Successful use of short‐term mechanical ventilation to manage respiratory failure secondary to profound hypokalemia in a cat with hyperaldosteronism

Objective – To report successful management of respiratory failure due to severe hypokalemia in a cat with hyperaldosteronism, including short‐term mechanical ventilation strategies and aspects of medical and surgical treatment. Case Summary – A cat presented with bilateral pelvic limb weakness that rapidly progressed to tetraparesis and respiratory muscle failure. Point‐of‐care testing revealed severe hypokalemia (1.9 mmol/L) and mild azotemia. Initial management included endotracheal intubation, mechanical ventilation, and aggressive potassium supplementation. Spironolactone was started due to a high index of suspicion for hyperaldosteronism. A right adrenal mass visualized during abdominal ultrasonographic examination and a serum aldosterone level greater than 3329 pmol/L confirmed the diagnosis. The cat made a full recovery following surgical removal of a right adrenal adenoma. New or Unique Information Provided – We report successful management of respiratory failure in a cat with hyperaldosteronism using short‐term mechanical ventilation. Respiratory failure due to severe hypokalemia should be considered a complication of hyperaldosteronism in cats and may require mechanical ventilation. However, full recovery is possible.     

Use of abdominal ultrasonography in the diagnosis of primary hyperaldosteronism in a cat

A 13-year-old castrated male cat was examined because of a 2-week history of weakness, cervical ventroflexion, and dysphagia. Clinicopathologic abnormalities included hypokalemia and high serum creatine kinase activity. Abdominal ultrasonography revealed a 15-mm spherical mass in the area of the left adrenal gland. Plasma aldosterone concentration was high, and plasma renin activity was low. Findings were diagnostic of primary hyperaldosteronism. The cat responded well to intravenous and oral potassium supplementation while in the hospital. The owner declined surgery; therefore, repeated follow-up abdominal ultrasonography was recommended. The cat did well clinically with medical management alone until day 334, when it was lost to follow-up.     

Primary hyperaldosteronism in two cats.

A condition of primary hyperaldosteronism resulting from an adrenal tumor in two cats is presented and was characterized by hypertension, hypokalemia, inappropriate kaliuresis, low normal plasma renin activity, and markedly increased serum aldosterone concentration. One of the two cats underwent a laparotomy, and in this case hypertension and hypokalemia resolved following the removal of an adrenal tumor.     

Primary hyperaldosteronism: expanding the diagnostic net

PRACTICAL RELEVANCE: Primary hyperaldosteronism is probably the most common adrenocortical disorder in cats. As in humans, it is often unrecognised, which excludes a potentially large number of cats from appropriate treatment. PATIENT GROUP: Affected cats present at a median age of 13 years (range 5-20 years). A breed or sex predilection has not been documented. The excessive secretion of mineralocorticoids usually leads to hypokalaemia and/or systemic arterial hypertension. Most affected cats present with muscular weakness and/or ocular signs of arterial hypertension. DIAGNOSTICS: In any cat presenting with hypokalaemia and/or arterial hypertension, other potential causes should be excluded. The ratio of plasma aldosterone concentration to plasma renin activity (aldosterone:renin ratio) is currently the best screening test for feline primary hyperaldosteronism. Diagnostic imaging is required to differentiate between adrenocortical neoplasia and bilateral hyperplasia, and to detect any distant metastases. CLINICAL CHALLENGES: The differentiation between adrenocortical neoplasia and bilateral hyperplasia is imperative for planning optimal therapy, but the limited sensitivity of diagnostic imaging may occasionally pose a problem. For confirmed unilateral primary hyperaldosteronism, unilateral adrenalectomy is the treatment of choice, and offers an excellent prognosis, but potentially fatal intra- and postoperative haemorrhage is a reported complication and risk factors have yet to be identified. EVIDENCE BASE: Only a few case reports are available on which to base the optimal diagnostic and therapeutic approach to feline primary hyperaldosteronism. This article reviews the physiology of aldosterone production and the pathophysiology of primary hyperaldosteronism, and summarises the currently available literature on the feline disease. Practical suggestions are given for the diagnostic investigation of cats with suspected primary hyperaldosteronism.     

Aldosteronoma in a dog with polyuria as the leading symptom.

In a 10-year-old castrated male shorthaired German pointer polyuria was associated with slight hypokalemia, hypophosphatemia and alkalosis, as well as elevated plasma concentrations of a glucocorticoid-inducible iso-enzyme of alkaline phosphatase. Repeated measurements of urinary corticoids and normal suppressibility of the hypothalamus-pituitary-adrenocorticial axis excluded glucocorticoid excess.Urine osmolality (Uosm) did not increase during administration of the vasopressin analogue desmopressin. At the time water deprivation had caused Uosm to rise from 300 to 788 mOsm/kg, there was also plasma hypertonicity. During hypertonic saline infusion the osmotic threshold for vasopressin release was increased.The combination of elevated plasma aldosterone concentrations and unmeasurably low plasma renin activity pointed to primary hyperaldosteronism. As initially computed tomography (CT) did not reveal an adrenocortical lesion, the dog was treated with the aldosterone antagonist spironolactone. This caused Uosm to rise in a dose-dependent manner. However, well-concentrated urine was only achieved with doses that gave rise to adverse effects.Once repeated CT, using 2-mm-thick slices, had revealed a small nodule in the cranial pole of the left adrenal, unilateral adrenalectomy was performed which resolved the polyuria completely. Also the plasma concentrations of kalium, aldosterone and renin activity returned to within their respective reference ranges. The adrenocortical nodule had the histological characteristics of an aldosteronoma, with the non-affected zona glomerulosa being atrophic.In this dog with primary hyperaldosteronism the polyuria was characterized by vasopressin resistance and increased osmotic threshold of vasopressin release, similar to the polyuria of glucocorticoid excess. The possibility is discussed that the polyuria of glucocorticoid excess is actually a mineralocorticoid effect.     

Urinary aldosterone to creatinine ratio in cats before and after suppression with salt or fludrocortisone acetate

Background: The endocrine diagnosis of primary hyperaldosteronism in cats currently is based on an increased plasma aldosterone to renin ratio, which has several disadvantages for use in veterinary practice. Objectives: To establish a reference range for the urinary aldosterone to creatinine ratio (UACR) and to determine whether oral administration of either sodium chloride or fludrocortisone acetate is effective for use in a suppression test. Animals: Forty‐two healthy cats from an animal shelter and 1 cat with primary hyperaldosteronism from a veterinary teaching hospital. Methods: Morning urine samples for determination of the basal UACR were collected from 42 healthy cats. For the suppression tests, urine samples for the UACR were collected after twice daily oral administration for 4 consecutive days of either sodium chloride, 0.25 g/kg body weight (n = 22) or fludrocortisone acetate, 0.05 mg/kg body weight (n = 15). Results: The median basal UACR was 7.2 × 10^?9 (range, 1.8–52.3 × 10^?9), with a calculated reference range of <46.5 × 10^?9. Administration of sodium chloride resulted in adequate salt loading in 10 of 22 cats, but without significant reduction in the UACR. Administration of fludrocortisone resulted in a significant decrease in the UACR (median, 78%; range, 44–97%; P < .001) in healthy cats. In the cat with an aldosterone‐producing adrenocortical carcinoma, the basal UACR and the UACR after fludrocortisone administration were 32 × 10^?9 and 36 × 10^?9, respectively. Conclusions and Clinical Importance: Using the UACR for an oral fludrocortisone suppression test may be useful for the diagnosis of primary hyperaldosteronism in cats.     

Idiopathic hyperaldosteronism in a dog

Idiopathic hyperaldosteronism was diagnosed in an 8-year-old castrated male Yorkshire Terrier, based on increased concentration of plasma aldosterone, hypertension, hypernatremia, decreased natriuresis, hypokalemia, and hyperkaluria. Unilateral adrenalectomy was performed after visualization of a nodule on the right adrenal gland. Hyperplasia of the zona glomerulosa and increased postoperative aldosterone concentrations supported the diagnosis of idiopathic hyperaldosteronism.     

Hyperaldosteronism in a cat with metastasised adrenocortical tumour

In a 12-year-old male shorthaired cat with attacks of hypokalaemic muscular weakness in spite of oral potassium supplementation, highly elevated plasma aldosterone concentrations in combination with low plasma renin activity pointed to primary hyperaldosteronism. Ultrasonography and computed tomography revealed a large left-sided adrenal tumour growing into the phrenicoabdominal vein and the caudal vena cava. The tumour and its intravascular extension were surgically removed, but the subsequent stenosis of the caudal vena cava caused congestion and renal failure. At autopsy pulmonary micrometastases of the aldosteronoma were found.     

Potassium depletion in cats: renal and dietary influences

Excessive urinary potassium loss was diagnosed in 7 cats with persistent hypokalemia and high serum creatinine concentrations. Renal tubular acidosis (proximal or distal) was not evident in the affected cats. Plasma aldosterone concentrations and plasma renin activities in affected cats were not significantly different from control values. Potassium depletion and hypokalemia were attributed to the combined effects of decreased dietary potassium intake and excessive urinary potassium losses. It was concluded that increased urinary potassium excretion may represent a basic response to renal dysfunction in cats. Data suggested that dietary potassium supplementation improved renal function in most cats in this study.     

Presumptive pseudohypoaldosteronism secondary to chronic urinary tract obstruction from sloughed urinary bladder mucosa and urinary tract infection in a cat

Objective – To describe a case of presumptive secondary pseudohypoaldosteronism (PHA) in a cat with urinary tract infection and chronic urethral obstruction. The obstruction was believed to have resulted from sloughed urinary bladder mucosa secondary to pressure necrosis. Case Summary – A 5‐year‐old, 4 kg, castrated male Siamese cat presented for vomiting and stranguria. Medical history included a perineal urethrostomy for urethral obstruction. Physical examination revealed a large, painful, nonexpressible urinary bladder. Point‐of‐care testing demonstrated electrolyte derangements consistent with a postrenal azotemia and metabolic acidosis. Results of urine culture was positive for bacterial growth. Diagnostic imaging revealed presence of retroperitoneal fluid, marked urinary bladder wall thickening, bilateral hydroureter, mild bilateral pyelectasia, and small nephroliths. The patient was treated for a urinary tract obstruction and infection. In the 3 weeks following initial discharge, the patient was evaluated on multiple occasions for lethargy, intermittent vomiting, inappropriate urination, and progressive polyuria and polydipsia. Although the urinary bladder was easily expressed during repeat examinations, it was persistently distended and subjectively thickened upon palpation. Repeat ultrasound of the urinary tract showed evidence of sloughed tissue in the bladder lumen, likely secondary to chronic urethral obstruction and pressure necrosis. A cystotomy was performed to remove the necrotic tissue, and a revised perineal urethrostomy was done due to a partial urethral stricture. Bladder biopsies were obtained at this time. Postoperatively, the cat was reported by the owners to be urinating normally but continued to be polyuric and polydipsic in the week following discharge. One week after surgery, the cat presented in hypovolemic shock with laboratory findings consistent with a presumptive diagnosis of secondary PHA. New or Unique Information Provided – PHA has not been reported previously in a cat. This case report suggests that aldosterone resistance should be considered in cats with consistent laboratory findings and a history of documented obstructive uropathy and urinary tract infection.     

Organic acidemia in a young cat associated with cobalamin deficiency

Objective: To describe a case of severe metabolic acidosis and encephalopathy secondary to cobalamin (Cbl) deficiency in a young cat. Case summary: A 4‐year‐old spayed female domestic short hair cat weighing 2.5 kg, presented with a 2‐day history of neurological signs referable to the cerebrum. The cat was evaluated for similar episodes twice before, however, no definitive diagnosis was made for either visit. On presentation the cat was minimally responsive and had a metabolic acidosis and ketonuria with no apparent reason, such as lactic acidosis or diabetic ketoacidosis. The patient was diagnosed postmortem with an organic acidemia secondary to low Cbl levels. New or unique information provided: The purpose of this report is to alert emergency clinicians to be suspicious of an organic acidemia in any case of metabolic acidosis and ketonuria that cannot be explained. Early identification of inherited organic acidemias in domestic animals may allow prompt and appropriate treatment of these conditions.     

Primary hyperaldosteronism, a mediator of progressive renal disease in cats

In recent years, there has been renewed interest in primary hyperaldosteronism, particularly because of its possible role in the progression of kidney disease. While most studies have concerned humans and experimental animal models, we here report on the occurrence of a spontaneous form of (non-tumorous) primary hyperaldosteronism in cats. At presentation, the main physical features of 11 elderly cats were hypokalemic paroxysmal flaccid paresis and loss of vision due to retinal detachment with hemorrhages. Primary hyperaldosteronism was diagnosed on the basis of plasma concentrations of aldosterone (PAC) and plasma renin activity (PRA), and the calculation of the PAC:PRA ratio. In all animals, PACs were at the upper end or higher than the reference range. The PRAs were at the lower end of the reference range, and the PAC:PRA ratios exceeded the reference range. Diagnostic imaging by ultrasonography and computed tomography revealed no or only very minor changes in the adrenals compatible with nodular hyperplasia. Adrenal gland histopathology revealed extensive micronodular hyperplasia extending from zona glomerulosa into the zona fasciculata and reticularis. In three cats, plasma urea and creatinine concentrations were normal when hyperaldosteronism was diagnosed but thereafter increased to above the upper limit of the respective reference range. In the other eight cats, urea and creatinine concentrations were raised at first examination and gradually further increased. Even in end-stage renal insufficiency, there was a tendency to hypophosphatemia rather than to hyperphosphatemia. The histopathological changes in the kidneys mimicked those of humans with hyperaldosteronism: hyaline arteriolar sclerosis, glomerular sclerosis, tubular atrophy and interstitial fibrosis. The non-tumorous form of primary hyperaldosteronism in cats has many similarities with "idiopathic" primary hyperaldosteronism in humans. The condition is associated with progressive renal disease, which may in part be due to the often incompletely suppressed plasma renin activity.     

Primary hyperaldosteronism in the cat: a series of 13 cases

Thirteen cases of feline primary hyperaldosteronism were diagnosed based on clinical signs, serum biochemistry, plasma aldosterone concentration, adrenal imaging and histopathology of adrenal tissue. Two cases presented with blindness caused by systemic hypertension, whilst the remaining 11 cases showed weakness resulting from hypokalaemic polymyopathy. Elevated concentrations of plasma aldosterone and adrenocortical neoplasia were documented in all cases. Seven cases had adrenal adenomas (unilateral in five and bilateral in two) and six had unilateral adrenal carcinomas. Three cases underwent medical treatment only with amlodipine, spironolactone and potassium gluconate; two cases survived for 304 and 984 days until they were euthanased because of chronic renal failure, whilst the third case was euthanased at 50 days following failure of the owner to medicate the cat. Ten cases underwent surgical adrenalectomy following a successful stabilisation period on medical management. Five cases remain alive at the time of writing with follow-up periods of between 240 and 1803 days. Three cases were euthanased during or immediately following surgery because of surgical-induced haemorrhage. One cat was euthanased 14 days after surgery because of generalised sepsis, whilst the remaining cat was euthanased 1045 days after surgery because of anorexia and the development of a cranial abdominal mass. It is recommended that primary hyperaldosteronism should be considered as a differential diagnosis in middle-aged and older cats with hypokalaemic polymyopathy and/or systemic hypertension and should no longer be considered a rare condition.     

Primary aldosteronism (Conn's syndrome) in a cat; a case report and review of comparative aspects

An aged cat was presented with a history of chronic relapsing weakness and depression. Profound hypokalaemia was detected in association with increased serum aldosterone levels and marginally subnormal plasma renin activity. A diagnosis of primary aldosteronism (Conn's syndrome) was made and the cat was successfully treated for 2 ½ months with spironolactone. When renal failure developed, the cat was destroyed and at autopsy a large adrenal cortical adenocarcinoma was found.     

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

Abstract: 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.     

Effect of benazepril and robenacoxib and their combination on glomerular filtration rate in dogs

Combined use of angiotensin‐converting enzyme inhibitors and nonsteroidal anti‐inflammatory drugs may induce acute kidney injury, especially when combined with diuretics. The objective of this investigation was to evaluate the effect of benazepril, robenacoxib and their combination in healthy dogs. In each of two studies (studies 1 and 2), 32 beagle dogs were randomized into one of four groups in a parallel‐group design. Groups received once‐daily oral treatment for 7 days with placebo, benazepril, robenacoxib or benazepril plus robenacoxib. In study 2, all dogs received additionally 2 mg/kg furosemide orally twice daily. The primary endpoint was the glomerular filtration rate (GFR) estimated from the plasma clearance of iohexol. Secondary endpoints included standard clinical monitoring and, in study 2, plasma renin activity, urine volume, specific gravity and aldosterone concentration and water intake. Administration of furosemide induced diuresis, reduced GFR and activated the renin–aldosterone–angiotensin system. Benazepril and robenacoxib, administered alone or in combination, were tolerated well, did not decrease GFR with or without co‐administration of furosemide and significantly reduced urinary aldosterone concentrations. No increased risk of acute kidney injury was identified with the combination of benazepril and robenacoxib in healthy dogs. Different effects might occur in dogs with heart or renal disease.     

Plasma renin activity and plasma concentrations of aldosterone, cortisol, adrenocorticotropic hormone, and alpha-melanocyte-stimulating hormone in healthy cats

A pathogenetic role of the renin-angiotensin-aldosterone system has been implicated in cats in both systemic arterial hypertension and hypokalemic myopathy. Yet, measurement of plasma aldosterone concentrations (PACs) and plasma renin activity (PRA) has not unequivocally pointed to hyperaldosteronism as a cause of these conditions. To obtain appropriate reference ranges, this study included a large number (130) of healthy house cats of different breeds without a history of recent illness and plasma concentrations of urea and creatinine below the upper limit of the respective reference ranges. In addition, the pituitary-adrenocortical axis was studied by measuring plasma concentrations of adrenocorticotropic hormone (ACTH), alpha-melanocyte-stimulating hormone (alpha-MSH), and cortisol. Reference ranges for PACs (110-540 pmol/L; 40-195 pg/mL), PRA (60-630 fmol/L/s; 0.3-3 ng/mL/h), and the aldosterone to renin ratio (ARR) (0.3-3.8) were very similar to those established in the same laboratory for humans in a supine position. No breed differences were found. The ARRs in neutered cats were significantly higher than in intact cats, primarily because of low PRA in neutered cats. The ARRs of cats > or = 5 years of age were significantly higher than those of cats < 5 years of age. The plasma concentrations of ACTH, alpha-MSH, and cortisol did not correlate significantly with PAC. Thus, although blood sampling was performed in cats in nonstandardized positions and was associated with a wide variation of stress responses, the references ranges of PAC, PRA, and ARR were similar to the relatively narrow limits established for humans under standardized conditions. The effects of neutering and aging on PRA and ARR warrant further investigation.     

Primary hyperaldosteronism in a dog with concurrent lymphoma

An 11-year-old, male castrated English springer spaniel was presented for muscle weakness, lethargy and anorexia while undergoing treatment of Stage IV lymphoma. Persistent hypokalemia prompted multiple diagnostic tests. Serum aldosterone levels, surgical exploration and histopathology confirmed primary hyperaldosteronism. Hyperaldosteronism is a rarely reported endocrinopathy in the dog. This report describes a case in which immunohistochemistry was utilized to confirm the diagnosis of an aldosterone-secreting tumour.     

Canine distal renal tubular acidosis and urolithiasis

Distal RTA is characterized by decreased distal renal tubular hydrogen ion secretion, decreased ability to acidify urine, hypercalciuria, hyperphosphaturia, hypocitraturia, and metabolic acidosis. Because of the resulting alterations in urine composition and pH, patients with distal RTA are predisposed to urolithiasis and renal calcification. Diagnosis of distal RTA is important because it is a potentially reversible disorder that, left untreated, may cause nephrocalcinosis, recurrent urolith formation, moderate to severe metabolic acidosis, and renal failure.