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Abstract
Insulin-mineral corticoids effects on extrarenal K+ metabolism in dialysis patients. During the inter-dialytic interval in dialyzed patients, hydrogen and potassium ions are regulated by extrarenal mechanisms. We studied the hormonal and acidotic effects on the extrarenal potassium metabolism, in selected, anuric and stable, hemodialysis patients. Fifteen patients, were grouped according to the mean mid-week pre-dialysis K+ over the past 12 months: > 6.0 mEq/L (G1, n = 5), = 5.1–6.0 mEq/L (G2, n = 5), ≤5.0 mEq/L (G3, n = 5). After a mid-week hemodialysis session and 12 h fasting, they received 1 g/Kg glucose p.os (A). Insulin, aldosterone, renin, pH, HCO3−, glucose, body weight, blood pressure and heart rate were measured before and 60′ after the meal. We recorded the same parameters, except insulin, in 15 patients, similarly grouped, before hemodialysis (T0) and on 3 consecutive off dialysis days (T1–T3); G1 received fluorohydrocortisone (FHC) 0.1 mg–0.3 mg/day, according to body weight and G3 spironolactone (SLT) 200 mg per day. G2 were controls (B). (A) A significant rise in glycemia (81 ± 23 to 157 ± 52 mg/dL, P < 0.001) and insulin (11.8 ± 6.2 to 46.8 ± 19.5 μU/mL, P<0.001), with a drop in K+ (5.1 ± 0.6 to 4.8 ± 0.7 mEq/L, P= 0.001) and aldosterone (453 ± 373 to 383 ± 364 pg/mL, P<0.01), were noted at T60 vs. T0, in all groups. Insulin levels correlated negatively (r = −0.54, P<0.04) to serum K+ at T60, in all patients. (B) No major pH, HCO3 and aldosterone changes were observed in the 3 groups. Despite that, K+ dropped in G1 by FHC (6.7 ± 0.9 to 5.9 ± 0.6 mEq/L, P<0.05), rose in G3 by SLT (4.4 ± 0.4 to 5.4 ± 0.3 mEq/L, P<0.05) and remained unchanged in controls (5.8 ± 0.2 to 5.8 ± 0.6 mEq/L), (T0 vs T3 pre-dialysis values). Glucose significantly lowered K− by promoting adequate insulin secretion. Drugs affecting aldosterone action significantly influenced potassium metabolism. Acid-base balance was not important in K+ handling in steady state anuric dialysis patients.