OBJECTIVE: Although hypertension is a well known risk factor for microalbuminuria, it is unclear whether blood pressure less than 140/90 mmHg could be a risk for microalbuminuria. We assessed the relationship between baseline blood pressure and the future onset of microalbuminuria in the general population. METHODS: We studied 2603 town inhabitants of Watari, located in the southeastern part of Miyagi prefecture, Japan. Demographic data, medical history, sitting blood pressure, fasting blood chemistry, and urinary albumin-creatinine ratio were measured at baseline and were followed annually during the next 3 years. RESULTS: Among 2338 individuals who were normoalbuminuric at baseline (albumin-creatinine ratio <30 mg/g Cr), 161 developed microalbuminuria (albumin-creatinine ratio 30-299 mg/g Cr) during a mean follow-up period of 2.4 years. Incident microalbuminuria patients were older (63.7 ± 8.6 vs. 61.4 ± 10.5 years; P < 0.01), included fewer men (31.1 vs. 40.1%; P < 0.05), had a greater BMI (23.8 ± 3.6 vs. 23.1 ± 3.1 kg/m²; P < 0.01), higher blood pressures (133.5 ± 18.1/75.8 ± 11.9 vs. 127.6 ± 18.1/73.4 ± 11.0 mmHg; P < 0.01 for both systolic and diastolic), higher triglycerides (median 1.18 vs. 1.02 mmol/l; P < 0.01), higher fasting blood glucose (median 5.05 vs. 4.94 mmol/l; P < 0.01), higher urinary albumin excretion (median 13.0 vs. 5.9 mg/g Cr; P < 0.001), and lower serum creatinine concentrations (59.2 ± 12.8 vs. 61.4 ± 13.2 μmol/l; P < 0.05) compared to persistent normoalbuminuric individuals. Multivariate Cox proportional hazards analysis including all covariates revealed that only baseline urinary albumin excretion was an independent predictor for future microalbuminuria, whereas high-normal DBP, triglyceride, and fasting blood glucose concentrations were all significant predictors in the model excluding urinary albumin excretion. CONCLUSIONS: High-normal DBP associated with metabolic disorders could initiate glomerular damage, leading to future microalbuminuria.
OBJECTIVE: Although hypertension is a well known risk factor for microalbuminuria, it is unclear whether blood pressure less than 140/90 mmHg could be a risk for microalbuminuria. We assessed the relationship between baseline blood pressure and the future onset of microalbuminuria in the general population. METHODS: We studied 2603 town inhabitants of Watari, located in the southeastern part of Miyagi prefecture, Japan. Demographic data, medical history, sitting blood pressure, fasting blood chemistry, and urinary albumin-creatinine ratio were measured at baseline and were followed annually during the next 3 years. RESULTS: Among 2338 individuals who were normoalbuminuric at baseline (albumin-creatinine ratio <30 mg/g Cr), 161 developed microalbuminuria (albumin-creatinine ratio 30-299 mg/g Cr) during a mean follow-up period of 2.4 years. Incident microalbuminuria patients were older (63.7 ± 8.6 vs. 61.4 ± 10.5 years; P < 0.01), included fewer men (31.1 vs. 40.1%; P < 0.05), had a greater BMI (23.8 ± 3.6 vs. 23.1 ± 3.1 kg/m²; P < 0.01), higher blood pressures (133.5 ± 18.1/75.8 ± 11.9 vs. 127.6 ± 18.1/73.4 ± 11.0 mmHg; P < 0.01 for both systolic and diastolic), higher triglycerides (median 1.18 vs. 1.02 mmol/l; P < 0.01), higher fasting blood glucose (median 5.05 vs. 4.94 mmol/l; P < 0.01), higher urinary albumin excretion (median 13.0 vs. 5.9 mg/g Cr; P < 0.001), and lower serum creatinine concentrations (59.2 ± 12.8 vs. 61.4 ± 13.2 μmol/l; P < 0.05) compared to persistent normoalbuminuric individuals. Multivariate Cox proportional hazards analysis including all covariates revealed that only baseline urinary albumin excretion was an independent predictor for future microalbuminuria, whereas high-normal DBP, triglyceride, and fasting blood glucose concentrations were all significant predictors in the model excluding urinary albumin excretion. CONCLUSIONS: High-normal DBP associated with metabolic disorders could initiate glomerular damage, leading to future microalbuminuria.