Heparin-induced hyperkalaemia due to hyporeninaemic hypoaldosteronism
O Idowu, K Muralidhara, Department of Diabetes and Endocrinology, Northwick Park Hospital
Heparin induces hyperkalaemia via a number of mechanisms including by inducing reversible aldosterone suppression without affecting the metabolism of corticosteroids. These effects are compounded by the presence of renal insufficiency, diabetes mellitus, in the elderly and the use of certain medications. It usually occurs after 4 – 6 days of therapy in about 7% of patients and resolve on discontinuing the drug.
Here we present a case of heparin-induced mineralocorticoid suppression in a 68-year-old female with left renal infarct caused by abdominal aortic thrombus in the immediate post-operative period following an emergency laparotomy for perforated duodenal ulcer that required the commencement of unfractionated heparin at therapeutic doses due to impaired renal function. Her thrombophilia, viral and autoimmune screen were negative.
During her prolonged hospital stay (173 days), she was found to have recurrent hyponatraemia (123 – 129 mmol/L), hyperkalaemia (5-6.4 mmol/L) with persistent renal impairment (Cr 249 µmol/L, urea 20.2 mmol/L). Her serum bicarbonate ranged between 21 – 33 mmol/L. Her TSH was 5.41mIU/L (raised) and FT4 15.4pmol/L (normal). She did not have diabetes. She also had short synacthen test performed thrice during her admission which all demonstrated adequate adrenal cortisol response (60 min cortisol > 889 nmol/L). Her serum renin and aldosterone were suppressed at 0.1nmol/L/hr (reference range 0.3 -2.2 nmol/L/hr) and <50pmol/L (reference range: up to 630 pmol/L) respectively suggestive of hyporeninaemic hypoaldosteronism. Her sodium and potassium normalised with fludrocortisone 50 micrograms/day.
She also developed hypercalcaemia secondary to prolonged immobilisation (corrected calcium 3.12 mmol/L, intact PTH <0.7 pmol/L, alkaline phosphatase 92 IU/L– normal, vitamin D 50 nmol/L, Mg 1.15 mmol/L, PO4 1.78 mmol/L) which was managed with rehydration with infusion of 0.9% saline, intravenous frusemide and pamidronate infusion..
Our case demonstrates that the use of fludrocortisone is an effective therapeutic option that can bring about the significant and rapid resolution of hyperkalaemia where the continuation of heparin is necessary.