LETTERand separated within 30 min, minimizing with nephropathy. We concur with Oda-

wara et al. that considerable cautionrisk of haemolysis. Among the 67 with aLETTERserum potassium . 5.4 mmol l−1, 14 were should be exercised when treating dia-receiving drugs which might have contrib- betic patients with these agents. Potassiumuted to hyperkalaemia (6 taking ACE levels should be checked before initiation

of such therapy and carefully monitoredinhibitor drugs, 5 potassium-sparingdiuretics, and 3 non-steroidal anti- throughout treatment to reduce the small

but real risk of producing dangerousinflammatory drugs) and 12 other patientsLife-threatening Hyperkalaemia caused had renal impairment which might have hyperkalaemia. Potassium-sparingby ACE inhibitor and diuretics contributed (serum creatinine diuretics should not be administered

concurrently with ACE inhibitor drugs,. 140 mmol l−1). In the remaining 41,there was no other obvious explanation especially in patients with diabetes.

Odawara and colleagues report a patient for the observed hyperkalaemia. It iswith non-insulin-dependent diabetes of interest that the patient reported by P.R. Jarman, A.M. Keheley, H.M. Mathermellitus who developed life-threatening Odawara et al. had evidence of nephro- Ealing Hospital, Uxbridge Road, Southall,hyperkalaemia after the potassium-sparing pathy (serum creatinine 141 mmol l−1, cre- Middlesex UB1 3HW, UKdiuretic spironolactone (25 mg) was atinine clearance 60 ml min−1) since weadded to existing anti-hypertensive treat- found an association between elevatedment including an angiotensin-converting mean serum potassium and the presenceenzyme (ACE) inhibitor (lisinopril 10 mg of both proteinuria and retinopathy, whichdaily).1 The authors attribute the extreme remained significant even after the Referenceshyperkalaemia observed in this patient exclusion of patients with established(plasma potassium 8.9 mmol l−1) to the renal failure.combination of two potassium-retaining Physicians treating diabetes have long 1. Odawara M, Asano M, Yamashitadrugs in a patient with mild renal impair- recognized the occurrence of hyperkalae- K. Life-threatening hyperkalaemiament, but do not consider the role of mia in their patients, but there have been caused by angiotensin-convertingdiabetes itself in the observed hyperkalae- few studies of its prevalence and its enzyme-inhibitor and diuretics. Dia-mia. mechanisms are not fully understood. betic Med 1997; 14: 169–170.

In a study of the prevalence of hyperka- Dangerous hyperkalaemia following the 2. Jarman PR, Kehely AM, Mather HM.laemia in unselected diabetic outpatients, use of potassium-sparing diuretics includ- Hyperkalaemia in diabetes: preva-we found that hyperkalaemia was rela- ing spironolactone has been previously lence and associations. Postgrad Medtively common in patients with both non- described in diabetic patients3,4 and the J 1995; 71: 551–552.insulin-dependent, and insulin-dependent British National Formulary suggests cau- 3. Walmsley RN, White GH, Cain M,diabetes.2 Of 1764 patients attending tion in prescribing amiloride for patients McCarthy PJ, Booth J. Hyperkalaemiaa clinic over a 1-year period, serum with diabetes. The case reported by Oda- in the elderly. Clinical Chemistrypotassium concentration was wara et al. highlights these dangers. The 1984; 30: 1409–1412.. 5.0 mmol l−1 in 270 patients (15 %) and unexpectedly high prevalence of hyperka- 4. Large DM, Laing I, Carr PH, Davies M.. 5.4 mmol l−1 in 67 patients (4 %). Six laemia in diabetic outpatients is of parti- Hyperkalaemia in diabetes mellitus—patients had a serum potassium greater cular importance in view of the increasing potential hazards of co-existing hypo-than 6.0 mmol l−1. All the samples were use of ACE inhibitors to treat hypertension reninaemic hypoaldosteronism. Post-

grad Med J 1984; 60: 370–373.taken in a morning clinic and centrifuged and cardiac failure in diabetic patients

808 CCC 0742–3071/97/090808–01$17.50 1997 by John Wiley & Sons, Ltd. DIABETIC MEDICINE, 1997; 14: 808