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Incidence of hypertension in individuals with different blood pressure salt-sensitivity: results of a 15-year follow-up study

Barba, Gianvincenzoa; Galletti, Ferrucciob; Cappuccio, Francesco Pc; Siani, Alfonsoa; Venezia, Antonellab; Versiero, Marcob; Della Valle, Elisabettad; Sorrentino, Paolob; Tarantino, Giovannib; Farinaro, Eduardod; Strazzullo, Pasqualeb

doi: 10.1097/HJH.0b013e3281139ebd
Original papers: Kidney

Objective To evaluate the incidence of hypertension and the rate of decline in renal function in a sample of 47 Olivetti Heart Study (OHS) participants whose blood pressure (BP) salt-sensitivity and renal tubular sodium handling had been assessed in 1987–88.

Methods During the 2002–04 OHS follow-up examination, medical history, physical examination and blood and urine sampling were performed in 36 of the 47 participants to the baseline study (age 60 ± 6 years; average follow-up = 15.1 ± 0.6 years). The renal length was measured in 23 participants by kidney ultrasonography. Based on the baseline salt-sensitivity evaluation, the subjects were classified into a lower salt-sensitivity (LSS, n = 20) and a higher salt-sensitivity group (HSS, n = 16).

Results In comparison with the LSS group, HSS participants had a significantly higher incidence of hypertension (87.5 versus 50.0%, P = 0.02), a higher glomerular filtration rate (median, first to fourth quartile: 81.9, 72.3–95.2 versus 72.3, 59.9–81.2 ml/min; P = 0.03) and greater kidney length (median, first to fourth quartile: 68.2, 63.3–72.1 versus 61.9, 58.7–62.7 mm/m of height; P = 0.003). The incidence of hypertension remained significantly higher in HSS individuals after adjustment for age, intercurrent changes in body mass index and baseline blood pressure on low sodium diet (P = 0.04).

Conclusion Our findings indicate that individuals with higher BP salt-sensitivity have a higher rate of incident hypertension and suggest an altered renal tubular sodium handling involving a trend to increased glomerular filtration rate and blood pressure over time as a possible mechanism.

aEpidemiology and Population Genetics, Institute of Food Sciences, CNR, Avellino

bDepartment of Clinical and Experimental Medicine, ‘Federico II’ University of Naples, Naples, Italy

cDivision of Clinical Sciences, Clinical Sciences Research Institute, Warwick Medical School, Coventry, UK

dDepartment of Preventive Medical Sciences, ‘Federico II’ University of Naples, Naples, Italy

Received 3 August, 2006

Revised 4 February, 2007

Accepted 15 February, 2007

Correspondence to Gianvincenzo Barba, Epidemiology and Population Genetics, Institute of Food Science, National Research Council, Via Roma 52A/C, 83100 Avellino, Italy Tel: +39 0825299 353; fax: +39 0825299 423; e-mail: gbarba@isa.cnr.it

© 2007 Lippincott Williams & Wilkins, Inc.