Primary hyperaldosteronism in two cats

Flood, Shannon; Randolph, John F.; Gelzer, Anna R.; Refsal, Kent R.

doi:10.5326/15473317-35-5-411

Cited by 74 publications

(106 citation statements)

References 13 publications

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“…Several case series have described cats with hyperaldosteronism secondary to adrenal neoplasia 20, 21, 22, 23. Such cats usually demonstrate PAC substantially higher than cats in this study, and yet not all of them will have systemic hypertension.…”

Section: Discussionmentioning

confidence: 52%

Plasma Renin Activity and Aldosterone Concentrations in Hypertensive Cats with and without Azotemia and in Response to Treatment with Amlodipine Besylate

Jepson

Syme

Elliott

2013

Veterinary Internal Medicne

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BackgroundRole of renin‐angiotensin aldosterone system (RAAS) in feline systemic hypertension is poorly understood.ObjectivesExamine plasma renin activity (PRA) and plasma aldosterone concentrations (PAC) in normotensive and hypertensive cats with variable renal function and in response to antihypertensive therapy.AnimalsOne hundred and ninety‐six cats >9 years from first opinion practice.Methods PRA, PAC, and aldosterone‐to‐renin ratio (ARR) were evaluated in cats recruited prospectively and grouped according to systolic blood pressure (SBP) and renal function (nonazotemic normotensive [Non‐Azo‐NT], nonazotemic hypertensive [Non‐Azo‐HT], azotemic normotensive [Azo‐NT], azotemic hypertensive [Azo‐HT]). Changes in PRA and PAC were evaluated with antihypertensive therapy (amlodipine besylate).ResultsPlasma renin activity (ng/mL/h; P = .0013), PAC (pg/mL; P < .001), and ARR (P = 0.0062) differed significantly among groups. PRA (ng/mL/h) was significantly lower in hypertensive (Non‐Azo‐HT; n = 25, median 0.22 [25th percentile 0.09, 75th percentile 0.39], Azo‐HT; n = 44, 0.33 [0.15, 0.48]) compared with Non‐Azo‐NT cats (n = 57, 0.52 [0.28, 1.02]). Azo‐HT cats had significantly higher PAC (n = 22, 149.8 [103.1, 228.7]) than normotensive cats (Non‐Azo‐NT; n = 26, 45.4 [19.6, 65.0], Azo‐NT; n = 18, 84.1 [38.6, 137.8]). ARR was significantly higher in Azo‐HT (n = 20, 503.8 [298.8, 1511]) than Azo‐NT cats (n = 16, 97.8 [77.0, 496.4]). Significant increase in PRA was documented with antihypertensive therapy (pretreatment [n = 20] 0.32 [0.15–0.46], posttreatment 0.54 [0.28, 1.51]), but PAC did not change.Conclusions and Clinical ImportanceHypertensive cats demonstrate significantly increased PAC with decreased PRA. PRA significantly increases with antihypertensive therapy. Additional work is required to determine the role of plasma aldosterone concentration in the pathogenesis of hypertension and whether this relates to autonomous production or activation of RAAS without demonstrable increase in PRA.

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Section: Discussionmentioning

confidence: 52%

Plasma Renin Activity and Aldosterone Concentrations in Hypertensive Cats with and without Azotemia and in Response to Treatment with Amlodipine Besylate

Jepson

Syme

Elliott

2013

Veterinary Internal Medicne

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“…For cats that underwent surgical adrenalectomy in other studies, survival times were between 240 and 1,803 days 8, 9, 17. Unfortunately, perioperative complications resulted in a high frequency of euthanasia before discharge.…”

Section: Discussionmentioning

confidence: 99%

“…Hypertension also was refractory to medical management 17. Reported survival times for cats treated medically range from 50 to 984 days 8, 9, 17. However, medical management only addresses clinical signs and does not treat the underlying adrenal mass, acute tumor hemorrhage,32 distant metastasis,1, 6, 30 or tumor invasion into the caudal vena cava or renal vessels 1…”

Section: Discussionmentioning

confidence: 99%

“…This disease was considered rare in humans and companion animals for many decades,2, 3, 4, 5 but recently has been found to be more prevalent with improved screening tests and detection in both humans and cats 6, 7. Since the first reported case of primary hyperaldosteronism in a cat in 1983,8 there have been only a few case reports of feline primary hyperaldosteronism (PHA) 9, 10, 11, 12, 13, 14, 15, 16, 17, 18…”

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confidence: 99%

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Treatment of Aldosterone‐Secreting Adrenocortical Tumors in Cats by Unilateral Adrenalectomy: 10 Cases (2002–2012)

Holt

Brown

et al. 2013

Veterinary Internal Medicne

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BackgroundPrimary hyperaldosteronism (PHA) in cats occurs as a consequence of excessive hormone production by an adrenocortical tumor. Median survival time, association between tumor type and prognosis, and the likelihood that cats require continued medical therapy after surgery have not been systematically evaluated.ObjectivesTo determine the median survival time of cats with PHA treated by unilateral adrenalectomy. To examine if tumor type, anesthesia time, or tumor location (left or right side) affect survival and if affected cats require continued postoperative treatment for persistent hypertension or hypokalemia.AnimalsTen client‐owned cats.MethodsRetrospective study. Cats were diagnosed with PHA based on clinical signs, increased plasma aldosterone concentration, and advanced imaging. Cats underwent unilateral adrenalectomy. Survival time (days alive after surgery) was determined for each cat. Factors affecting median survival time were investigated, including histopathology, anesthesia time, and location (side) of the tumor.ResultsEight of 10 cats survived to discharge from the hospital post adrenalectomy. Overall median survival was 1,297 days (range 2–1,582 days). The only significant factor affecting median survival time was anesthesia time >4 hours. Tumor type and location (side) did not significantly affect median survival time. No cats required continued medical treatment for PHA.Conclusions and Clinical ImportanceAlthough PHA in cats is still considered an uncommon condition, it should be considered in middle to older aged cats with hypokalemic polymyopathy and systemic hypertension. Surgical correction by unilateral adrenalectomy is a viable approach to definitive treatment of PHA with no need for continued medical management.

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“…15,23 In contrast, in cats, suspicion of PHA arises with identification of hypokalemia, hypertension, and elevated plasma aldosterone concentration; diagnosis ultimately relies on identification of a discrete tumor within the adrenal glands. 1,2,4,[7][8][9]14,17,[19][20][21] However, in the absence of a discrete tumor, such as in cats with adrenocortical nodular hyperplasia, minimal or no adrenal gland changes may be detected via ultrasound. 10 In fact, in humans, following a diagnosis of PHA, further testing such as a computed tomography scan and adrenal vein blood sampling is conducted to differentiate between unilateral and bilateral hyperplasia, adenoma or adenocarcinoma.…”

Section: Introductionmentioning

confidence: 99%

Serum aldosterone and cortisol concentrations before and after suppression with fludrocortisone in cats

et al. 2015

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Abstract. Primary hyperaldosteronism is an increasingly recognized syndrome in cats, and diagnosis can be difficult. A potential diagnostic method has been reported, utilizing oral fludrocortisone administered twice daily for 4 days followed by collection of urine. In the current study, we sought to determine if blood sampling and a shorter dosing period would provide a possible means to test for primary hyperaldosteronism. Also, cortisol concentrations were measured to assess the potential of fludrocortisone to act as a glucocorticoid in cats. In phase I, 8 healthy laboratory cats were studied in a placebo-controlled, crossover design. Serum aldosterone and cortisol concentrations were measured before and on the second, third, and fourth day of treatment and compared within groups. In phase II, based on the results obtained in phase I, 8 healthy client-owned cats were administered 3 doses of fludrocortisone or placebo. Serum aldosterone and cortisol concentrations were compared before and after treatment within groups. In both phases, serum aldosterone and cortisol concentrations were significantly suppressed in fludrocortisone-treated cats. Thus, it was determined that oral administration of fludrocortisone causes suppression of serum aldosterone in healthy adult cats after only 3 doses. Further research is needed to determine the effects of oral fludrocortisone in cats with primary hyperaldosteronism and cats with other disorders causing hypertension and/or hypokalemia to determine if this protocol can be used as a tool for the definitive diagnosis of primary hyperaldosteronism.

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Primary hyperaldosteronism in two cats

Cited by 74 publications

References 13 publications

Plasma Renin Activity and Aldosterone Concentrations in Hypertensive Cats with and without Azotemia and in Response to Treatment with Amlodipine Besylate

Plasma Renin Activity and Aldosterone Concentrations in Hypertensive Cats with and without Azotemia and in Response to Treatment with Amlodipine Besylate

Treatment of Aldosterone‐Secreting Adrenocortical Tumors in Cats by Unilateral Adrenalectomy: 10 Cases (2002–2012)

Serum aldosterone and cortisol concentrations before and after suppression with fludrocortisone in cats

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