Metabolism of Protein, Amino Acids and Ammonia in Patients with Liver Disease

摘要

Renal function in patients with liver disease (hepatorenal syndromes), and the metabolic responses of man and animals to potassium deficiency and excess were studied. Renal responses to potassium loading were studied in salt-fed and salt-deprived normal subjects and in patients with ascites who are avid sodium retainers. The renal responses are conditioned by the degree of renal sodium conservation. Patients with ascites have abnormal responses to KC1 loading. They show decreased H+ excretion and develop systemic acidosis. These data are evaluated in relation to the Na+, H+, K+ exchange system in the kidney. Studies on the effects of feeding amino acids on potassium and hydrogen ion metabolism in the rat have continued. Feeding L-lysine caused displacement of potassium from muscle and increases in urinary potassium excretion. These effects of L-lysine depended upon the availability of exchangeable potassium in muscle. L-lysine behaved like potassium in altering the amino acid pattern of potassium-deficient rat muscle in vivo.