Independent impact of glycemia and blood pressure in albuminuria on high-risk subjects for metabolic syndrome.

BACKGROUND

Microalbuminuria may reflect diffuse endothelial damage. Considering that diabetes and hypertension cause vasculopathy, we investigated associations of albumin-to-creatinine ratio (ACR) with plasma glucose and blood pressure levels in high-risk subjects for metabolic syndrome.

METHODS

A sample of 519 (246 men) Japanese-Brazilians (aged 60 +/- 11 years), who participated in a population-based study, had their ACR determined in a morning urine specimen. Backward models of multiple linear regression were created for each gender including log-transformed values of ACR as dependent variable; an interaction term between diabetes and hypertension was included.

RESULTS

Macroalbuminuria was found in 18 subjects. ACR mean values for subjects with normal glucose tolerance, impaired fasting glycemia, impaired glucose tolerance and diabetes were 9.9 +/- 6.0, 19.0 +/- 35.4, 20.7 +/- 35.4, and 33.9 +/- 55.0 mg/g, respectively. Diabetic subjects showed higher ACR than the others (p < 0.05). An increase in the proportion of albuminuric subjects was observed as glucose metabolism deteriorated (4.9, 17.0, 23.0 and 36.0%). Stratifying into 4 groups according to postchallenge glycemia (< 7.8 mmol/l, n = 91; > or = 7.8 mmol/l, n = 410) and hypertension, hypertensive and glucose-intolerant subgroups showed higher ACR values. ACR was associated with gender, waist circumference, blood pressure, plasma glucose and triglyceride (p < 0.05); albuminuric subjects had significantly higher levels of such variables than the normoalbuminuric ones. In the final models of linear regression, systolic blood pressure and 2-hour glycemia were shown to be independent predictors of ACR for both genders (p < 0.05). In men, also waist was independently associated with ACR. No interaction was detected between "diabetes and hypertension".

CONCLUSIONS

These findings suggest that both glucose intolerance and hypertension could have independent but not synergistic effects on endothelial function--reflected by albumin loss in urine. Such hypothesis needs to be confirmed in prospective studies.