Microalbuminuria (MA) is a marker of adverse outcome in hypertension. The aim of this study was to investigate the association of MA with cardiovascular risk factors and glomerular hyperfiltration in the early stage of hypertension and to assess its predictive value for the development of sustained hypertension requiring antihypertensive treatment.
We studied 1041 young stage 1 hypertensive subjects. Study variables were 24-h ambulatory blood pressure and heart rate, anthropometric measures, metabolic variables, creatinine clearance and lifestyle factors analyzed as a function of ascending urinary albumin measured from 24-h collections. Subjects were followed until they developed sustained hypertension and were eligible for antihypertensive medication according to current guidelines.
Seventeen outpatient clinics in Italy.
Eighty-five percent of the subjects were normoalbuminuric, 9% had borderline MA, and 6% had overt MA. No between-group differences were found for age, body mass index, heart rate, lifestyle factors and biochemistry in both genders. Creatinine clearance was greater in the subjects with overt MA and borderline MA than in the normoalbuminuric subjects (P = 0.003 and 0.011, respectively). In a two-way ANCOVA, microalbuminuric subjects both with hyperfiltration (P < 0.001) and with normal filtration (P = 0.04) had higher 24-h systolic blood pressure than subjects with normoalbuminuria and normal filtration. In a Cox analysis, neither MA nor hyperfiltration were significant predictors of development of sustained hypertension.
MA is not associated with an adverse metabolic risk profile in the early stage of hypertension. MA is associated with greater hemodynamic load and with glomerular hyperfiltration in this clinical setting, but does not help in predicting those subjects destined to develop sustained hypertension requiring antihypertensive therapy.
aClinica Medica 4, University of Padova, Padova, bTown Hospital, Vittorio Veneto, cTown Hospital, San Daniele del Friuli and dTown Hospital, Sacile, Italy.
Sponsorship: This work was supported by grants from the University of Padova, Padova, Italy and from the Associazione ‘18 Maggio 1370', San Daniele del Friuli, Italy.
Correspondence and requests for reprints to Professor Paolo Palatini MD, Trial Coordinator, Clinica Medica 4, University of Padova, via Giustiniani, 2, 35128 Padova, Italy. Tel: +39 049 8212278; fax: +39 049 8754179; e-mail: firstname.lastname@example.org
Received 23 April 2004 Revised 16 July 2004 Accepted 21 July 2004