ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Endocrine Abstracts (2018) 59 EP32 | DOI: 10.1530/endoabs.59.EP32

A curious case of hypercalcaemia associated with proximal renal tubular acidosis

Punith Kempegowda1,2, Samuel Booth1, Rohan Desai1, Muhammad Usman Rashid1, Francesca Gizzi1 & Srikanth Bellary1,3


1University Hospitals Birmingham NHS Foundation Trust, Birmingham, UK; 2Institute of Metabolism and Systems Research, Birmingham, UK; 3Aston University, Birmingham; UK.


An 88-year-old Caucasian man with hypertension, single functioning kidney, vitamin D insufficiency and transurethral resection of the prostate was admitted with worsening confusion. On admission, he had acute on chronic renal impairment (Urea- 17.2 mmol/l (range: 2.5–7.5 mmol/l), Creatinine- 163 μmol/l (range: 60–120 μmol/l), eGFR- 35 (Baseline- 60 ml/min/1.73m2) and a normal serum/corrected calcium (2.51 mmol/l (range- 2.2–2.6mmol/l). He was commenced on IV fluids and was also started on high dose Vitamin D. Routine investigations did subsequently showed severe hypercalcaemia which was confirmed on repeat testing (corrected calcium 3.01 mmol/l and ionised calcium 1.888 mmol/l). On review, the patient had ongoing symptoms of constipation for several days but had normal calcium levels during this period until the incidental diagnosis. Clinical examination was unremarkable. Blood gas analysis revealed hyperchloremic metabolic acidosis (pH-,bicarbonate 16.6 mmol/l,chloride 15.1 mmol/l. Investigations for common causes of hypercalcaemia were negative (Parathyroid hormone 1.1pmol/l, vitamin D- 69.1 nmol/l, Immunoglobulin (Ig) G- 12.55, IgM- 0.80, IgA- 5.07, Magnesium- 0.86 mmol/l, Phosphate-0.64 mmol/l, Alkaline phosphatase- 134 IU/l). Following discussion with the renal team, a diagnosis of proximal renal tubular metabolic acidosis was made. He was treated with intravenous bicarbonate and fluid therapy. Over the next few days, his hypercalcaemia resolved as his metabolic acidosis improved. Although there are a number of causes for acute hypercalcaemia, we could not establish a definitive cause in this patient. To our knowledge, this is the first case of idiopathic hypercalcaemia associated with renal tubular acidosis. We observed a temporal association between onset of metabolic acidosis and hypercalcaemia and its subsequent resolution following correction of acidosis leading us to speculate that the hypercalcemia was due to decreased calcium excretion from the proximal tubule.

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