Advertisement

Proximal Renal Tubular Acidosis and Hypophosphatemia Induced by Arginine

  • Daniel Batlle
  • Steven Hays
  • Richard Foley
  • Yun Chan
  • Jose A. L. Arruda
  • Neil A. Kurtzman
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 151)

Abstract

Arginine monohydrochloride is a cationic amino acid widely used to test pituitary function (1). In the recent past, its use for the treatment of severe metabolic alkalosis and hepatic encephalopathy was often recommended (2–4). Recognition of its potential for severe hyperkalemia (5,6) prompted the cautious use of this compound. Its use, however, is bound to continue in view of the widespread administration of amino acids in the course of hyperalimentation. This study was undertaken to systematically examine the effect of arginine, at a dose similar to that commonly used clinically, on urinary acidification and plasma electrolyte composition. Our results are in keeping with previous studies showing the development of metabolic acidosis and hyperkalemia during a brief infusion. They further demonstrate that arginine, like other cationic amino acids (7–9), markedly impairs proximal bicarbonate reabsorption. Of interest, a significant fall in plasma phosphate was uncovered by these studies. This could not be ascribed to renal phosphate wastage because phosphate excretion decreased markedly. Hence, arginine induces proximal renal tubular acidosis associated with hypophosphatemia without a renal phosphate leak.

Keywords

Hepatic Encephalopathy Ammonium Chloride Plasma Potassium Cationic Amino Acid Phosphate Excretion 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. 1.
    Merimee TJ, Rabinowitz D, Riggs L, Burgess JA, Rimoin DL, McKusick VA: Plasma growth hormone after arginine infusion. N Engl J Med 276:434–439, 1967.PubMedCrossRefGoogle Scholar
  2. 2.
    Gennari FJ: Differential diagnosis and treatment of metabolic alkalosis, in Acid-Base and Electrolyte Balance, edited by Schwartz AB, Lyons H. New York, Grune and Stratton, 1977, p. 74.Google Scholar
  3. 3.
    Wolfe SJ, Fast BB, Stormont JM, Davidson CS: Treatment of hepatic coma: Use of certain Kreb’s urea cycle intermediates (L-arginine, DL-ornithine). J Lab Clin Med 51:627–689, 1958.Google Scholar
  4. 4.
    Reynolds TB, Redeker AG, Davis P: A controlled study of the effects of L-arginine on hepatic encephalopathy. Am J Med 25:359–367, 1958.PubMedCrossRefGoogle Scholar
  5. 5.
    Hertz P, Richardson JA: Arginine-induced hyperkalemia in renal failure patients. Arch Intern Med 130:778–780, 1972.PubMedCrossRefGoogle Scholar
  6. 6.
    Bushinsky DA, Gennari J: Life-threatening hyperkalemia induced by arginine. Ann Intern Med 89:632–634, 1978.PubMedGoogle Scholar
  7. 7.
    Wallin JD, Brennar JP, Long DL, Aronoff SL, Rector FC, Jr, Seidin DW: Effect of increased distal bicarbonate delivery on free water reabsorption in the dog. Am J Physiol 224:209–218, 1973.PubMedGoogle Scholar
  8. 8.
    Gougoux A, Lemieux G, Vinay P: Bicarbonaturic effect of lysine in the dog. Kidney Internat 14:215–227, 1978.CrossRefGoogle Scholar
  9. 9.
    Chan YL, Kurtzman NA: Effect of lysine on bicarbonate and fluid absorption in the rat proximal tubule. Am J Physiol (In press).Google Scholar
  10. 10.
    Kurtzman NA: Regulation of renal bicarbonate reabsorption by extracellular volume. J Clin Invest 49:586–595, 1970.PubMedCrossRefGoogle Scholar
  11. 11.
    Batlle D, Arruda JAL: The renal tubular acidosis syndromes. Min elect Metab 5:83–99, 1981.Google Scholar
  12. 12.
    Sabastian A, McSherry E, Morris RC, Jr: Metabolic acidosis with special reference to the renal acidosis, in The Kidney, edited by Brenner B and Rector FC, Jr, Sauders, Philadelphia, 1976, p. 615.Google Scholar
  13. 13.
    Relman AS, Shelbourne PF, Taiman A: Profound acidosis resulting from excessive ammonium chloride in previously healthy subjects. N Engl J Med 264:848, 1961.PubMedCrossRefGoogle Scholar
  14. 14.
    Dickerman HW, Walker WG: Effect of cationic amino acid infusion on potassium metabolism in vivo. Am J Phsyiol 206:403–408, 1964.Google Scholar
  15. 15.
    Levinsky NG, Tyson I, Miller RB, Relman AS: The relation between amino acids and potassium in isolated rat muscle, J Clin Invest 41:480–487, 1962.PubMedCrossRefGoogle Scholar
  16. 16.
    Sheldon GF, Grzyb S: Phosphate depletion and repletion: Relation to parenteral nutrition and oxygen transport. Ann Surg 182:683, 1975.PubMedCrossRefGoogle Scholar
  17. 17.
    Travis SJ, Sugeriman HJ, Rubery RL, Durick SJ, Delivoria-Papadopoulus M, Millor LD, Oski F: Alterations of red-cell glycolytic intermediates and oxygen transport as a consequence of hypophosphatemia in patients receiving hyperalimentation. N Engl J Med 285:763, 1971.PubMedCrossRefGoogle Scholar

Copyright information

© Plenum Press, New York 1982

Authors and Affiliations

  • Daniel Batlle
    • 1
  • Steven Hays
    • 1
  • Richard Foley
    • 1
  • Yun Chan
    • 1
  • Jose A. L. Arruda
    • 1
  • Neil A. Kurtzman
    • 1
  1. 1.Section of NephrologyUniversity of Illinois College of MedicineChicagoUSA

Personalised recommendations