Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2014) 34 P78 | DOI: 10.1530/endoabs.34.P78

SFEBES2014 Poster Presentations Clinical practice/governance and case reports (103 abstracts)

Severe hypercalcaemia and acute kidney injury secondary to Graves’ thyrotoxicosis

Thinzar Min , Lawrance Cozma & Silas Benjamin


Princess of Wales Hospital, Bridgend, UK.


A 46-year-old woman presented with 2 months history of thirst, polydipsia, polyuria, constipation, three-stone weight loss, and abdominal pain. She had no other significant medical problem except from personality disorder, which was controlled with antipsychotic medications. She denied use of over-counter medications. She had been off lithium for 5 years.

On examination, she was dehydrated, tachycardic and appeared anxious. She had palmar erythema, fine tremor, firm symmetrical non-tender goiter, and no evidence of thyroid ophthalmopathy.

Investigations revealed acute kidney injury (serum urea of 13.5 mmol/l and serum creatinine of 140 mcmol/l), severe hypercalcaemia (corrected serum calcium of 3.15 mmol/l), normal serum phosphate level (PO4 1.45 mmol/l), magnesium of 0.73 mmol/l, and suppressed PTH of 0.6 pmol/l. Subsequent thyroid function test showed suppressed TSH of <0.03 mU/l, FT4 of 68 pmol/l and FT3 of 27.8 pmol/l. She scored 50 points on Burch-Wartofsky score, which is suggestive of thyroid storm. Carbimazole, propranolol and i.v. glucocorticoid were commenced.

All investigations for causes of hypercalcaemia were proved to be normal. Her serum calcium level gradually declined and renal function returned to normal once thyroid function improved. At 8 weeks follow-up, TFT continued to improve and serum calcium level remained within normal range. TRAb was elevated. We concluded that hypercalcaemia was due to Graves’ thyrotoxicosis.

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