Page 121 - Clinical Small Animal Internal Medicine

11 Hypoadrenocorticism in Dogs and Cats 89

and lymphopenia) in a stressed cat should raise suspi- Hyperaldosteronism in Cats
VetBooks.ir cion for HOAC. Etiology/Pathophysiology
Diagnostic imaging is not necessary to diagnose
HOAC, but is often performed as part of the diagnostic
work‐up prior to suspicion for HOAC. Thoracic radio- Primary hyperaldosteronism (PHA) results from
graphs may reveal pulmonary hypoperfusion or micro- excessive aldosterone production by the zona glomer-
cardia due to dehydration; abdominal imaging is ulosa of the adrenal cortex, and usually leads to clinical
usually unremarkable. The ECG may reveal bradycar- signs related to hypokalemia and/or systemic hyper-
dia, but the other classic ECG abnormalities (spiked tension. Unilateral adrenocortical tumors are the most
T‐wave, decreased R‐wave, and absent P‐wave) are less common cause; carcinomas are more common than
consistent in hyperkalemic cats, though the reason for adenomas. Bilateral adenomas occur rarely. Idiopathic
this is unclear. adrenal hyperplasia (“non-tumorous hyperaldosteron-
Definitive diagnosis of HOAC in cats relies upon an ism”), characterized by bilateral micronodular hyper-
ACTH stimulation test. A serum sample is taken prior plasia of the zona glomerulosa, is reported less
to administering 5 μg/kg cosyntropin (or tetracosac- frequently than the tumorous forms. However, since
trin), which is given intravenously. A poststimulation definitive diagnosis requires histopathologic confirma-
sample is collected one hour later. The diagnosis of tion, and these cats are treated medically instead of
HOAC is consistent with a poststimulation cortisol surgically, idiopathic adrenal hyperplasia is likely
concentration of <2 μg/kg. underdiagnosed.
Measurement of endogenous ACTH concentrations Aldosterone is the most important endogenous miner-
can help determine whether an Addisonian cat with nor- alocorticoid in dogs and cats. It primarily acts on the
mal electrolyte concentrations has primary or secondary principal cells of the distal tubules and collecting ducts
HOAC. High concentrations are consistent with primary in the kidney, stimulating sodium and water reabsorp-
disease. Low concentrations are expected in cats with tion (thus expanding the vascular volume), and promot-
secondary disease. ing potassium and acid excretion.
Aldosterone is regulated by the renin‐angiotensin‐
aldosterone system (RAAS). Decreased renal perfu-
Therapy sion pressure and decreased delivery of sodium to the

Treatment of feline HOAC is similar to treatment of distal tubules stimulate the release of renin from
canine HOAC. Intravenous crystalloid fluids (0.9% juxtaglomerular cells. Renin cleaves angiotensinogen,
NaCl, LRS or Plasma‐Lyte A) should be administered produced by the liver, into angiotensin I. Angiotensin I
to cats in Addisonian crisis. One‐third of a shock dose is then converted to angiotensin II by angiotensin con-
(40–60 mL/kg) is given, and then the patient is reas- verting enzyme. Angiotensin II then stimulates aldos-
sessed. Dexamethasone (0.15 mg/kg BID) is given terone synthesis via the activity of aldosterone
intravenously until oral prednisolone is tolerated. synthase. Hyperkalemia also has a direct stimulatory
Prednisolone is started at 1 mg/kg/day, and slowly effect on aldosterone secretion, with ACTH contribut-
tapered to 0.1–0.2 mg/kg/day following discharge. Two ing to a lesser degree.
to four times the dose should be given when the cat Secondary hyperaldosteronism (“hyperreninemic
experiences stress (going to the veterinarian, visitors in hyperaldosteronism”) results from increased renin
the house, concurrent illness). produced in response to reduced arterial blood vol-
Mineralocorticoid supplementation can be provided ume, such as occurs with congestive heart failure,
using either desoxycorticosterone pivalate (DOCP, renal failure, and liver failure. Primary hyperaldoster-
2.2 mg/kg every 25 days) or fludrocortisone (0.05–0.1 mg/ onism, however, is due to autonomous secretion of
cat, SID–BID). Dosage adjustments are made based on aldosterone from the zona glomerulosa, and is associ-
electrolyte concentrations, as described for dogs. ated with low plasma renin activity. It is sometimes
referred to as “hyporeninemic hyperaldosteronism”
for this reason.
Prognosis In addition to expected consequences of hyperaldo-

Cats in Addisonian crisis tend to respond to treatment steronism, such as hypokalemia and hypertension, some
more slowly than dogs, and may require 3–5 days for cats with PHA develop progressive renal disease. There
significant improvement. Long‐term prognosis for cats is evidence that aldosterone itself mediates vascular
with hypoadrenocorticism is good, provided that the fibrosis and inflammation, resulting in glomerular scle-
owners continue to administer medication and moni- rosis, hyaline arteriolar sclerosis, tubular atrophy, and
tor as directed. interstitial fibrosis. Thus, in azotemic patients with