Plasma and Skeletal Muscle Free Aminoacids in Acute Renal Failure

  • Almerico Novarini
  • Isabella Simoni
  • Rossana Colla
  • Antonio Trifirò
  • Achille Guariglia
  • Emilio Sani
  • Alberto Montanari
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 212)


Abnormalities in protein metabolism are well known in acute renal failure (ARF) (1, 2). When renal function is acutely reduced or completely abolished, two phenomena contribute to derange protein metabolism: first, acute protein catabolism occurs inducing negative nitrogen balance, overproduction of urea and other nitrogen catabolites; second, these latter substances accumulate in the body, due to defective renal excretion, possibly contributing through their toxic effect to enhance proteolysis. In addition, if ARF is accompanied or is caused by catabolizing events (severe bleeding, surgery, sepsis, rhabdomiolysis), a further stimulus to protein breakdown contributes to a tremendous, acute malnutrition (1, 2). It is generally thought that the severity of protein catabolism may influence the clinical course of ARF (1). Acute malnutrition in ARF may be easily demonstrated by net loss of muscle mass (1, 2) and from a biochemical point of view by severely negative balance, fall of serum proteins and finally by changes in plasma amino acids (AA) levels, with reduction of essential AA (1). However, plasma free AA concentrations are not fully representative of the whole body pool of free AA, the concentrations of which are by far higher in intracellular water (ICW) than in plasma (3). Muscle tissue is the largest homogeneous cellular tissue in the body, thus containing the largest amount of free AA. Every catabolic condition is characterized primarily by increased net muscle protein degradation, which in turn causes increased flow of free AA to other organs, mainly to the liver. Accelerated muscle proteolysis is reflected also by changes in muscle free AA concentrations, as it has been demonstrated under several conditions, such as surgical trauma, sepsis, diabetes mellitus (4, 5, 6, 7). On the other hand it has been shown that sufficient and equilibrated concentrations of cellular free AA are needed to fully regulate equilibrium between muscle protein synthesis and breakdown (8).


Plasma Amino Acid Acute Malnutrition Free Amino Acid Pool Negative Nitrogen Balance Free Amino Acid Concentration 
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  1. 1).
    Kopple J.D., Cianciaruso B., 1984, The role for nutrition in acute renal failure, in: “Acute Renal Failure”, V.E. Andreucci ed., Martinus Nijhoff, Boston.Google Scholar
  2. 2).
    Knochel J.P.: Complications of total parenteral nutrition. Kidney International, 27: 489 (1985).PubMedCrossRefGoogle Scholar
  3. 3).
    Bergström J., Fürst P. et al.: Intracellular free aminoacid concentration in human muscle tissue. J. Appl. Physiol. 36: 693 (1974).PubMedGoogle Scholar
  4. 4).
    Elwin D.M., Fürst P. et al.,1981, Effect of fasting on the muscle concentration of BCAA. In: “Metabolism and Clinical Implications of BCAA and BCKA”, Elsevier, North Holland.Google Scholar
  5. 5).
    Askanazi J., Fürst P. et al.: Muscle and plasma amino acids after injury. Hypocaloric glucose Vs. Amino acid infusion. Ann. Surg. 191: 465 (1980).PubMedCrossRefGoogle Scholar
  6. 6).
    Askanazi J., Carpentier J.A. et al.: Muscle and plasma Amino acids following injury. Influence of recurrent infection. Ann. Surg. 192: 78 (1980).PubMedCrossRefGoogle Scholar
  7. 7).
    Borghi L.,Lugari R. et al.: Plasma and skeletal muscle free amino acids in type I insulin treated diabetic subjects. Diabetes 34, 812 (1985).PubMedCrossRefGoogle Scholar
  8. 8).
    Fulks R.M., Li J.B. et al: Effects of insulin, glucose and amino acids on protein turnover in rat diaphragm. J. Biol. Chem. 250: 290 (1975).PubMedGoogle Scholar
  9. 9).
    Bergström J.: Muscle electrolytes in man. Scand. J. Clin. Lab. Invest. 14 (suppl. 68): 1 (1962).Google Scholar
  10. 10).
    Montanari A., Borghi L. et al: Skeletal muscle cell abnormalities in acute hypophosphatemia during total parenteral nutrition. Mineral Electrolyte Metabolism 10: 52 (1984).Google Scholar
  11. 11).
    Flügel-Link R.M., Salusky I.B. et al: Enhanced muscle protein degradation and urea nitrogen appearance (UNA) in rats with acute renal failure. Am. J. Physiol. 244: 615 (1983).Google Scholar
  12. 12).
    Christensen H.N.: Organic ion transport during seven decades.The amino acids, Bioch. Biophys. Acta 779: 255 (1984).CrossRefGoogle Scholar
  13. 13).
    Tizianello A., Deferrari al: Renal metabolism of amino acids and ammonia in subjects with normal renal function and in patientswith CRI. J.Clin. Invest. 65: 1162 (1980).CrossRefGoogle Scholar
  14. 14).
    )Frohlich J., Hoppe-Seyler G. et al: Possible sites of interaction of acute renal failure with amino acid utilization for gluconeogenesis in isolated perfused rat liver. Eur. J. Clin. Invest. 7: 261 (1977).PubMedCrossRefGoogle Scholar
  15. 15).
    Felig P.: Amino acid metabolism in man. Ann. Rev. Biochem. 9: 44: 933 (1975).CrossRefGoogle Scholar
  16. 16).
    Tischler M.E., Fagan J.M.: Response to trauma of protein, amino acid, and carbohydrate metabolism in injured and uninjured rat skeletal muscles. Metabolism Clin. Exp., 32, 853 (1983).CrossRefGoogle Scholar

Copyright information

© Plenum Press, New York 1987

Authors and Affiliations

  • Almerico Novarini
    • 1
  • Isabella Simoni
    • 1
  • Rossana Colla
    • 1
  • Antonio Trifirò
    • 2
  • Achille Guariglia
    • 3
  • Emilio Sani
    • 1
  • Alberto Montanari
    • 1
  1. 1.Istituto di Semeiotica MedicaParmaItaly
  2. 2.Stazione Sperimentale per le Conserve AlimentariParmaItaly
  3. 3.Istituto di Clinica Medica e NefrologiaParmaItaly

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