Aging-associated perifollicular changes and calcium deposition in poodles.

BACKGROUND: It is commonly accepted that canine dystrophic mineralization of the hair follicle glassy membrane can be seen in hyperadrenocorticism and as a senile change in poodles. Pathology textbooks define this change as deposition of calcium salts in the form of basophilic, amorphous, granular material along collagen fibrils. HYPOTHESIS/OBJECTIVES: The aim was to evaluate whether the incidence of the lesion is specific to poodles and if it is always associated with calcium deposition. ANIMALS: One hundred and forty-seven dogs divided into three groups: (i) 91 normal poodles; (ii) 40 dogs of other breeds; and (iii) 16 dogs with clinical/histopathological diagnosis of hyperadrenocorticism. METHODS AND MATERIALS: Retrospective study; with haematoxylin and eosin, and von Kossa staining. RESULTS: Our findings demonstrate that perifollicular changes of the hair follicle glassy membrane of poodles are not always associated with calcium deposition. CONCLUSIONS AND CLINICAL IMPORTANCE: A specific staining is needed to identify true calcium deposition when performing histological examination of the skin of poodles.

Sex-hormone producing adrenal tumors causing behavioral changes as the sole clinical sign in 3 cats.

Three neutered cats with adrenocortical tumors that were presented with behavioral changes but no evidence of hyperaldosteronism or hypercortisolism are described. All 3 cats had resolution of their clinical signs following adrenalectomy. For neutered cats presenting with behavior changes, a sex-hormone secreting adrenal tumor should be considered as a differential diagnosis.

Tumeurs surrénaliennes produisant des hormones sexuelles causant des changements de comportement comme seul signe clinique chez 3 chats. Les cas de trois chats stérilisés ayant des tumeurs surrénaliennes qui ont été présentés avec des changements comportementaux mais aucun signe d'hyperaldostéronisme ou hypercortisolisme sont décrits. Les trois chats ont eu une résorption de leurs signes cliniques après une surrénalectomie. Pour les chats stérilisés présentant des changements comportementaux, une tumeur surrénalienne sécrétant des hormones sexuelles devrait être considérée comme un diagnostic différentiel.(Traduit par Isabelle Vallières).

Evaluation of coagulation profile in dogs with ACTH-dependent hyperadrenocorticism compared to healthy dogs by rotational thromboelastometry (ROTEM).

Despite their low morbidity, thromboembolic events in hyperadrenocorticism are associated with high mortality. Identifying the main hemostatic abnormalities will improve the prophylactic approach of these canine patients. The aim of this study was to evaluate hemostatic alterations related with ACTH-dependent HAC and its association with hypercoagulable state. For this purpose, 25 dogs diagnosed with ACTH-dependent HAC were compared with 28 healthy dogs as a control group. The hemostatic variables included platelet count, antithrombin, fibrinogen, D-dimer, PT, aPTT, rotational thromboelastometry (ROTEM) and platelet aggregation. Results showed a hypercoagulable state in 32% (8/25) dogs by ROTEM, which had at least 2 of the next features: decreased coagulation time (CT) or clot formation time (CFT) on INTEM (5/25) or EXTEM (4/25); increased maximum clot firmness (MCF) on INTEM (9/25), EXTEM (6/25) and FIBTEM (9/25). These same variables had a significant difference (P≤ 0.05) compared with the control group, as well as the parameters of α-angle and CT. Median fibrinogen levels (310 vs.178 mg/dL), mean platelet aggregation (11.1 vs. 7.9 Ohms), median platelet count (360 vs. 225 ×103/µL) and mean antithrombin activity (140 vs. 119%) were increased in ACTH-dependent HAC dogs compared to control group. PT (7.1 vs. 8.0 seconds) and aPTT (11.6 vs. 15.2 seconds) were also shortened in ACTH-dependent HAC dogs. Our findings confirm the presence of a hypercoagulable tendency in dogs with HAC. Although multifactorial, fibrinogen concentration and MCF FIBTEM showed the relevance of this protein for hypercoagulability in HAC.

Evaluation of oral telmisartan administration as a suppression test for diagnosis of primary hyperaldosteronism in cats.

BACKGROUND: Development of a telmisartan-based suppression test may facilitate the diagnosis of primary hyperaldosteronism (PHA) in cats, which remains difficult today. OBJECTIVES: To develop a telmisartan suppression test (TST) that is safe, and able to suppress aldosterone secretion in healthy cats but not in cats with PHA. ANIMALS: Ten healthy cats and 6 cats with PHA. METHODS: Prospective study using a placebo-controlled crossover design to investigate a TST in healthy cats, and evaluation of TST in cats with PHA. Plasma aldosterone concentration, potassium concentration, and systolic blood pressure (SBP) were measured before (T0), and 1 hour (T1) and 1.5 hours after (T1.5) PO administration of 1 mg/kg of telmisartan, 2 mg/kg of telmisartan or placebo. RESULTS: Median age in healthy cats was 3 years old (range, 1-7). In healthy cats, a telmisartan dose of 2 mg/kg significantly decreased aldosterone concentration at T1 and T1.5 compared with T0. Placebo had no significant effect on aldosterone concentration. In cats diagnosed with PHA, a 2-mg/kg dose of telmisartan did not induce any significant change in aldosterone concentration at T1 or T1.5 compared with T0. No adverse effects of telmisartan (e.g., hyperkalemia, systemic hypotension) were observed in any cats. CONCLUSIONS AND CLINICAL IMPORTANCE: The oral TST shows promise as a diagnostic test for the diagnosis of PHA in cats.

Prospective evaluation of a telmisartan suppression test as a diagnostic tool for primary hyperaldosteronism in cats.

BACKGROUND: In a previous study, telmisartan suppressed aldosterone secretion in healthy cats but not in cats with primary hyperaldosteronism (PHA). HYPOTHESES: Telmisartan suppresses aldosterone secretion in middle-aged healthy cat and cats with diseases that may result in secondary hyperaldosteronism, but not in those with PHA. ANIMALS: Thirty-eight cats: 5 with PHA; 16 with chronic kidney disease (CKD), subclassified as hypertensive (CKD-H) or non-hypertensive (CKD-NH); 9 with hyperthyroidism (HTH); 2 with idiopathic systemic arterial hypertension (ISH); and 6 healthy middle-aged cats. METHODS: Prospective, cross-sectional study. Serum aldosterone concentration, potassium concentration, and systolic blood pressure were measured before and 1 and 1.5 hours after PO administration of 2 mg/kg of telmisartan. The aldosterone variation rate (AVR) was calculated for each cat. RESULTS: No significant difference in the minimum AVR was observed among groups (median [quartile 1 (Q1); quartile 3 (Q3)]: 25 [0; 30]; 5 [-27; -75]; 10 [-6; -95]; 53 [19; 86]; 29 [5; 78]) for PHA, CKD, HTH, ISH, and healthy cats, respectively (P = .05). Basal serum aldosterone concentration (pmol/L) was significantly higher in PHA cats (median [Q1; Q3]: 2914 [2789; 4600]) than in CKD-H cats (median [Q1; Q3]: 239 [189; 577], corrected P value = .003) and CKD-NH cats (median [Q1; Q3]: 353 [136; 1371], corrected P value = .004). CONCLUSIONS AND CLINICAL IMPORTANCE: The oral telmisartan suppression test using a single dose of 2 mg/kg telmisartan did not discriminate cats with PHA from healthy middle-aged cats or cats with diseases that may result in secondary hyperaldosteronism.

Surgical findings and outcomes after unilateral adrenalectomy for primary hyperaldosteronism in cats: a multi-institutional retrospective study.

CASE SERIES SUMMARY: Twenty-nine cats from different institutions with confirmed or highly suspected primary hyperaldosteronism treated by unilateral adrenalectomy were retrospectively included in this study. The most frequent clinical signs were lethargy (n = 20; 69%) and neck ventroflexion (n = 17; 59%). Hypokalaemia was present in all cats, creatinine kinase was elevated in 15 and hyperaldosteronism was documented in 24. Hypertension was frequently encountered (n = 24; 89%). Preoperative treatment included potassium supplementation (n = 19; 66%), spironolactone (n = 16; 55%) and amlodipine (n = 11; 38%). There were 13 adrenal masses on the right side, 15 on the left and, in one cat, no side was reported. The median adrenal mass size was 2 × 1.5 cm (range 1-4.6 × 0.4-3.8); vascular invasion was present in five cats, involving the caudal vena cava in four cats and the renal vein in one. Median duration of surgery was 57 mins. One major intraoperative complication (3%) was reported and consisted of haemorrhage during the removal of a neoplastic thrombus from the caudal vena cava. In 4/29 cats (14%), minor postoperative complications occurred and were treated medically. One fatal complication (3%) was observed, likely due to disseminated intravascular coagulation. The median duration of hospitalisation was 4 days; 97% of cats survived to discharge. The potassium level normalised in 24 cats within 3 months of surgery; hypertension resolved in 21/23 cats. Follow-up was available for 25 cats with a median survival of 1082 days. Death in the long-term follow-up was mainly related to worsening of comorbidities. RELEVANCE AND NOVEL INFORMATION: Adrenalectomy appears to be a safe and effective treatment with a high rate of survival and a low rate of major complications. Long-term medical treatment was not required.

[Primary hyperaldosteronism in cats]. / Primärer Hyperaldosteronismus bei Katzen.

Primary hyperaldosteronism is a clinical syndrome characterized by an elevated aldosterone secretion by the adrenals. The present case series describes 7 cats with primary hyperaldosteronism, which were presented between 2002 and 2011. Common clinical symptoms were weakness, anorexia, cervical ventroflexion and blindness. All cats showed hypokalemia. In 6 cats, blood pressure was determined: 5 cats showed hypertension, of which 4 animals exhibited retinal detachment and blindness. In the ultrasonographic examination, unilateral adrenomegaly was present in 6 cats whereas one animal showed normal adrenals. In 4 cats, the serum aldosterone concentration was above the reference range. Five cats underwent unilateral adrenalectomy, which was accomplished uneventfully and returned the electrolytes back to normal. Histopathological examination of the adrenals revealed 2 carcinomas and 4 adenomas; one cat with ultrasonographic normal adrenals exhibited bilateral nodular hyperplasia.

Suspected primary hyperreninism in a cat with malignant renal sarcoma and global renin-angiotensin-aldosterone system upregulation.

A 14-year-old male castrated domestic medium-hair cat with diabetes mellitus was evaluated for vomiting, diarrhea, and anorexia. Two weeks before presentation, the cat had been diagnosed with congestive heart failure and started on furosemide. Initial diagnostic testing identified hypokalemia, systemic hypertension, and hypertrophic cardiomyopathy phenotype, and plasma aldosterone concentration was moderately increased. Abdominal ultrasound examination disclosed bilateral adrenomegaly and a right renal mass, and cytology of a needle aspirate of the mass was consistent with malignant neoplasia. The cat was treated with amlodipine and spironolactone. Because of the unusual presentation for hyperaldosteronism, a comprehensive profile of renin-angiotensin-aldosterone system (RAAS) peptides was performed. Results from multiple timepoints indicated persistently and markedly increased plasma renin activity and generalized RAAS upregulation. In addition to the lack of adrenal tumor, the markedly increased plasma renin activity was atypical for primary hyperaldosteronism. These clinical findings are suggestive of primary hyperreninism, a condition previously unreported in cats. The concurrent presence of a renal neoplasm suggests the possibility of a renin-secreting tumor.

Presumptive renal tubular acidosis secondary to topiramate administration in a cat.

OBJECTIVE: To describe renal tubular acidosis (RTA) and secondary acquired hyperaldosteronism in a cat as an adverse effect of topiramate therapy. CASE SUMMARY: An 8-year-old neutered female cat on chronic oral topiramate therapy at a recommended dose (11.9 mg/kg q 8 h) for seizure control was presented with severe metabolic acidosis and hypokalemia. Plasma electrolyte and acid-base analysis identified a severe metabolic acidosis (pH 7.153, reference interval: 7.31-7.46), hypokalemia (2.08 mmol/L [2.08 mEq/L], reference interval: 3.5-4.8 mmol/L [3.5-4.8 mEq/L]), and ionized hypercalcemia (1.85 mmol/L [1.85 mEq/L], reference range: 1.1-1.4 mmol/L [1.1-1.4 mEq/L]). Urinalysis revealed a urine specific gravity of 1.021 and a pH of 7.0. Diagnostic workup suggested distal RTA as a cause of the cat's acid-base and electrolyte disturbances. Aldosterone concentration was moderately increased, suggestive of secondary hyperaldosteronism. The metabolic abnormalities resolved with supportive care and discontinuation of topiramate. NEW OR UNIQUE INFORMATION PROVIDED: Topiramate is suggested to have led to the development severe RTA in a cat.

Multiple corticosteroid abnormalities in cats with hyperaldosteronism.

BACKGROUND: The frequency with which multiple corticosteroid abnormalities occur in cats with aldosterone secreting adrenocortical tumors is unknown. OBJECTIVES: To evaluate adrenal-derived corticosteroids in cats in which blood samples were submitted for measure of aldosterone. ANIMALS: Two hundred ninety-seven cats. METHODS: Retrospective study. Analysis of a convenience sample of previously submitted serum or plasma. Progesterone, corticosterone, and cortisol were measured in feline serum or plasma samples submitted to an endocrinology laboratory for aldosterone measurements. Demographics and clinical history were retrieved from submittal forms when provided. Statistical testing was performed to investigate associations among the adrenal corticosteroids. RESULTS: Progesterone and corticosterone concentrations were strongly correlated (ρ = 0.74; P < .001). Progesterone (median, 5 nmol/L; interquartile range, 3-10 nmol/L) and corticosterone (113 nmol/L, 38-250 nmol/L) in cats with markedly increased aldosterone concentrations (≥3000 pmol/L) were higher than progesterone (1 nmol/L, 1-2 nmol/L) and corticosterone (12 nmol/L, 3-25 nmol/L) in cats with normal aldosterone concentrations (P < .001 for both comparisons). Progesterone concentrations ≥10 nmol/L (normal, ≤2 nmol//L) occurred in 24 of 76 (32%) cats with aldosterone concentrations ≥3000 pmol/L. Cortisol was lower in cats with aldosterone concentrations ≥3000 pmol/L as compared to those with aldosterone concentrations <500 pmol/L (59 nmol/L, 27-103 nmol/L vs 103 nmol/L, 49-182 nmol/L; P = .002). CONCLUSIONS AND CLINICAL IMPORTANCE: Multiple corticosteroid abnormalities occur in a subset of cats with hyperaldosteronism. The magnitude of increases in progesterone and corticosterone in some cats with hyperaldosteronism is likely to be clinically relevant.

Retrospective study of aldosterone and progesterone secreting adrenal tumors in 10 cats.

BACKGROUND: Primary hyperaldosteronism caused by adrenal neoplasia has been well described in cats. Multiple corticosteroid abnormalities occur in a subset of affected cats, but characterizations of this syndrome are limited to several case reports. OBJECTIVES: To describe a series of cats with adrenal tumors secreting aldosterone and additional corticosteroids. ANIMALS: Ten cats with multiple corticosteroid secreting adrenocortical tumors. METHODS: Retrospective case series. Medical records of cats with adrenal tumors secreting both aldosterone and progesterone were identified. Data concerning historical findings, clinicopathologic features, treatments, and outcomes were retrieved from medical records. RESULTS: All 10 cats had diabetes mellitus in addition to biochemical features of hyperaldosteronism such as hypokalemia. High corticosterone concentrations were observed in all 3 cats in which this corticosteroid was measured. Ultrasound examinations revealed unilateral adrenal tumors in all 10 cases, and the contralateral adrenal gland was either atrophied or not identified in 5 cats. Three of 4 cats developed hypoadrenocorticism after surgical adrenalectomy. Three cats achieved diabetic remission after adrenalectomy. Two cats treated with adrenalectomy survived >1 year, 1 cat survived 6.5 months, and 1 cat was alive 5.5 months after diagnosis. Survival >1 year occurred in 2 of 4 cats treated with medical management alone. Two cats were not treated. CONCLUSIONS AND CLINICAL IMPORTANCE: The presence of multiple corticosteroid abnormalities should be considered in cats with aldosterone secreting adrenal tumors, especially those with concurrent diabetes mellitus. Both surgical and medical management can result in long-term survival, although diabetic remission was documented only in cats undergoing adrenalectomy.

A preclinical pharmacokinetic and pharmacodynamic approach to determine a dose of spironolactone for treatment of congestive heart failure in dog.

Fifteen Beagle dogs were used to describe the anti-aldosterone effect of spironolactone (0, 0.8, 2 and 8 mg/kg) in a hyperaldosteronism model. The magnitude of the aldosterone response observed in this model was very similar to the one described in a dog with congestive heart failure (CHF). Each dog was allocated to a treatment group according to a 5 x 5 Latin square crossover design for five periods with a washout period of 7 days between each period. A maximal possible effect (E(max)) model was employed to determine the basic pharmacodynamic parameters of spironolactone, measured by high-performance liquid chromatography, in antagonizing the renal effects of aldosterone. The change in urinary sodium/potassium ratio in response to a single dose of aldosterone was calculated. The inhibition of this response by oral spironolactone administration was assessed. Aldosterone alone decreased sodium excretion by approximately 35% and urinary potassium concentrations increased by 25%, whereas the urine volume decreased, as expected. The effect of aldosterone on the Na(+)/K(+) ratio was completely reversed (88% inhibition) at a dose of 2 mg spironolactone/kg, while at the dose of 0.8 mg/kg, partial reversal was seen (27.5% inhibition). Urine flow rate was not significantly modified by either aldosterone treatment or aldosterone with spironolactone. The dose of spironolactone required to inhibit the action of aldosterone by 50% (ED(50)) was estimated to be 1.08 +/- 0.28 mg/kg. The E(max) was a ratio of 1.089 +/- 0.085, close to the observed value in negative control group (1.00 +/- 0.18). The proposed spironolactone dose using this E(max) model was 2 mg/kg b.w. once daily for the management.

Primary Hyperaldosteronism in Cats: An Underdiagnosed Disorder.

Primary hyperaldosteronism, also known as Conn's syndrome, is the most common adrenocortical disease in cats. As in humans, this disease is underdiagnosed in cats. Cats presenting with systemic arterial hypertension, hypokalemia, or both quite often are only treated symptomatically without further investigations. This practice may potentially exclude a significant number of cats from receiving appropriate treatment. It is therefore important for general practitioners to be aware of the disease. This article describes the (patho)physiology, clinical presentation, diagnostic approach, and treatment options of for feline primary hyperaldosteronism.

Endocrine diseases in animals.

BACKGROUND: Several endocrine disorders that affect humans also occur as endocrinopathies in companion animals. Spontaneous endocrine disorders in animals may provide valuable information for their counterparts in human endocrinology. For example, the discovery of progesterone-induced growth hormone production in the mammary gland of dogs may have important consequences for understanding the pathogenesis of breast cancer in women. In addition, the majority of diabetic cats have a type of diabetes mellitus that closely resembles type 2 diabetes mellitus in humans and therefore may serve as an animal model for this disease in humans. This review describes several endocrine diseases in companion animals that are quite similar to those in humans and emphasizes their usefulness as spontaneous animal models for human endocrine disorders.

Accuracy of an adrenocorticotropic hormone (ACTH) immunoluminometric assay for differentiating ACTH-dependent from ACTH-independent hyperadrenocorticism in dogs.

BACKGROUND: Adrenocorticotropic hormone (ACTH) determination has been used for 30 years to distinguish ACTH-dependent hyperadrenocorticism (ADHAC) from ACTH-independent hyperadrenocorticism (AIHAC) in dogs. However, the few studies that have evaluated its diagnostic accuracy, based in the majority of cases on older assays, have been associated with systematic, but highly variable proportions of misclassified or unclassified cases. OBJECTIVE: The purpose of the present study is to evaluate the accuracy of a validated ACTH immunoluminometric assay (ILMA) for differentiating between ADHAC and AIHAC. ANIMALS: One hundred and nine dogs with hyperadrenocorticism were included: 91 with ADHAC and 18 with AIHAC. METHODS: Retrospective study. Dogs displaying feedback inhibition after the dexamethasone suppression test, adrenal symmetry, or both were considered to have ADHAC. AIHAC was demonstrated by adrenal tumor histology. For each group, ACTH determination by ILMA was reviewed. RESULTS: In the ADHAC group, plasma ACTH measurements ranged between 6 and 1250 pg/mL (median, 30 pg/mL). In the AIHAC group, all ACTH concentrations were below the lower quantification limit of the assay (<5 pg/mL). The 95% confidence interval was 85-100% for sensitivity and 97-100% for specificity in AIHAC diagnosis. CONCLUSION AND CLINICAL IMPORTANCE: No overlap in ACTH concentrations was observed between dogs with ADHAC and dogs with AIHAC. The use of a new technique with high analytical sensitivity made it possible to use a low threshold (5 pg/mL), avoiding the misclassification of some ADHAC cases with low, but quantifiable concentrations of ACTH. The assessment of ACTH concentrations by ILMA is an accurate tool for differentiating between ADHAC and AIHAC.

Hyperaldosteronism and hyperprogesteronism in a cat.

UNLABELLED: CLINICAL FINDINGS AND INVESTIGATIONS: A 14-year-old female neutered domestic shorthair cat was referred for investigation of progressive hair loss, muscle wasting and hind limb weakness. Diabetes mellitus had been diagnosed 8 months earlier and was well controlled. Abnormalities on serum biochemistry included persistent mild azotaemia, hypochloridaemia, hypokalaemia, metabolic alkalosis and elevated creatine kinase. Physical examination revealed a pot-bellied appearance, with muscle wasting, marked thinning and fragility of the skin, bilaterally symmetrical alopecia, a gallop rhythm and systolic hypertension (173 mmHg). A large, lobulated left adrenal mass was identified using abdominal ultrasound. CONFIRMATION OF DIAGNOSIS: Primary hyperaldosteronism was diagnosed based on an elevated plasma aldosterone concentration and normal plasma renin activity. Hyperprogesteronism was confirmed by adrenocorticotrophic hormone stimulation test. PRACTICAL RELEVANCE: This is only the second reported case of hyperaldosteronism and hyperprogesteronism in the cat. Clinicians should be alert to the possibility of concurrent hyperaldosteronism and hyperprogesteronism in cats with adrenal tumours showing clinical signs referable to both conditions. The putative mechanism is either increased secretion of aldosterone and progesterone from neoplastic cells of the zona glomerulosa and fasciculata/reticularis, respectively, or increased production of progesterone, as an intermediate in the synthesis of aldosterone, from neoplastic cells of the zona glomerulosa alone.

What is your diagnosis? Abdominal mass aspirate in a cat with an increased Na:K ratio.

A 13-year-old domestic shorthair cat was presented for evaluation of pollakiuria. Laboratory abnormalities included mild hypercholesterolemia, moderate hypertriglyceridemia, and a mild increase in the Na:K ratio (43, reference interval 32-41). Abdominal ultrasonography revealed urinary calculi and a soft tissue mass between the right caudate liver lobe and the right kidney. Surgery was done to remove the cystic calculi, and aspirates of the mass were obtained. Cytologic specimens contained a population of large, round to angular cells with round nuclei, coarse irregularly stippled chromatin, 1-2 prominent round to angular nucleoli, and abundant pale basophilic cytoplasm distended by numerous well-delineated vacuoles. Rare binucleated cells and micronuclei, and moderate anisocytosis, anisokaryosis, and anisonucleoleosis were noted. The cytologic interpretation was adrenal neoplasia, consistent with adrenal carcinoma. Approximately 4 months later, the cat developed vomiting, dehydration, weakness, and cervical ventroflexion. Serum biochemical alterations at that time included marked hypokalemia (2.4 mmol/L, reference interval 3.4-5.6 mmol/L) and a markedly increased Na:K ratio (65, reference interval 32-41). Mean systolic blood pressure was 205 mmHg. Surgical removal of the mass was accomplished via right adrenalectomy and a diagnosis of adrenal carcinoma was confirmed histologically. Plasma aldosterone concentration (measured preoperatively) was 1358 pmol/L (reference interval 194-388 pmol/L). Primary hyperaldosteronism caused by a functional adrenal carcinoma is an uncommon condition in cats.

Primary hyperaldosteronism in a domestic ferret with an adrenocortical adenoma.

CASE DESCRIPTION: A 6-year-old spayed female domestic ferret was evaluated because of lethargy, alopecia, pruritus, and an abdominal mass. CLINICAL FINDINGS: On initial examination, nonregenerative anemia, mild azotemia, and a large left adrenal gland mass were identified. However, deterioration of the ferret's general condition prevented excision of the mass, and dyspnea, weakness, hypertension, and severe hypokalemia developed. Plasma aldosterone concentration was >3329 pmol/L, confirming a provisional diagnosis of hyperaldosteronism. High concentrations of sex hormones were also observed, but baseline cortisol concentration was within reference limits. TREATMENT AND OUTCOME: Medical treatment included oral administration of spironolactone, potassium gluconate, leuprolide acetate, amlodipine, and benazepril. Inhalation of albuterol proved effective in reducing the dyspnea. In the following weeks, serum potassium concentration returned to within reference limits and hypertension decreased, but dyspnea persisted. Two months after initial examination, the ferret became anorectic and was euthanized. Histologic examination revealed a large left adrenal gland adenoma, progressive chronic nephropathy, severe pulmonary edema, and focal fibrosis in the left ventricle. Immunohistochemical staining of the adrenal gland mass revealed aldosterone within neoplastic adrenocortical cells. CLINICAL RELEVANCE: Findings suggested that primary hyperaldosteronism should be considered as a possible cause in ferrets with hypokalemia, hypertension, and an adrenal gland mass. Early detection of aldosterone-secreting masses might allow for removal of the tumor before irreversible complications occur.

Adrenalectomy and caval thrombectomy in a cat with primary hyperaldosteronism.

A 13-year-old, castrated male, domestic longhaired cat was diagnosed with primary hyperaldosteronism from an adrenal gland tumor and a thrombus in the caudal vena cava. Clinical signs included cervical ventriflexion, lethargy, weakness, inappetence, and diarrhea. Laboratory tests revealed hypokalemia, normonatremia, hyperglycemia, hypophosphatemia, and elevated creatine kinase activity. Hypokalemia worsened despite oral potassium supplementation. An adrenalectomy and caval thrombectomy were successfully performed utilizing deliberate hypothermia followed by progressive rewarming.