Conn’s Syndrome is one of those diseases  I knew existed but understood little else about purely due to my assumption that this was a condition rarely encountered in general practice. That was until recently where more discussion has centred around Conn’s syndrome especially in the feline world and it is believed that, given this is a condition which mimics other feline diseases such as chronic kidney failure, it is likely to be more commonly encountered than had been originally assumed.

James McMurrough BVSc Cert AVP(SAM) Cert AVP(VC) MRCVS discussed this fascinating syndrome in last week’s Lite webinar and he advised that if you are to remember nothing else from this webinar, remember this: Conn’s Syndrome in cats has two major presenting signs , hypertension and hypokaleamia. If you see these two changes together in a sick cat, alarm bells should ringing loudly and Conn’s syndrome should be placed high on your list of differentials.

An attempt to diagnose Conn’s syndrome in cats presenting with simultaneous hypertension and hypokaleamia is the next challenge and James explained it is important to understand the pathophysiology behind this disease. Conn’s syndrome is a disorder of the adrenal cortex which produces an excess of mineralocorticoids (which mainly constitutes aldosterone). Aldosterone is responsible for maintaining extravascular volume and systemic blood pressure via sodium homeostasis. It also regulates potassium homeostasis. The amount of aldosterone produced is controlled by the renin – angiotensin- aldosterone system. The release of renin, due to a drop of blood pressure for example, will lead to the production of aldosterone . Excessive aldosterone however, as is seen in Conn’s syndrome, will lead to the reduction of renin production via a negative feedback loop. This excess production of aldosterone is usually caused by either a functional adenoma (in about 50% of cases) or an adenocarcinoma (in about 50% of cases) of the adrenal gland. Very occasionally there will also be cases of bilateral adrenal hyperplasia as well as idiopathic hyperaldosteronism.

Given the pathophysiology of this disease the gold standard diagnostic test is to ascertain the aldosterone: plasma renin ratio. This ratio should be increased in Conn’s syndrome as the aldosterone will be high and the renin low  due to the negative feedback loop. This is not always as straightforward as it seems however as renin levels can be challenging to obtain. At least 4mls of blood must be taken from a cat, which then needs to be immediately centrifuged and frozen. This is assuming you can find a laboratory to perform the test as they are few and far between. A simpler approach is to perform an aldosterone level in the face of hypokaleamia which if within normal limits or elevated is most definitely not normal and indicates the cat is suffering from Conn’s syndrome.

 Imaging is also key and useful as an aid in determining the appropriate treatment regime. Ultrasound is the in practice tool which offers the most information. The adrenals should be visualised, with any masses or altered echogenicity being noted. The size the adrenals are also important with normal adrenal glands being between <4.8-<12.5mm in size. Adrenal tumours tend to be between 9 and 30mm in size. The one caveat in all of this however is that the adrenal glands in some cats with Conn’s Syndrome can in some cases appear completely normal on ultrasound. A CT or MRI scan are more sensitive methods for detecting adrenal changes and it is also important to perform thoracic imaging to ensure metastatic spread has not occurred.

 James went on to discuss treatment options available to cats with Conn’s syndrome some of which depend very much on the underlying cause. For example surgical removal is a real option for patients  with unilateral masses without any evidence of metastasis. James stresses however that this type of surgery should always be performed by a board certified surgeon as they are very difficult high risk surgeries which can culminate in potentially fatal complications including thrombosis, bleeding and sepsis. If successful however surgery may be curative with the resolution of signs and cessation of medical therapy in many cases.

Drug therapy is the alternative option where surgery is not a viable option as well as in cases of benign hyperplasia and idiopathic hyperaldosteronism. The mainstay of drug therapy for cats with Conn’s involves the use of spironolactone, an aldosterone receptor antagonist, potassium supplementation and antihypertensives such as amlodipine. James explained, in his experience, these cases can do well with survival times varying from months to years. Blood pressure and biochemistry should be monitored weekly in these patients until their potassium has normalised and their blood pressure has stabilised to less than 160mm/hg. These cats can then be checked at 3 monthly intervals but it must be remembered that if present an adrenal mass may continue to grow and dosages of the above medications may need to be increased over time.

On reflection I suspect I have encountered cats with Conn’s syndrome  previously but had assumed these patients were suffering from chronic kidney disease. In fact some cats with Conn’s syndrome will also produce an excess of progesterone which can lead to hyperglycaemia  so it is not out of the question that there have been a few misdiagnosed diabetics as well. The good news is that webinars like this are getting the message through to general practitioners and we are now starting to consider Conn’s syndrome as a potential differential in cats with hypertension and hypokalaemia. In fact within the past year our practice has actually been able to confirm some cases of Conn’s syndrome in cats using the aldosterone: renin ratio and given this disease’s obscurity up until recently, this has to be a step in the right direction.