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Incidence of hypertension in individuals with different blood
pressure salt-sensitivity: results of a 15-year follow-up study
Gianvincenzo Barba
a
, Ferruccio Galletti
b
, Francesco P. Cappuccio
c
,
Alfonso Siani
a
, Antonella Venezia
b
, Marco Versiero
b
, Elisabetta Della Valle
d
,
Paolo Sorrentino
b
, Giovanni Tarantino
b
, Eduardo Farinaro
d
and
Pasquale Strazzullo
b
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 W 6 years; average follow-
up U 15.1 W 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 U 20) and a
higher salt-sensitivity group (HSS, n U 16).
Results In comparison with the LSS group, HSS
participants had a significantly higher incidence of
hypertension (87.5 versus 50.0%, P U 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 U 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 U 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 U 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.
J Hypertens 25:1465–1471 Q 2007 Lippincott Williams &
Wilkins.
Journal of Hypertension 2007, 25:1465–1471
Keywords: blood pressure, glomerular filtration rate, prospective study,
renal function, sodium dependent hypertension
a
Epidemiology and Population Genetics, Institute of Food Sciences, CNR,
Avellino,
b
Department of Clinical and Experimental Medicine, ‘Federico II’
University of Naples, Naples, Italy,
c
Division of Clinical Sciences, Clinical
Sciences Research Institute, Warwick Medical School, Coventry, UK and
d
Department of Preventive Medical Sciences, ‘Federico II’ University of Naples,
Naples, Italy
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
Received 3 August 2006 Revised 4 February 2007
Accepted 15 February 2007
Introduction
A heterogeneous blood pressure (BP) response to
changes in dietary sodium chloride intake, a phenom-
enon generally referred to as BP salt-sensitivity, is
observed in both hypertensive patients and normotensive
individuals [1–3]. On the basis of the feature character-
istics of well described forms of monogenic hypertension
[4–6], it is conceivable that a different ability of the
kidney to excrete sodium and water is involved in this
phenomenon [7].
We have previously reported on BP, renal function and
tubular sodium handling in a sample of healthy normo-
tensive male volunteers drawn from a middle-aged male
working population in 1987–88 [3]. Our results showed
that those with higher salt-sensitivity, estimated by their
BP response to low salt diet, had increased BP, greater
proximal tubular sodium reabsorption and higher glomer-
ular filtration rate (GFR) when on habitual high sodium
diet compared to those with a lower degree of salt-
sensitivity. These alterations were no longer apparent
when the subjects were placed on a low sodium diet
(40 mmol Na/day for 3 days). We speculated that the
trend to greater tubular sodium reabsorption detected
in the more salt-sensitive subjects elicited humoral
adaptive responses to overcome the difficulty in sodium
excretion at the cost of an increase in BP and GFR.
Other studies have reported increased GFR and/or
intraglomerular pressure in salt-sensitive hypertension
[8–13]. In turn, hyperfiltration could heighten suscepti-
bility to renal function deterioration and actually it has
been found to be associated with early organ damage in
hypertensive patients [14].
Original article 1465
0263-6352 ß 2007 Lippincott Williams & Wilkins