Familial pseudohyperkalaemia: inhibition of erythrocyte K+ efflux at 4 degrees C by quinine.

1. Mechanisms responsible for increased erythrocyte K+ efflux in vitro have been investigated in a patient with familial pseudohyperkalaemia. Mean net K+ efflux (4 degrees C) was 108 nmol h-1 10(-9) erythrocytes, seven times greater than the mean for controls (15.2 nmol h-1 10(-9) erythrocytes). Net K+ efflux was not increased at 22 degrees C or 37 degrees C and losses at 4 degrees C were reversed by subsequent incubation at 37 degrees C. 2. Erythrocyte glucose consumption (4 degrees C) was 14 nmol h-1 10(-9) erythrocytes, similar to the mean for controls of 16.8 nmol h-1 10(-9) erythrocytes. This suggests that the increased net K+ efflux (4 degrees C) was not associated with abnormal energy consumption and was therefore unlikely to be due to an abnormality of the Na+, K+-pump. 3. Incubation of erythrocyte suspensions with ouabain (0.1 mmol/1) or frusemide (1 mmol/1) at 4 degrees C or 37 degrees C resulted in no differences in K+ efflux between patient and controls. Incubation with quinine (2 mmol/1), an inhibitor of the erythrocyte Ca2+-dependent K+ channel, reduced net K+ efflux at 4 degrees C, but the effect persisted in Ca2+-depleted erythrocytes, implying that quinine was acting in a non-specific fashion. 4. Chemical pathologists and clinicians must be aware of this condition if inappropriate treatment of pseudohyperkalaemia is to be avoided.