Abstract
In order to investigate the role of aldosterone and catecholamines in the pathogenesis of hyperkalemia in diabetics without renal failure and diabetic ketoacidosis, 32 diabetics (fasting blood sugar<160mg/dl, creatinine clearance>40ml/min) with or without persistent hyperkalemia (serum potassium>5mEq/L) and orthostatic hypotension (OH) were divided into four groups as follows. Group I (n=7): diabetics with hyperkalemia and OH;Group II (n=4): diabetics with hyperkalemia and without OH;Group III (n=14): diabetics without hyperkalemia and with OH;Group IV (n=7): diabetics without hyperkalemia and OH.
The changes in plasma renin activity (PRA), plasma aldosterone concentration (PAC), plasma norepinephrine (PNE) and plasma epinephrine (PE), caused by maintaining the upright posture for 2 hours were evaluated in each group and 7 normal controls. Increase in PRA, PAC, PNE and PE by upright posture are indicated by δPRA, δPAC, δPNE and δPE. Group III was divided into two groups as follows: Group IIIA: δPNE was more than 2 SD (SD: standard deviation) below the normal mean ofδPNE ;Group IIIBδPNE was less than 2 SD below the normal mean of δPNE.
Groups I, II and IIIA showed a significant decrease in PNE response to upright posture and in δPNE compared with controls, groups IIIB and IV.Furthermore groups I and HIA showed a slight decrease in PNE response to upright posture and in δPNE compared with group II.Groups I and II showed a significant decrease in PRA and PAC response to upright posture and in A PRA and δPAC compared with the controls, groups IIIA, HIB and IV.Groups I, II, IIIA, IIIB and IV showed no significant difference in PE response to upright posture and APE compared with the controls.
We concluded that a decreased response of PRA and PAC to upright posture was responsible for hyperkalemia in diabetics without renal failure and diabetic ketoacidosis.
