Ciência Rural ISSN: 0103-8478 [email protected] Universidade Federal de Santa Maria Brasil
Diola Bento, Daniel; Soares Zahn, Fabíola; Duarte, Laura Carolina; de Araújo Machado, Luiz Henrique Feline primary hyperaldosteronism: an emerging endocrine disease Ciência Rural, vol. 46, núm. 4, abril, 2016, pp. 686-693 Universidade Federal de Santa Maria Santa Maria, Brasil
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Feline primary hyperaldosteronism: an emerging endocrine disease
Hiperaldosteronismo primário felino: uma enfermidade endócrina emergente
Daniel Diola BentoI Fabíola Soares ZahnII Laura Carolina DuarteIII Luiz Henrique de Araújo MachadoIV
– REVIEW –
ABSTRACT aumento da excreção de potássio, que ocasionarão, respectivamente, hipertensão arterial sistêmica e hipocalemia grave. O diagnóstico The primary hyperaldosteronism, an endocrine é realizado com base na comprovação da hipersecreção hormonal disease increasingly identified in cats, is characterized by adrenal com supressão da liberação de renina, além de exames de imagem gland dysfunction that interferes with the renin-angiotensin- e avaliação histopatológica da adrenal. O tratamento pode ser aldosterone system, triggering the hypersecretion of aldosterone. curativo, com a adrenalectomia, em enfermidades unilaterais, Pathophysiological consequences of excessive aldosterone ou conservativo, por meio de antagonistas da aldosterona, secretion are related to increased sodium and water retention, suplementação de potássio e anti-hipertensivos. O prognóstico é and increased excretion of potassium, which induce hypertension bom e reservado com a terapia apropriada. and severe hypokalemia, respectively. The most common clinical findings in cats include: polydipsia, nocturia, polyuria, Palavras-chave: medicina felina, endocrinologia, enfermidade generalized weakness, neck ventroflexion, syncope, anorexia, adrenocortical, hipertensão. weight loss, pendulous abdomen and blindness. Diagnosis is based on the evidence of hormonal hypersecretion with suppression of renin release, imaging and histopathological evaluation of adrenal glands. Treatment may be curative with adrenalectomy, in cases INTRODUCTION of unilateral disease, or conservative, through administration of aldosterone antagonists, potassium supplementation and First described in humans in antihypertensives. Prognosis varies from fair to good with the appropriate therapy. This article reviews the main aspects of 1955, primary hyperaldosteronism, also called primary aldosteronism in cats, providing the clinician with Conn syndrome, is an adrenocortical disorder important information for the diagnosis of this disease. characterized by autonomous adrenal hypersecretion
Key words: feline medicine, endocrinology, adrenocortical of aldosterone. Initially considered to be rare, disease, hypertension. hyperaldosteronism is found in approximately 6% of all hypertensive human patients and accounts for RESUMO 11% of those with hypertension non- responding O hiperaldosteronismo primário, doença endrócrina to therapy (FOGARI et al., 2007). The first case in cada vez mais identificada em felinos, caracteriza-se pela cats was reported in 1983 and currently, though little disfunção da glândula adrenal com interferência no sistema renina- known and diagnosed, it is considered an important angiotensina-aldosterona, desencadeando a hipersecreção de adrenocortical disease in the species (BISGNANO aldosterona. As consequências da secreção excessiva de aldosterona estão relacionadas com o aumento da retenção de sódio e água e & BRUYETTE, 2012).
IHospital Veterinário Santa Inês, São Paulo, SP, Brasil. IIDepartamento de Reprodução Animal e Radiologia Veterinária, Faculdade de Medicina Veterinária e Zootecnia (FMVZ), Universidade Estadual Paulista (UNESP), Botucatu, SP, Brasil IIIEspecialidades Veterinárias VESP, Campinas, SP, Brasil IVDepartamento de Clínica Veterinária, Faculdade de Medicina Veterinária e Zootecnia (FMVZ), Universidade Estadual Paulista (UNESP), 18618-970, Botucatu, SP, Brasil. E-mail: [email protected]. Corresponding author. Received 09.06.14 Approved 09.22.15 Returned by the author 12.15.15 CR-2014-1327.R7 Ciência Rural, v.46, n.4, abr, 2016. 687 Bento et al.
Aldosterone plays important roles both of sodium and chloride in the distal convoluted tubules. in the modulation of vascular tone and in the Through this mechanism, it regulates systemic blood central nervous system function. Mineralocorticoid pressure and homeostasis of extracellular fluid in receptors have been identified in non-epithelial response to hemodynamic and electrolyte changes tissues such as heart fibroblasts, endothelial cells, (SCHULMAN, 2010). vascular smooth muscle cells and brain. Experiments Its secretion is primarily regulated by indicate that increased aldosterone concentrations the renin-angiotensin-aldosterone system and the are associated with increased sympathetic excitatory extracellular concentrations of potassium. In addition responses and elevated blood pressure. Aldosterone to these mechanisms, there is evidence that aldosterone is considered pro-inflammatory and pro-fibrotic secretion is also influenced by the adrenocorticotropic in blood vessels periphery and plays a key role hormone (ACTH), natriuretic peptides and certain in vascular remodelling and vasoconstriction, neurotransmitters. In spite of the significant difference in thus leading to endothelial dysfunction. Persistent plasma concentrations of aldosterone observed before hypertension in primary aldosteronism is therefore and after administration of synthetic ACTH (DECLUE a consequence of the synergic effects of sodium et al., 2011), none of these compounds was proven to and fluid retention, increased sympathetic tone, directly or indirectly regulate the secretion of aldosterone endothelial dysfunction and increased total (DJAJADININGRAT-LAANEN et al., 2011). peripheral resistance (JEPSON, 2011). Potassium has a direct effect on the zona glomerulosa of the adrenal glands for the secretion Endocrine physiology of aldosterone of aldosterone. Hyperkalemia stimulates aldosterone Target organs and tissues secretion by depolarization of the zona glomerulosa Aldosterone is a steroid hormone with cells and hypokalemia inhibits such depolarization. strong mineralocorticoid activity. It was previously Sodium (Na+) and potassium (K+) ions are thought to be produced only in the adrenal glands; extremely important and are directly involved in recent studies have shown its production by other establishing the resting membrane potential. Low tissues including heart, brain and blood vessels, in serum potassium concentrations prevent the cell which it presents both autocrine and paracrine action from exercising its action potential thus leading to (CONNELL et al., 2008). muscle weakness. The nerve cell remains in idle state The circulating aldosterone, whose classical and can not perform the ion exchange necessary for targets are kidney epithelium, colon and salivary impulse conduction and muscle tone. glands, overpasses the plasma membrane of such Through the signaling of kidney tissues and binds to the cytoplasmic mineralocorticoid baroreceptors located in the afferent arterioles, receptor. Although this receptor presents equal affinity juxtaglomerular apparatus cells increase or reduce for cortisol and aldosterone, the mineralocorticoid the renin secretion in response to decreased or receptors in these tissues enzymatically convert cortisol increased circulating blood volume or renal blood to cortisone, which has little affinity to the receptor, flow, respectively. The baroreceptors have the function ensuring the availability of mineralocorticoid receptors of regulating blood pressure; when blood pressure is for the circulating aldosterone (DJAJADININGRAT- decreased, kidney baroreceptors are activated and LAANEN et al., 2011). sympathetic activity is increased, resulting in increased Additionally, aldosterone affects other heart rate and peripheral vasoconstriction. epithelial and non-epithelial tissues that contribute to Sympathetic stimulation acts directly the homeostasis of blood pressure, including cardiac on the macula densa, a group of modified cells in tissue. Aldosterone increases blood pressure both by the distal tubules near the end of the loop of Henle the expanding the extracellular fluid, and by increasing and closely associated with juxtaglomerular cells. peripheral vascular resistance (CONNELL et al., 2008). The concentration of sodium in the tubular lumen is As demonstrated in humans, long-term excessive monitored by the macula densa cells, and its reduction mineralocorticoids can trigger microangiopathy, can trigger communication between the macula densa fibrosis and proliferation of endothelium and smooth and juxtaglomerular cells, resulting in renin release. muscle in tissues such as the heart and kidneys. This released renin is responsible for cleavage of angiotensinogen, produced by hepatic metabolism, in Regulation of aldosterone secretion angiotensin I, an inactive peptide which is hydrolyzed in Aldosterone works by increasing the the kidneys to angiotensin II by angiotensin converting excretion of potassium and hydrogen and resorption enzyme (ACE) (SCHULMAN, 2010).
Ciência Rural, v.46, n.4, abr, 2016. Feline primary hyperaldosteronism: an emerging endocrine disease. 688
Besides its vasoconstrictor effect, In humans, six different primary angiotensin II stimulates aldosterone secretion. hyperaldosteronism subtypes have been identified, Moreover, circulating concentrations of renin, including familial hyperaldosteronism. In contrast angiotensin II, and aldosterone are all increased when to what is observed in humans, in which the primary blood flow to the kidneys is reduced, thus leading to bilateral idiopathic hyperaldosteronism (60-65% of increased sodium retention, increased extracellular cases), and aldosterone secretory adenoma (30-35% fluid and low concentration of extracellular potassium of cases) represent the majority of cases (YOUNG, because of urine losses. Once homeostasis has 2003; YOUNG, 2007), in cats, hyperaldosteronism been restored, renin production is reduced and, is mostly attributed to adenomas or adenocarcinomas consequently, so does the concentration of aldosterone of adrenal glands (DJAJADININGRAT-LAANEN et (SCHULMAN, 2010). al., 2011). Of 25 cases in cats with histopathological confirmation described in the literature, 13 were related Metabolism of aldosterone to carcinoma, seven to unilateral adenomas, two to Little is known about the metabolism of bilateral adenomas and three to bilateral hyperplasia aldosterone in cats. The liver is often regarded as the (DJAJADININGRAT-LAANEN et al., 2011). most important site of steroid hormones conjugation DeCLUE et al. (2005) reported one case and inactivation. In cats, cortisol, estradiol of adenocarcinoma in a cat, with the adrenal glands and progesterone are mainly excreted via bile secreting significant amounts of both aldosterone and (GRAHAM & BROWN, 1996). Due to the structural progesterone. Young (2003) reported adrenocortical similarity, it is expected that the same would occur cancer as part of a recognized syndrome in humans, with aldosterone. According to SYME et al. (2007), known as multiple endocrine neoplasia (MEN), in urinary excretion of the free form of aldosterone in which, in the presence of autosomal dominance, cats is about 77 times lower than in humans and seven the patient develops tumors in endocrine organs, times lower when compared to dogs. especially pancreas, thyroid, and pituitary. In another case reported the cat presented adrenal adenoma, Etiology and pathophysiology of hyperaldosteronism insulinoma and parathyroid adenoma (REIMER Two pathophysiological mechanisms et al., 2005). Despite the data in the literature, can lead to hypersecretion of aldosterone. The DJAJADININGRAT-LAANEN et al. (2011) reduction in effective arterial blood volume suggested that the occurrence of adrenocortical caused by heart failure, kidney disease or severe hyperplasia may be greater than that reported in cats hypoproteinemia, activates the renin-angiotensin- and suggested that histopathological examination aldosterone system. This physiological response should be essential to determine the cause of the is called secondary hyperaldosteronism primary hyperaldosteronism in cats, even though it is or hyperreninemic hyperaldosteronism rarely performed. (DJAJADININGRAT-LAANEN et al., 2011). Although not identified until the present In the primary or hyporeninemic time, it is believed that some stimulating factor, hyperaldosteronism, autonomous hypersecretion of probably a pituitary peptide present in the circulation, aldosterone is held by neoplastic tissue, adrenocortical is responsible for adrenocortical hyperplasia (JAVADI adenomas or adenocarcinomas, or by nodular et al., 2005). The idiopathic form of the disease can hyperplasia of the zona glomerulosa of the adrenal lead to incomplete suppression of renin, while in the cortex, also known as primary hyperaldosteronism or neoplastic form there is a complete suppression (ASH non neoplastic hyperaldosteronism. In contrast, the et al, 2005; JAVADI et al., 2005; DJAJADININGRAT- secretion of aldosterone in these situations is associated LAANEN et al., 2011). In cats presenting incomplete with suppressed renin activity (SCHULMAN, 2010). suppression of renin, the primary hyperaldosteronism Pathophysiological consequences of becomes an important mediator of the progression excessive aldosterone secreted are related to the of kidney failure. This occurs because of the two increase in sodium and water retention, and increased circulating mediators of fibroproliferative destruction potassium excretion, which can trigger systemic arterial and vascular changes, aldosterone and angiotensin II hypertension and severe hypokalemia, respectively. (JAVADI et al., 2005). Furthermore, as soon as potassium is shifted to the According to JAVADI et al. (2005), extracellular compartment, hydrogen ions are moved chronic kidney failure has been related to intracellularly, thus leading to metabolic alkalosis tubulointerstitial and glomerular injury as well as (DJAJADININGRAT-LAANEN et al., 2011). the excessive accumulation of extracellular matrix
Ciência Rural, v.46, n.4, abr, 2016. 689 Bento et al. in the kidney. The extracellular matrix accumulation Potassium is the major intracellular may be mediated by a number of factors, including electrolyte and the relationship between its angiotensin II. Its action is believed to stimulate both intracellular and extracellular levels is the main renal interstitial fibrosis and mesangial, glomerular determinant of the electric potential of the endothelial and tubular epithelial hyperplasia and membranes; any significant change in extracellular hypertrophy. Regarding aldosterone, JAVADI et potassium concentration can therefore have al. (2005) reported its contribution to renal injury effects not only on metabolic functions, but also in by promoting vascular fibrosis and thrombosis. nerve conduction, with muscular repercussions; In addition, many cats may present evidence of hypokalemic polymyopathy is a reflection of cardiovascular damage secondary to hypertension this. Hind limbs weakness, episodic spasticity because of increased intravascular volume, such as of forelimbs, plantigrade positioning, impaired murmur, cardiomegaly evidenced by radiographic jumping, flaccid paresis associated to hyporeflexia, evaluation and ventricular hypertrophy evidenced dysphagia, respiratory distress, lethargy, and mental by echocardiography (DECLUE et al., 2005). depression have been described (ASH et al., 2005; In humans, the cardiovascular effects of DJAJADININGRAT-LAANEN et al., 2011). From aldosterone hypersecretion are well understood 33 feline cases reported by SCHULMAN (2010), (GIACCHETTI et al., 2009); in cats, however, blindness due to retinal detachment or intraocular the role of the primary hyperaldosteronism in the bleeding as a consequence of systemic hypertension development or progression of heart diseases has was observed in 11 animals. not been determined (SCHULMAN, 2010). Care Other deleterious effects of hypertension should be taken in cases where the hypersecretion include myocardial hypertrophy and kidney damage of aldosterone to the cardiovascular system (DECLUE et al., 2005). Polyuria, polydipsia, is observed, as in many patients, especially polyphagia or anorexia, urinary incontinence or geriatric ones, hypertension, hypokalemia, and nocturia, weight loss, and diarrhea are other reported azotemia or evidence of cardiovascular changes clinical manifestations (SCHULMAN, 2010). Physical are misattributed to chronic kidney failure or examination may reveal a palpable mass in the heart failure as primary disorders rather than hypogastric region, pronounced muscular atrophy, the the direct effect of primary aldosteronism skin fragility syndrome, systolic murmur and irregular (DJAJADININGRAT-LAANEN et al., 2011). heartbeat (BISIGNANO & BRUYETTE, 2012). According to a review of 40 cats diagnosed Clinical presentation with the disorder (DJAJADININGRAT-LAANEN et Cats diagnosed with primary al., 2011), hypertension was observed in 31 of 37 aldosteronism are mostly geriatrics, although cats submitted to blood pressure assessment; ocular the disturb had already been identified in cats changes, including hyphema, mydriasis, increased younger than five years (SCHULMAN, 2010). tortuosity of the retinal vessels, edema and retinal From 40 confirmed or suspected cases of primary detachment, were observed in 10 of 19 animals hyperaldosteronism reported, the average age was 13 submitted to ophthalmologic evaluation; hypokalemic years (DJAJADININGRAT-LAANEN et al., 2011). polymyopathy was observed in 19 of 40 cases; signs Apparently there is no predilection for gender or of congestive heart failure was present in one cat, and breed (SCHULMAN, 2010). no abnormalities were reported in two patients by the Primary hyperaldosteronism was first physical assessment. reported in 24 domestic shorthair cats, in three Regarding laboratory findings in cats, domestic longhair cats, two British Shorthairs, and moderate to severe hypokalemia is typically one individual of each of the following breeds: found, although in the early course of the disease Siamese, Persian, Tonkinese, Burmese, Burmilla the concentrations are within the reference range (DJAJADININGRAT-LAANEN et al., 2011). (DECLUE et al., 2005; JAVADI et al., 2005). Sodium Weakness, of sudden or insidious onset, is the most levels are generally normal or slightly increased and common clinical manifestation, followed by cervical indicate a proportional water absorption in relation ventroflexion related to hypokalemic polymyopathy, to the tubular absorption of sodium, triggered by that occurs most commonly with potassium aldosterone (SCHULMAN, 2010). If hypokalemic concentrations close to 2.5mmol/L-1 (EGER et al., polymyopathy is observed, the levels of creatine 1983; MACKAY et al., 1999; ASH et al., 2005; kinase (CK) are markedly increased (AHN, 1994). REIMER et al, 2005). This is explained as severe hypokalemia can lead to
Ciência Rural, v.46, n.4, abr, 2016. Feline primary hyperaldosteronism: an emerging endocrine disease. 690 an acute muscular injury, which triggers the release of clinician to use the assessment of aldosterone activity extremely toxic components into the circulation, most as a single test (DECLUE et al., 2005). JAVADI et al. notably myoglobin and CK (GOTO et al., 2009). (2004) determined a reference value of 80-450pmol Because of the potential to precipitate L-1 (28.8 to162.2pg ml-1) for plasma aldosterone or worsen an existing chronic renal injury, the activity from studies in healthy cats, and reported cats may also present isosthenuria and increased that neither stress nor body condition affected the serum creatinine and the concentrations of nitrogen concentrations. Nevertheless, the same authors compounds (EGER et al., 1983; ASH, 2005). recommend that plasma aldosterone activity should Furthermore, proteinuria is a common finding due to always be based on serum potassium concentrations, both the direct action of aldosterone hypersecretion as hypokalemia is decisive for reduced aldosterone and hypertension (JAVADI et al., 2005). Although secretion. Thus, an aldosterone activity at or above no study has effectively demonstrated its prevalence, the laboratory reference values is inappropriate in metabolic alkalosis can be observed in patients with hypertensive or hypokalemic cats (JAVADI et al., primary hyperaldosteronism since extracellular 2004; LO et al., 2014.). potassium translocation leads to hydrogen ions moving into the intracellular compartment Urinary aldosterone: creatinine ratio (DJAJADININGRAT-LAANEN et al., 2011). The assessment of the urinary aldosterone Primary hyperaldosteronism in humans to creatinine ratio was recently investigated in cats. may be associated with metabolic syndrome, Although the amount of excreted aldosterone through characterized by insulin resistance, inadequate urine in cats is smaller than in humans or dogs function of beta cells, circulating pro-inflammatory (SYME et al., 2007), the ratio can be determined and proteins and prothrombotic tendency (FALLO et the sample is both easy to obtain and representative al., 2006; SCHULMAN, 2010). Although there of the aldosterone circulation during the whole period is no parameter established in feline medicine, of the collected urine production (SCHULMAN, DJAJADININGRAT-LAANEN et al. (2011), reported 2010). This has been shown to be a practical and in their review that all four cats with specified glucose noninvasive method in the diagnosis of primary determination were hyperglycemic. hyperaldosteronism in cats when combined with the suppression induced by salt or fludrocortisone acetate Diagnosis (DJAJADININGRAT-LAANEN et al., 2013). This Aldosterone: plasma renin ratio drug was shown to cause a significant reduction on In cats, the gold standard to differentiate urinary aldosterone to creatinine ratio in healthy the primary hyperaldosteronism from the secondary cats, but not in an animal with confirmed primary hyperaldosteronism is the aldosterone: renin hyperaldosteronism. ratio, being 0.3 to 3.8 the established reference value (JAVADI et al., 2004; JAVADI et al., 2005). Other tests Thus, cats with adrenocortical tumors have very The adrenocorticotropic hormone (ACTH) high plasma aldosterone activity and, in general, stimulates the production of aldosterone and may be completely suppressed plasma renin activity, since used to evaluate adrenal mineralocorticoid production the secretion is independent of the stimulation of (BISIGNANO & BRUYETTE, 2012). Exogenous the renin-angiotensin-aldosterone system (JAVADI ACTH causes reliable increase in aldosterone et al., 2005). In the case of bilateral hyperplasia, secretion and a recommended IV dose of 125mg however, the obtained plasma renin activity may be ACTH per cat has been used, followed by blood slightly increased or within the upper reference limits sample collection 60 to 75 minutes after the hormone (DJAJADININGRAT-LAANEN et al., 2011). administration (DECLUE et al., 2011). Despite Care must be taken in obtaining the this possibility of ACTH use, BISIGNANO & samples to ensure the accuracy of the test, p.e. the BRUYETTE (2012) concluded that such a test is of obtainment of appropriate amount (>4mL) and questionable utility. immediate freezing after centrifugation. The reference An ideal test based on the suppression of ranges for plasma renin activity vary widely between aldosterone production in normal cats, but presenting laboratories, which complicates the interpretation little or no effect on those patients with primary and standardization of the test (DJAJADININGRAT- hyperaldosteronism, would be the best method to LAANEN et al., 2011). Moreover, few laboratories confirm that hyperactivity of zona glomerulosa is offer the plasma renin test, which often requires the the responsible for the increased activity of plasma
Ciência Rural, v.46, n.4, abr, 2016. 691 Bento et al. aldosterone (BISIGNANO & BRUYETTE, 2012). glands on ultrasound or CT scan and all the others In a study by DJAJADININGRAT-LAANEN et presented minor visible abnormalities. al. (2013) the fludrocortisone suppression test Abnormalities in adrenal glands may still was effective to exclude the diagnosis of primary correspond to cortisol or progesterone secreting hyperaldosteronism in cats presenting plasma masses, pheochromocytomas or nonfunctional aldosterone: renin ratio within the reference range. masses and the finding of abnormal adrenal This test should be performed in cats with plasma glands do not necessarily imply hypersecretion of aldosterone: renin ratio between 7.5x10-9 and aldosterone. For this reason, imaging evaluation is 46.5x10-9 ; fludrocortisone should be given at 0.05mg only performed after confirming hyperaldosteronism kg-1 12h-1 for 4 days. in humans (DECLUE et al., 2005). The ratio is determined in the morning urine before, during and after the fourth day of Treatment and prognosis administration; a suppression lower than 50% For cats with unilateral primary indicates inadequate secretion of aldosterone. The aldosteronism with no evidence of metastasis, fludrocortisone suppression test cannot predict the adrenalectomy is the therapy of choice and is etiology of the disease and before performing the test, curative for both adenoma and adenocarcinoma blood pressure of the animal should be evaluated; with signs of hypokalemia or hypertension, hypertension was not observed in this study. Potassium with resolution of the clinical manifestations levels should be assessed before and during the test, as eliminating additional postoperative therapy (ASH fludrocortisone can lead to hypokalemia. Some tests are et al., 2005; ROSE et al, 2007; LO et al., 2014). already available in human medicine, p.e. the captopril In human patients, in which aldosterone is secreted stimulation test, the saline infusion test and the oral by adenomas, the control of blood pressure after administration of sodium test (DJAJADININGRAT- adrenalectomy is achieved in 50-60% of cases LAANEN et al., 2011). (DUESBERG & PETERSON, 1997). Post operative complications may occur Imaging and include sepsis, bleeding and thromboembolism Imaging tests, aiming on checking the (DECLUE et al., 2005). These complications were laterality of the disease (essential in guiding the reported in 8 of 18 surgical cases in cats, 6 of them choice of therapy), should be performed in all being fatal (MACKAY et al., 1999; RIJNBERK et patients in which primary hyperaldosteronism is al., 2001; ASH et al., 2005; DECLUE et al., 2005). suspected, specially when screening tests indicate Drug therapy with administration of abnormal regulation of aldosterone secretion. spironolactone, potassium supplementation and The clinical and laboratory suspicion must antihypertensive agents is required in many coexist, as changes in the image not necessarily cats, especially those presenting idiopathic corresponding to hyperaldosteronism but to the hyperaldosteronism. The reported survival time other kind of hormone producing or non producing in cats with conservative therapy ranges from lesion may occur. In these cases, surgery may be several months up to years (ASH et al., 2005). unnecessary or even lead to death, for example in Spironolactone, an aldosterone receptor antagonist the case of a pheochromocytoma that is operated in the distal convoluted tubules and renal collecting without adequate pharmacological preparation ducts, promotes potassium retention and sodium (BISIGNANO & BRUYETTE, 2012). excretion. The initial dose of 2mg kg-1 every 12 In cats, the abnormalities observed hours may be increased up to a maximum of 4mg during ultrassonographic examination in patients kg-1, above which it may cause anorexia, diarrhea with primary hyperaldosteronism may vary from and emesis. Potassium supplementation, preferably the presence of calcification and masses to changes oral, is required in refractory cases. The medication in echogenicity of the adrenal glands (MACKAY of choice for persistent hypertension is amlodipine, et al., 1999; ASH et al., 2005). Both computed a calcium channel blocker, at an initial dose of 0.1mg tomography and magnetic resonance imaging kg-1 every 24 hours (BISIGNANO & BRUYETTE, can be used to improve the image obtained from 2012; DJAJADININGRAT-LAANEN et al., 2011). the adrenal glands in cats (ASH et al., 2005). In Mainly because of non-selective a study performed by JAVADI et al. (2005), from affinity of spironolactone for androgen, estrogen 11 cats diagnosed with hyperaldosteronism, only and progesterone receptors in humans, a new two exhibited normal appearance of the adrenal generation of aldosterone antagonists, eplerenone,
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