In a 10-year-old castrated male shorthaired German pointer polyuria was ass
ociated with slight hypokalemia, hypophosphatemia and alkalosis, as well as
elevated plasma concentrations of a glucocorticoid-inducible iso-enzyme of
alkaline phosphatase. Repeated measurements of urinary corticoids and norm
al suppressibility of the hypothalamus-pituitary-adrenocorticial axis exclu
ded glucocorticoid excess,
Urine osmolality (Uosm) did not increase during administration of the vasop
ressin analogue desmopressin. At the time water deprivation had caused Uosm
to rise from 300 to 788 mOsm/kg, there was also plasma hypertonicity. Duri
ng hypertonic saline infusion the osmotic threshold for vasopressin release
was increased.
The combination of elevated plasma aldosterone concentrations and unmeasura
bly low plasma renin activity pointed to primary hyperaldosteronism. As ini
tially computed tomography (CT) did not reveal an adrenocortical lesion, th
e dog was treated with the aldosterone antagonist spironolactone. This caus
ed Uosm to rise in a dose-dependent manner. However, well-concentrated urin
e was only achieved with doses that gave rise to adverse effects.
Once repeated CT, using 2-mm-thick slices, had revealed a small nodule in t
he cranial pole of the left adrenal, unilateral adrenalectomy was performed
which resolved the polyuria completely. Also the plasma concentrations of
kalium, aldosterone and renin activity returned to within their respective
reference ranges. The adrenocortical nodule had the histological characteri
stics of an aldosteronoma, with the non-affected zona glomerulosa being atr
ophic.
In this dog with primary hyperaldosteronism the polyuria was characterized
by vasopressin resistance and increased osmotic threshold of vasopressin re
lease, similar to the polyuria of glucocorticoid excess. The possibility is
discussed that the polyuria of glucocorticoid excess is actually a mineral
ocorticoid effect. (C) 2001 Elsevier Science Inc. All rights reserved.