resistance and renal dysfunction and to study MA’s relation to insulin resistance, type 2 diabetes, and hypertension.

RESEARCH DESIGN AND METHODS—MA was assessed using 24-h, timed, and/or random urine samples in a cross-sectional sample (n = 289) from a cohort of African-American women with a history of GDM and followed for a median of 11 years (range 3.0–18.4) since their diabetic pregnancy. Subjects with a urine albumin excretion rate of 30–300 g/24 h or 30–300 μg/mg creatinine in a random sample were classified as having MA if two of three samples over a 3- to 6-month period were positive. These women were evaluated for family history of diabetes, smoking and alcohol use, BMI, diabetes, hypertension, and lipid abnormalities. Insulin sensitivity was determined using the homeostasis model assessment (HOMA) estimates, which used fasting insulin and glucose measurements obtained at the same time as the MA urine sample.

RESULTS—At MA assessment, the women ranged in age from 22 to 57 years, with a median of 39 years. The overall prevalence of MA was 20%; 36% in those with diabetes. Those women with MA had higher rates of diabetes (63.8 vs. 28.6%, odds ratio [OR] = 4.4, P < 0.05), hypertension (82.8 vs. 42.9%, OR = 6.4, P < 0.05), and family history of diabetes (85.7 vs. 61.7%, OR = 3.7, P < 0.05). The proportion of subjects with MA with a family history of hypertension was nonsignificantly increased (92.9 vs. 82.4%). Subjects with MA were more obese (BMI 37.2 ± 8.9 vs. 34.4 ± 8.6 kg/m2) and had higher levels of HbA1c (8.8 ± 3.3 vs. 6.6 ± 1.8%, P < 0.001) and systolic (144.3 ± 25.9 vs. 122.8 ± 17.2 mmHg, P < 0.0001) and diastolic (95.1 ± 15.4 vs. 82.5 ± 11.9 mmHg, P < 0.0001) blood pressures. Lipid fractions were similar in those with and without MA. Although fasting glucose was much higher in subjects with MA (10.3 ± 5.8 vs. 7.1 ± 4.2 mmol/l, P = 0.0002), insulin levels were not significantly higher in subjects with MA (17.4 ± 21.2 vs. 15.2 ± 12.4 pmol/l). Insulin sensitivity, as measured using log HOMA, was similar (1.5 ± 0.6 vs. 1.6 ± 0.6) in women with and without MA, respectively. Multivariable logistic regression analyses indicated that HbA1c, OR = 1.16 (1.07, 1.27), and systolic blood pressure, OR = 1.27 (1.14, 1.41), were independent risk factors for MA. In those with diabetes, the subjects with MA had higher rates of hypertension—83.8 vs. 56.1%, OR = 4.1 (1.5, 11.10)—which was reflected by their higher systolic and diastolic blood pressures, 146.1 mmHg (P = 0.001) and 94.8 mmHg (P = 0.002), respectively, and lower levels of VLDL (0.45 ± 0.22 vs. 0.61 ± 0.33 mmol/l, P = 0.021). In the multivariable analyses of those with diabetes, the two independent risk factors for MA were similar: HbA1c, OR = 1.13 (1.01, 1.28), and systolic blood pressure, OR = 1.21 (1.04, 1.41).

CONCLUSIONS—African-American women with a history of GDM have one of the highest rates for MA. Presence of MA was not associated with insulin resistance but was significantly independently associated with HbA1c levels and hypertension. These results, taken in context of the literature, suggest that hypertension and glucose intolerance, in part, influence MA through different mechanisms. Because of the high prevalence of MA in this population and MA’s relation to all-cause and cardiovascular mortality, screening for MA should be considered.

Recently, there has been a strong interest in microalbuminuria (MA) due to its association with increased all-cause mortality and cardiovascular disease (CVD) mortality (1,2,3,4,5) in both normal (6) and diabetic populations (7,8,9). MA also predicts the progression to diabetic nephropathy (8,10,11,12) and retinopathy (13). The MA prevalence in those with diabetes varies among different ethnic groups, ranging from 19 to 36% in Caucasians (14,15), 26 to 64% in Polynesians (16), and 25 to 36% in African-Americans (17,18). Reported MA prevalence in those in the U.S. without diabetes has ranged from 3.4 to 13%, but these studies vary in the ethnic groups and age ranges studied (19,20).

Several factors have been found to be associated with these increased rates. The most consistent, in all ethnic groups, has been the presence of hypertension or elevated systolic blood pressure (14,16,17,21). Level of diabetic control in type 2 diabetic subjects is also associated with the rates of MA (22,23,24,25,26). The relationship of MA to insulin sensitivity is unresolved; some studies have shown that type 2 diabetic subjects with MA have lower sensitivity (27,28,29), whereas others have shown no difference in insulin sensitivity (30,31).

Very little is known of the relation of MA to other CVD risk factors in African-American women, a group at high risk for cardiovascular events (32,33,34); nothing is reported in African-American women with a history of gestational diabetes (GDM) who are at high risk of both diabetes and hypertension (35). Also, the prevalence of MA in this latter high-risk group is unknown. This study was designed to investigate MA in a cohort of African-American women with a history of GDM, who have been followed for a median of 11 years post-GDM pregnancy for development of diabetes and CVD risk factors. MA was cross-sectionally studied to assess its prevalence and to determine which CVD risk factors, and whether insulin sensitivity, as determined by HOMA, were associated with the presence of MA.

The original cohort of 664 African-American women who had their first prenatal visit at any of the eight Jefferson County Health Department Clinics between 1981 and 1988 and who were screened and diagnosed with GDM was described previously (35). During 1992–1995, 450 women in this original cohort were still enrolled in the study, and were contacted in 1996–1999 to assess MA. MA was not assessed at baseline. In this period, 341 women (341/450 = 76%) were examined and interviews and venipunctures were performed. Of these 341 women, 289 (289/341 = 85%) were used in the analyses presented. The other 52 women either did not follow the protocol for timed urinary albumin excretion or had other reasons for making the assay unreliable (e.g., had a urinary tract infection, were menstruating, were pregnant, or were taking ACE inhibitors and had normal urinary albumin excretion rates). Blood and urine samples were assayed by the Hospital Clinical Pathology Laboratories at University of Alabama at Birmingham. Comparisons of key baseline variables (e.g., age at delivery, proteinuria, insulin requirement, hypertension, and smoking during pregnancy) between those sampled and those lost to follow-up revealed no significant differences.

Urinary albumin excretion rates were obtained from either a random (66%) or a timed urine sample (24-h or overnight, 34%). Women with at least two positive out of three tests within a 3- to 6-month period for albumin excretion were classified as having MA (34). In all, 24% were diagnosed from two timed urine samples, 59% from one timed and one random urine sample, and 17% from two random urine samples. Every woman was initially evaluated with a random urine assessment for MA. A positive test for a timed sample was defined as albumin excretion of 30–300 mg/24 h, whereas that for a random urine was a urinary albumin of 30–300 μg/mg creatinine. Date of onset of MA was the date the woman was classified as having MA based on the above-listed criteria (i.e., date of the second positive test). Those 24-h collections containing <70% of the predicted creatinine excretion, based on the equations of Cockroft and Gault (37) were collected. Urine microalbumin assays were conducted on a Beckman LX-20 (Beckman Instruments, Brea, CA) using reagents and procedures provided by Diagnostics Chemical Limited (Oxford, CT).

Women with a fasting blood glucose ≥140 mg/dl, a random blood glucose ≥300 mg/dl, a glucose tolerance test sample at 120 min of ≥200 mg/dl, or who were being treated for diabetes were classified as having diabetes. A woman was classified as hypertensive if she was ever told by a physician that she had hypertension and was taking medications for it or had an average (based on two blood pressure readings per visit) diastolic blood pressure >90 mmHg or average systolic blood pressure >140 mmHg. Obesity was defined as 120% over ideal body weight according to Metropolitan Life tables. Albumin, creatinine, glucose, and insulin levels were assessed by the Bacillus of Calmette and Guerin (BCG) dye binding, alkaline pictrate, hexokinase, and chemiluminescence methods, respectively. Glucose levels were measured on a YSI model 23A glucose analyzer according to the manufacturer’s recommendations; insulin levels reported in International Units were determined by use of Coat-A-Count Insulin solid-phase radioimmunoassay procedure (Diagnostic Products, Los Angeles), standardized to the World Health Organization’s First International Reference Preparation of Insulin for Immunoassay and HbA1c levels, reported as percentages, were determined using a Tosoh 2.2 glycohemoglobin analyzer (Tosoh Medics, San Francisco, CA). Estimates of insulin sensitivity (homeostasis model assessment [HOMA]) were calculated by the formula of Matthews et al. (36), insulin/22.5e−ln glucose. Lipid levels were obtained from fasting blood samples. Serum cholesterol and triglycerides were analyzed using enzymatic methods to produce quinoneimine-colored products on a SYNCHRON LX System (Beckman Instruments). HDL cholesterol was analyzed on a SYNCHRON LX system using a unique detergent that solubilizes HDL only and an enzymatic method to produce a colored product. LDL cholesterol was calculated using the equation of Friedewald et al. (39). LDL values were excluded for hypertriglyceridemic subjects with values of triglycerides >4.57 mmol/l. VLDL was calculated as the triglyceride concentration divided by five.

For statistical analyses, means of continuous variables were compared with use of the Student’s t test, and the χ2 test was used to test proportions for categorical variables. HOMAs and triglyceride levels were transformed to the natural log to normalize their distribution. All tests were two sided, with α <0.05 treated as statistically significant. Risk factors of MA were determined using the multiple logistic regression model (40). Results are reported as prevalence odds ratios (PORs). PORs were calculated for continuous and class variables, and all variables significant at α <0.05 were included in the multivariable analysis. Backward and forward selection procedures were used to determine the best explanatory models. All analyses were performed with SAS Version 6.12 (SAS Institute, Cary, NC) (39).

Table 1 gives the characteristics of the 58 women with MA (20.1%) and the 231 women without MA (79.9%). No association with age was found. Presence of diabetes (odds ratio [OR] = 4.4, 2.4–8.1), hypertension (6.4, 3.1–13.3), and family history of diabetes (3.7, 1.7–8.1) was significantly higher in women with MA. Those being treated with hypertensive medications had an elevated risk of MA (OR = 3.4, 1.9–6.6); however, those who were regulated by their medications were at lower risk of MA (0.3, 0.1–0.8). Family history of hypertension, though higher in those with MA (92.9 vs. 82.4%), was not significantly different. Women with MA had significantly higher BMI (37.2 vs. 34.4 kg/m2, P = 0.026), HbA1c (8.8 vs. 6.6%, P < 0.0001), fasting glucose values (10.2 vs. 7.07 mmol/l, P = 0.0002), average systolic blood pressure (144.3 vs. 122.8 mmHg, P < 0.0001), and average diastolic blood pressure (95.1 vs. 82.5 mmHg, P < 0.0001). Lipid levels did not differ significantly. The log HOMA means in women with and without MA were remarkably similar, 1.4 vs. 1.2, respectively, P = 0.107, despite women with MA having higher rates of diabetes.

Among those women with diabetes (n = 103), the prevalence of those also having MA was 36% (n = 37). Comparisons of characteristics in diabetic women with and without MA are given in Table 2. Family history of diabetes did not differ (OR = 1.1, 0.4–3.6). As found in the total sample, hypertension (OR = 4.1, 1.5–11.0), mean HbA1c levels (10.2 vs. 8.4%, P = 0.004), and systolic (146.1 vs. 129.2 mmHg, P < 0.0001) and diastolic blood pressure (94.8 vs. 85.4 mmHg, P = 0.002) were higher in the diabetic women with MA. Fasting glucose levels were higher in the diabetic women with MA, 12.8 vs. 11.3 mmol/l, but this difference was not significant. VLDL was found to be significantly lower in those diabetic women with MA (0.45 vs. 0.61 mmol/l, P = 0.021); however, the other lipid levels were not significantly different.

In the normoglycemic women (n = 186), the prevalence of MA was 11% (n = 21). The proportions with hypertension (OR = 7.1, 2.3–21.9), diabetes family history (5.1, 1.4–18.2), and mean systolic (141.1 vs. 120.3 mmHg, P = 0.001) and diastolic (95.8 vs. 81.3 mmHg, P = 0.0005) blood pressures, were significantly higher among normoglycemic women with MA. HDL (1.07 vs. 1.31 mmol/l, P = 0.023) was significantly lower. Mean fasting glucose was higher in nondiabetic women with MA, but the difference was not significant (5.5 vs. 4.8 mmol/l, P = 0.27).

Multivariable logistic regression analysis using a model including all of the significant results from the univariate comparisons in Table 1 found that only HbA1c (OR = 1.16 [1.07, 1.27]) and systolic blood pressure (1.27 [1.14, 1.41]) were independently associated with MA among the entire sample. These same models in type 2 diabetic women only, but including years since diabetes was first diagnosed, found that, as in the total sample, HbA1c (OR = 1.13 [1.01–1.28]) and systolic blood pressure (1.21 [1.04–1.40]) were the only significant independent associations. Fasting blood glucose, however, was not significantly associated with MA. Both of these models provided a good fit to the data (X2 = 6.6, eight df, and X2 = 4.6, six df, respectively). Analyses of this same model in normoglycemic women only found that systolic blood pressure and diabetes family history had independent significant associations with MA. The ORs were 1.68 (1.28, 2.22) and 3.88 (1.03, 14.59), respectively. However, this model fit the data poorly for the normoglycemic women (P = 0.004).

When comparing MA women with and without diabetes, not surprisingly the distinguishing characteristics are that the diabetic women with MA had higher HbA1c levels (10.2 vs. 6.3%, P < 0.0001) and higher fasting blood glucose (12.8 vs. 5.5 mmol/l, P < 0.0001). Blood pressures in both groups were similar, reflecting the high proportion of hypertensive subjects in each group (83.8% [with diabetes] and 80.9% [without diabetes]). The average systolic blood pressures were 146.1 and 141.0 mmHg, and the average diastolic blood pressures were 94.8 and 95.8 mmHg, respectively. The log of the HOMA values was lower in the diabetic women, reflecting their lower insulin sensitivity and higher resistance (1.3 vs. 1.6, P = 0.13), although this did not reach significance.

End-stage renal disease (ESRD) is a major cause of morbidity and mortality in African-Americans (42) and MA is considered an early marker of proteinuria, a risk factor for ESRD (43). The primary determinants of ESRD in the African-American population are hypertension and diabetes (43,44,45). The prevalence of MA and its determinants in African-Americans is uncertain; therefore, the objective of this study was to evaluate them in a cohort of women with a history of GDM, a group with presumably high risk for ESRD. The primary intermediate outcome for this study became MA, which has been associated with all-cause mortality (2) and CVD mortality (1,3,4,5,7,8,9) and has been shown to predict the development of albuminuria in diabetic subjects (3,7,46).

There have been no previous reports of MA prevalence in African-American women with a history of GDM. However, previous studies in other non-Caucasian racial groups with high prevalences of diabetes, hypertension, and obesity have found high rates of MA in diabetic subjects: 26% in Mexican-Americans (12), 26% in Pima Indians (24), 64.1% in Naurans (25), and 26.1% in Wanigelas (16). Two studies in African-Americans have also found high rates of albuminuria in diabetic subjects: 24–36% (17,18). The prevalence of MA in our diabetic subset was 36%, similar to the higher range of the other studies, even though the average age at MA assessment in our cohort was only 39 years of age, which is 10 years younger than that of the two previous reports. Although the prevalence of MA is higher—49.7% in women with both diabetes and hypertension, compared with 22.4% in women with only diabetes and 30.4% in women only with hypertension—the number of end points, unfortunately, is too small to conclude that the effects of these two conditions on the prevalence are more than just additive.

The proportion of women with MA who were free of hypertension and type 2 diabetes was 11%. It is difficult to compare the prevalence of MA in the nondiabetic portion of this cohort, because there is only one published report of MA in a nondiabetic sample of African-American women, that by Jiang et al. (19), and the mean age of that sample was younger than ours, and only a single random urine sample was used to identify those with MA. Nonetheless, the prevalence reported by that study (5.7%) was only slightly more than half of the prevalence we found. Although not definitive, our results suggest that the prevalence of MA is quite high among African-American women with a history of GDM.

Unlike the studies by Goldschmid et al. (17) and Dasmahapatra et al. (44), our study found that glycemic control among subjects with diabetes was a very significant determinant of MA, although the mean level of HbA1c in our diabetic population with MA was 10.2%, similar to the mean HbA1c in the diabetic subjects in the study by Goldschmid et al (17). Several recent studies attempting to identify predictors of progression to MA (47) and predictors of progression from MA to proteinuria in Finnish (47) and Korean (48) type 2 diabetic populations, respectively, found that glycemic control in both populations was a significant predictor of myocardial infarction. Two possible explanations for the differences between our positive results and the two negative studies are 1) there was less variability in their samples, thereby decreasing their ability to detect any association with HbA1c, and/or 2) the shorter duration of diabetes in our subjects.

Results of this study provide evidence of a strong link of elevated systolic blood pressure and hypertension to MA in this population of African-American women with and without diabetes. Studies on diabetic subjects (10,49,50) have shown an increased risk of MA in diabetic subjects with hypertension and, in particular, systolic blood pressure. In fact, our study shows that women who were adequately treated for their hypertension, i.e., had normal blood pressures, were protected from MA (OR = 0.3), whereas those women not being adequately treated had an increased risk to MA (OR = 3.4). Our study indicates that these same risk factors are etiologically related to MA in normoglycemic women who are at high risk of hyperglycemia. Thus, these results support the hypothesis that it is not a single underlying factor for both type 2 diabetes and hypertension that is causing MA, such as insulin resistance, but that at least two separate pathways may be involved and may interact to cause MA.

Using the HOMA estimate as an indicator of insulin sensitivity, we found that HOMA values were not significantly different between subjects with and without MA in all the subgroups we studied. This is contrary to some studies in diabetic Caucasians that have previously found associations of insulin resistance with MA (27,28,29,51). The Insulin Resistance Atherosclerosis Study on nondiabetic subjects (52) found that those with MA had significantly lower estimated insulin sensitivity than normoalbuminuric subjects. This relationship remained significant even after adjustment for age, sex, ethnicity, hypertension, fasting glucose, and BMI. However, results of the Hoorn Study (30) and other studies (31,53) failed to find any MA association with insulin resistance and HOMA in their Caucasian populations. The study by Hodge et al. (16) of two different ethnic populations in New Guinea also failed to find an association between insulin resistance and MA. The differences found among these studies may reflect that adjustment for other factors reduced the differences, that variability in some studies was too small to detect a difference, or that the effect was small and therefore association of MA with insulin resistance could not be detected given the sample sizes.

A number of studies have examined the relationship between BMI and MA. Some (54,55,56) reported a positive association, whereas others (20,57) did not. Even though there were positive associations between MA and blood pressure and blood glucose level, both in part related to obesity, we found no association between BMI and MA in our sample. It is possible that this reflects the relatively narrow range of BMI in our sample of subjects, most of whom were overweight.

Our results demonstrate that African-American women with a history of GDM are at very high risk for MA and suggest that screening to identify those with MA and earlier effective treatment may reduce their risk to subsequent renal dysfunction, CVD, and mortality.

Table 1—

Characteristics of women in GDM cohort with and without MA

FactorWithout MAWith MAUnadjusted OR (95% CI)P
Type 2 diabetes     
 No 71.4 (165) 36.2 (21) 4.4 (2.4–8.1)*  
 Yes 28.6 (66) 63.8 (37)   
Hypertensive     
 No 57.1 (132) 17.2 (10) 6.4 (3.1–13.3)*  
 Yes 42.9 (99) 82.8 (48)   
Diabetes family history     
 No 38.3 (87) 14.3 (8) 3.7 (1.7–8.3)*  
 Yes 61.7 (140) 85.7 (48)   
Hypertension family history     
 No 17.6 (40) 7.1 (4) 2.8 (0.9–8.1)  
 Yes 82.4 (187) 92.9 (52)   
Age at last interview (years) 38.8 ± 6.6 39.1 ± 6.8  0.814 
BMI (kg/m2) 34.4 ± 8.6 37.2 ± 8.9  0.026* 
Log HOMA 1.2 ± 0.8 1.4 ± 0.8  0.107 
HbAlc (%) 6.6 ± 1.8 8.8 ± 3.3  <0.0001* 
Average systolic BP (mmHg) 122.8 ± 17.2 144.3 ± 25.9  <0.0001* 
Average diastolic BP (mmHg) 82.5 ± 11.9 95.1 ± 15.4  <0.0001* 
LDL (mmol/l) 3.2 ± 1.0 3.5 ± 1.1  0.113 
Triglycerides (mmol/l) 2.43 ± 1.3 2.4 ± 1.0  0.714 
VLDL (mmol/l) 0.49 ± 0.26 0.44 ± 0.20  0.198 
Cholesterol (mmol/l) 5.0 ± 1.1 5.2 ± 1.1  0.294 
HDL (mmol/l) 1.3 ± 0.4 1.2 ± 0.4  0.224 
Insulin (pmol/l) 15.2 ± 12.4 17.4 ± 21.2  0.469 
Fasting glucose (mmol/l) 7.1 ± 4.2 10.3 ± 3.8  0.0002* 
FactorWithout MAWith MAUnadjusted OR (95% CI)P
Type 2 diabetes     
 No 71.4 (165) 36.2 (21) 4.4 (2.4–8.1)*  
 Yes 28.6 (66) 63.8 (37)   
Hypertensive     
 No 57.1 (132) 17.2 (10) 6.4 (3.1–13.3)*  
 Yes 42.9 (99) 82.8 (48)   
Diabetes family history     
 No 38.3 (87) 14.3 (8) 3.7 (1.7–8.3)*  
 Yes 61.7 (140) 85.7 (48)   
Hypertension family history     
 No 17.6 (40) 7.1 (4) 2.8 (0.9–8.1)  
 Yes 82.4 (187) 92.9 (52)   
Age at last interview (years) 38.8 ± 6.6 39.1 ± 6.8  0.814 
BMI (kg/m2) 34.4 ± 8.6 37.2 ± 8.9  0.026* 
Log HOMA 1.2 ± 0.8 1.4 ± 0.8  0.107 
HbAlc (%) 6.6 ± 1.8 8.8 ± 3.3  <0.0001* 
Average systolic BP (mmHg) 122.8 ± 17.2 144.3 ± 25.9  <0.0001* 
Average diastolic BP (mmHg) 82.5 ± 11.9 95.1 ± 15.4  <0.0001* 
LDL (mmol/l) 3.2 ± 1.0 3.5 ± 1.1  0.113 
Triglycerides (mmol/l) 2.43 ± 1.3 2.4 ± 1.0  0.714 
VLDL (mmol/l) 0.49 ± 0.26 0.44 ± 0.20  0.198 
Cholesterol (mmol/l) 5.0 ± 1.1 5.2 ± 1.1  0.294 
HDL (mmol/l) 1.3 ± 0.4 1.2 ± 0.4  0.224 
Insulin (pmol/l) 15.2 ± 12.4 17.4 ± 21.2  0.469 
Fasting glucose (mmol/l) 7.1 ± 4.2 10.3 ± 3.8  0.0002* 

Data are % (n) or means ± SD, unless otherwise stated. BP, blood pressure.

*

P < 0.05.

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Table 2—

Characteristics of women with and without MA in GDM cohort who have type 2 diabetes

FactorWithout MAWith MAUnadjusted OR (95% CI)P
Hypertensive     
 No 43.9 (29) 16.2 (6) 4.1 (1.5–11.0)*  
 Yes 56.1 (37) 83.8 (31)   
Diabetes family history     
 No 15.4 (10) 13.9 (5) 1.1 (0.4–3.6)  
 Yes 84.6 (55) 86.1 (31)   
Hypertension family history     
 No 12.3 (8) 5.6 (2) 2.4 (0.5–11.9)  
 Yes 87.7 (57) 94.4 (34)   
Age at last interview (years) 39.9 ± 7.1 39.3 ± 6.7  0.661 
Duration of diabetes (years) 7.0 ± 4.1 6.4 ± 3.4  0.430 
BMI (kg/m2) 36.8 ± 7.7 37.5 ± 7.9  0.662 
Log HOMA 1.5 ± 0.6 1.6 ± 0.6  0.617 
HbAlc (%) 8.4 ± 2.2 10.2 ± 3.1  0.004* 
Average systolic BP (mmHg) 129.2 ± 17.5 146.1 ± 26.5  0.001* 
Average diastolic BP (mmHg) 85.4 ± 11.2 94.8 ± 15.3  0.002* 
LDL (mmol/l) 3.1 ± 1.1 3.2 ± 0.9  0.775 
Triglycerides (mmol/l) 2.9 ± 1.6 2.5 ± 1.1  0.147 
VLDL (mmol/l) 0.6 ± 0.3 0.4 ± 0.2  0.021* 
Cholesterol (mmol/l) 5.0 ± 1.0 5.1 ± 0.9  0.652 
HDL (mmol/l) 1.3 ± 0.5 1.3 ± 0.4  0.849 
Insulin (pmol/l) 16.6 ± 10.4 18.8 ± 25.3  0.627 
Fasting glucose (mmol/l) 11.3 ± 5.8 12.8 ± 5.8  0.211 
FactorWithout MAWith MAUnadjusted OR (95% CI)P
Hypertensive     
 No 43.9 (29) 16.2 (6) 4.1 (1.5–11.0)*  
 Yes 56.1 (37) 83.8 (31)   
Diabetes family history     
 No 15.4 (10) 13.9 (5) 1.1 (0.4–3.6)  
 Yes 84.6 (55) 86.1 (31)   
Hypertension family history     
 No 12.3 (8) 5.6 (2) 2.4 (0.5–11.9)  
 Yes 87.7 (57) 94.4 (34)   
Age at last interview (years) 39.9 ± 7.1 39.3 ± 6.7  0.661 
Duration of diabetes (years) 7.0 ± 4.1 6.4 ± 3.4  0.430 
BMI (kg/m2) 36.8 ± 7.7 37.5 ± 7.9  0.662 
Log HOMA 1.5 ± 0.6 1.6 ± 0.6  0.617 
HbAlc (%) 8.4 ± 2.2 10.2 ± 3.1  0.004* 
Average systolic BP (mmHg) 129.2 ± 17.5 146.1 ± 26.5  0.001* 
Average diastolic BP (mmHg) 85.4 ± 11.2 94.8 ± 15.3  0.002* 
LDL (mmol/l) 3.1 ± 1.1 3.2 ± 0.9  0.775 
Triglycerides (mmol/l) 2.9 ± 1.6 2.5 ± 1.1  0.147 
VLDL (mmol/l) 0.6 ± 0.3 0.4 ± 0.2  0.021* 
Cholesterol (mmol/l) 5.0 ± 1.0 5.1 ± 0.9  0.652 
HDL (mmol/l) 1.3 ± 0.5 1.3 ± 0.4  0.849 
Insulin (pmol/l) 16.6 ± 10.4 18.8 ± 25.3  0.627 
Fasting glucose (mmol/l) 11.3 ± 5.8 12.8 ± 5.8  0.211 

Data are % (n) or mean ± SD, unless indicated otherwise. BP, blood pressure.

*

P < 0.05.

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This work was supported by grant DK-32767 from the National Institute of Diabetes and Digestive and Kidney Diseases (to R.T.A.).

We thank the many African-American women who donated their time to participate in this study and Debra Dixon for her recruiting efforts. We especially thank the late Dr. Buris R. Boshell for his leadership and guidance.

1.
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Address correspondence and reprint requests to Rodney C.P. Go, PhD, Department of Epidemiology and International Health, School of Public Health, 1665 University Blvd., Ryals Public Health Bldg, Room 230N, Birmingham, AL 35294-0022. E-mail: [email protected].

Received for publication 22 February 2001 and accepted in revised form 6 July 2001.

A table elsewhere in this issue shows conventional and Système International (SI) units and conversion factors for many substances.

2001