Abstract

Objective: Dietary potassium is known to lower the blood pressure but high attentions should be paid not to induce hyperkalemia in patients with renal impairment. Recently we experienced a case postprandial hyperkalemia (from 4.8 to 6.0mmol/L). We investigated the pathophysiology of postprandial hyperkalemia in healthy volunteers. Design and method: Twelve healthy volunteers (age: 23 to 58 years old, eGFR: 76.1 to 119.9 mL / min / 1.73 m2) who obtained informed consent took potassium-rich diet (2000 mg, with avogado, tomato juice and banana), serum K, urinary K, and urinary creatinine (CRE) were measured before, 1 hour and 2 hours after the meal. Urinary K was corrected by urinary CRE. Results: The serum K level increased significantly at 1 hour (p < 0.01) and 2 hours (p < 0.05) after the meal, and the urinary K / CRE increased 2 hours (p < 0.01) compared to the pre-meal value. In two cases, serum K level increased by 0.7 mmol / L 1 hour after the meal and urinary K / CRE increased by 60 mmol / g · CRE 2 hours after meal. Other 10 cases, those with little change in serum K levels urinary K/CRE were constant during the examination. In 5 of 12 patients, the serum K level increased by 0.3 mmol / L or more, and in this group, the excretion of urinary K 1 hour after meal was small and increased significantly 2 hours after the meal. Conclusions: Potassium-rich diet may increase serum K levels in healthy human. We can not predict the postprandial elevation of K by regular biomarkers. The delay of urinary excretion plays a role in postprandial hyperkalemia. To assess K status, we should consider the status of fasting in patients. Further investigations are required to reveal precise mechanism in alteration of K handling in the kidney.

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