Rossi E, Sani C, Perazzoli F, Casoli MC, Negro A, Dotti C.
Alterations of calcium metabolism and of parathyroid function
in primary aldosteronism and their reversal by spironolactone
or by surgical removal of aldosterone-producing adenomas
Am J Hypert
(Sep) 8:884-893 1995
This paper confirms and extends previous studies linking alterations
in sodium and in calcium metabolism in hypertension secondary to
aldosterone excess. The control and the hypertensive groups (primary
hyperaldosteronism, low renin hypertension, normal renin hypertension) are
well matched (age, sex, duration of hypertension, arterial pressure and
CrCl) and the data are carefully analysed. Serum intact PTH (1-84) was
measured by a radiometric assay.
The main results (raised PTH in primary hyperaldosteronism, reversal of
raised PTH after surgery in patients with adenoma) are in line with a
previous paper by Resnick (Am J Med 1985;385-390) but the increase in serum
PTH was comparatively much less than in the cases described by Resnick. To
my knowledge this paper includes the largest series of hypertensives with
hyperaldosteronism in which alterations in Ca metabolism have been
characterized,
and it is the first that documents reversal of the Ca abnormalities
after spironolactone.
Plasma ionized Ca levels in hypertensives with hyperaldosteronism was less
than those in
control subjects and comparable to levels in patients with low and normal
renin hypertension. Interestingly, ionized Ca levels in the latter
two groups were
slightly reduced and accompanied by a normal to slightly reduced serum
PTH. The authors discuss at length this finding which contrasts with data
by Resnick (Ann Int Med 1986; 105:649-654) and attribute the difference to
the fact that their sample size is relatively small. A more plausible
explanation is that they studied only white hypertensives while Resnick
most likely included black hypertensives (the race was not indicated in
Resnick's paper). It is worth noting that in another European study in
white hypertensives, serum intact PTH was (inappropriately) normal in a
group of essential hypertensives with frank hypercalciuria and mild
hypocalcemia (Zoccali C. Contrib. Nephrol. 1991;90:49-53).
All in all, this study nicely revisits the alterations in calcium
metabolism in hypertension and indicates that a frank derangement of
parathyroid function occurs only in patients with primary
hyperaldosteronism.
(Zoccali)
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