Feline hyperaldosteronism

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Feline Primary Hyperaldosteronism (PHA) is perhaps the most common adrenocortical disorder in cats. In both primary and secondary hyperaldosteronism, concentrations of the hormone aldosterone are elevated.[1] Secondary hyperaldosteronism is a normal physiological response to decreased arterial blood volume, wherein hypovolemia activates the renin-angiotensin system to stimulate aldosterone synthesis and thus increase fluid retention.[2]

Primary hyperaldosteronism[edit]

Primary hyperaldosteronism is a disorder of the adrenal cortex that causes increased circulating aldosterone levels. There are two types of PHA. One type is caused by a unilateral aldosterone-producing adenoma or adenocarcinoma. The other type, known as idiopathic hyperaldosteronism, occurs with bilateral adrenal hyperplasia.[1]

The pathophysiological consequences of PHA are a result of abnormal increases in the hormone aldosterone. Aldosterone receptors are present on the epithelial cells of the distal nephron in the kidney. Aldosterone activates sodium channels that result in sodium resorption from the urine.[1] Increased sodium and water retention results in systemic arterial hypertension.[2] This increase in active sodium reabsorption generates an electrochemical gradient that leads to passive transfer of potassium from the tubular cells into the urine. This causes a lower total body concentration of potassium and potentially, hypokalemia.[1] Hypokalemia affects polarization of nerve and muscle membranes, which causes episodic muscle weakness.[2]

Symptoms[edit]

Affected cats present with a median age of 13 years. A breed or sex predilection has not been documented. Most affected cats present with muscular weakness and/or ocular signs of hypertension. Signs of muscle weakness can include a plantigrade stance of the hindlimbs, cervical ventroflexion, inability to jump, lateral recumbency, or collapse. Ocular signs of arterial hypertension include mydriasis, hyphema, or blindness due to retinal detachment and/or intraocular hemorrhages.[1] A palpable mass in the cranial abdomen is another potential finding.[2]

Differential diagnosis[edit]

Blood pressure should be measured in sick cats, especially at older ages. If the blood pressure is persistently increased, common causes of hypertension, especially kidney disease and hyperthyroidism, should be ruled out with basic laboratory tests. When a cause is not readily apparent, and especially when hypokalemia is identified, hyperaldosteronism should be considered. Diagnostic imaging, usually beginning with abdominal ultrasound, may identify that one or both adrenal glands are enlarged. Imaging may also detect metastasis and usually includes radiographs of the chest in addition to abdominal ultrasound and/or computerized tomography (CT).[1]

Screening test[edit]

The ratio of plasma aldosterone concentration (PAC) to plasma renin activity (PRA) is currently the best screening test for feline PHA. In cats with unilateral or bilateral zona glomerulosa tumors, the PAC may be very high and the PRA is usually completely suppressed. In cats with idiopathic bilateral nodular hyperplasia of the zona glomerulosa, the PAC may be slightly elevated or high normal. In the presence of hypokalemia even a mildly elevated aldosterone should be considered inappropriately high. A high-normal or elevated PAC with a low PRA indicates persistent aldosterone synthesis in the presence of little or no stimulation of the renin-angiotensin system.

Treatment[edit]

Unilateral primary hyperaldosteronism due to an adrenocortical adenoma or adrenocarcinoma can be potentially cured surgically. Unilateral adrenalectomy is the treatment of choice for unilateral PHA. Potential complications include hemorrhage and postoperative hypokalemia. With complete removal of the tumor, prognosis is excellent.[1]

Bilateral primary hyperaldosteronism due to hyperplasia of the zona glomerulosa or metastasized adrenocortical adenocarcinoma should be treated medically. Medical therapy is aimed at normalizing blood pressure and plasma potassium concentration. Mineralocorticoid receptor blockers, such as spironolactone, coupled with potassium supplementation are the most commonly used treatments. Specific therapy for treating high blood pressure (e.g., amlodipine), should be added if necessary.[2]

References[edit]

  1. ^ a b c d e f g Djajadiningrat-Laanen, S.; Galac, S.; Kooistra, Hans (2011). "Primary Hyperaldosteronism: Expanding the diagnostic net". Journal of Feline Medicine and Surgery 13 (9): 641–650. 
  2. ^ a b c d e Kooistra, Hans S. (2006). "Hyperaldosteronism in Cats.". World Small Animal Veterinary Association World Congress Proceedings.