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The 49th Annual Meeting of the Irish Endocrine Society (IES) featured an outstanding line-up of national and international experts in their field who discussed the current hot topics in endocrinology, networked with colleagues, met industry participants, and enjoyed a range of excellent oral and poster presentations.
The event began with a trainees’ meeting and RCPI and sub-committees meetings, as well as a ‘Meet the Professor’ session. This was followed with case presentations by trainees, followed by a clinical discussion.
Prof Steven Hunter, IES President, and Consultant Endocrinologist, Royal Victoria Hospital, Belfast, officially opened the meeting. He introduced four oral presentations on original clinical and scientific content that were specially selected by the organisers.
One of the presenters, Dr Maria Tomkins, spoke on the topic of steroid metabolism in patients with chronic kidney disease (CKD) to shed light on renal determinants of adrenal steroid biosynthesis and metabolism. “When we think of the kidney and adrenal steroids, the first one that comes to mind is aldosterone,” said Dr Tomkins. “When aldosterone is elevated in patients with CKD, it drives pro-inflammatory and fibrotic changes, which can then drive cardiovascular risk.”
Manipulating the renin-angiotensin system is the mainstay of treatment in patients with CKD, she explained. “ACE [angiotensin converting enzyme] inhibitors and ARBs [angiotensin 2 receptor blockers] are widely used in patients with CKD and mineralocorticoid receptor antagonist use is somewhat curtailed by the risk of hyperkalaemia, with newer agents with less risk of hyperkalaemia coming on the market.
“But what we sometimes fail to remember is that cortisol can also bind to the mineralocorticoid receptor… the mineralocorticoid receptor is exposed to far more cortisol than it is aldosterone.” Dr Tomkins presented data from studies conducted by herself and her colleagues and noted that steroid enzyme activity can be evaluated by looking at steroid ratios. She also observed that patients with CKD share some of the clinical markers of Cushing’s syndrome, such as excess cardiovascular risk, bone disease, muscular atrophy, and a greater risk of liver disease. Dr Tomkins and colleagues set out to identify the effect renal dysfunction has on steroid metabolism and biosynthesis, particularly looking at glucocorticoids and mineralocorticoids.
“We can confirm that the kidneys do play a major role in adrenal regulation, and this goes beyond just aldosterone,” she said. “Where patients with CKD do have elevated aldosterone, which can then cause mineralocorticoid receptor over-activation, cortisol is also a major player. Reducing 11β-hydroxysteroid dehydrogenase type 2 drives excess cortisol and reduces cortisone, which then have the dual effect of increasing mineralocorticoid effects, but also increasing glucocorticoid tissue exposure, leading to some of these adverse clinical signs that we see in patients with CKD.
“We also showed reduced classic androgens in patients with CKD – most marked in men – and in both sections we found reduced 11-oxygenated androgen biosynthesis in CKD from our previous studies,” Dr Tomkins concluded.
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