Abstract
Extrarenal mechanisms are important in the defense against hyperkalemia. During a potassium load, cellular uptake is essential to avoid severe hyperkalemia. Liver and muscles represent the major buffering system, partially mediated by insulin, in the distribution of potassium between intracellular and extracellular fluids. To study the potential role of the liver, we administered an oral load of potassium (0.75 mEq/kg) to nine male patients with compensated cirrhosis and ten normal subjects of similar age, sex, and weight. Despite identical renal excretion, cirrhotic patients had higher potassium levels two and three hours after oral administration. Moreover, only cirrhotic patients presented a clear-cut increase in serum C-peptide concentration after the potassium load without any change in glucose level. It is likely that, in cirrhosis, liver failure contributes to the decrease in hepatic cellular potassium uptake despite insulin hypersecretion.
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