Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2013) 31 P124 | DOI: 10.1530/endoabs.31.P124

SFEBES2013 Poster Presentations Clinical practice/governance and case reports (79 abstracts)

Accelerated renal impairment in a patient with type 2 diabetes with an inadequately investigated incidental adrenal adenoma

Marie-France Kong 1, , Zin Zin Htike 1, , Michael Pieridies 1, & Nigel Brunskill 1,


1Centre Hospitalier Universitaire Brugmann, Brussels, Belgium; 2University Hospitals of Leicester NHS Trust, Leicester, UK.


A 54-year-old Asian man with type two diabetes diagnosed 6 years ago was admitted to hospital in May 2011 because of deteriorating renal function. His eGFR had been stable until April 2011 when his eGFR dropped from 37 in January 2011–2021. Repeat eGFR 2 weeks later was 17 and his family doctor felt he needed to be admitted to hospital. He was on metformin alone which was stopped. His HbA1c was 6.4% (48 mmol/mol). He had hypertension and was on four antihypertensive agents. He had no retinopathy and no peripheral neuropathy. As he was well he was discharged and was seen in our joint renal/diabetes clinic. His renal immunology was negative and he proceeded to a renal biopsy. This showed features of diabetic nephropathy and moderate chronic damage with associated arterio- and arteriolosclerosis. The number of viable glomeruli present was small and it was not possible to perform immunohistochemistry or electron microscopy. It was noted that he had an adrenal adenoma approximately one cm in diameter which was found incidentally in 1999. Renin and aldosterone levels were suggestive of primary hyperaldosteronism but this had not been followed up. He had a repeat scan in 2005 and the adrenal lesion had not increased in size after 6 years and was not followed up again. A repeat scan in July 2011 showed that there was minimal increase in size of the adrenal mass to 1.2 cm. Twenty-four hours urine collections excluded phaechromocytoma and Cushing’s syndrome. Renin aldosterone ratio confirmed primary hyperaldosteronism. His eGFR had dropped further and he started haemodialysis. As it was planned for him to have a renal transplant he was referred for adrenalectomy which was carried out laparoscopically. Two cortical adrenal adenomas were excised. Appearances were consistent with Conn’s syndrome. His blood pressure dropped and he came off all his antihypertensives.

Inadequate follow up/delay in investigating his incidental adrenal adenoma may have resulted in accelerated deterioration of his renal function.

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