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Answers on p 57.
A 76 year old man was referred to casualty with a non-haemolysed serum potassium of 6.6 mmol/l. He was entirely asymptomatic. He had a past medical history of type II diabetes mellitus with diabetic nephropathy, hypercholesterolaemia, and cerebrovascular disease with a residual left hemiparesis from a previous stroke. He had recently increased his coffee intake and had started drinking four glasses of orange juice daily. His medications were aspirin 75 mg daily, cerivastatin 100 μg daily, gliclazide 160 mg twice a day, and nebivolol 5 mg daily (recently started for newly diagnosed hypertension)
On examination his blood pressure was 172/88 mm Hg and he had both left upper and lower limb weakness consistent with a previous stroke. He had some evidence of peripheral neuropathy but nothing to suggest a proximal myopathy. Examination was otherwise unremarkable. His electrocardiograph showed peaked T waves in most leads.
Initial investigations showed: serum sodium concentration 145 mmol/l, serum potassium 6.6 mmol/l, urea 11.1 mmol/l, creatinine 172 μmol/l, glucose 4.5 mmol/l, albumin 36 g/l, glycated haemoglobin (HbA1c) 8.3% (reference range 4.5–6.5). A 24 hour urinary creatinine clearance was 56 ml/min while 24 hour urinary protein was raised at 1.67 g/24 hours. Serum aldosterone was 100 (100–450) pmol/l and serum renin was <0.2 (1.1–2.7) pmol/ml/hour. One year previously his biochemistry showed: serum sodium 143 mmol/l, potassium 5.4 mmol/l, urea 9.9 mmol/l, creatinine 143 μmol/l, and glucose 5.9 mmol/l.
(1) What are the factors causing his hyperkalaemia?
(2) Why are elderly patients prone to developing hyperkalaemia?
(3) How would you manage this patient?