Metabolic Alkalosis, Prostaglandins, Low Chloride, or Something Else?

  • Jose R. Salcedo
Part of the Developments in Nephrology book series (DINE, volume 3)


The recent epidemic of metabolic alkalosis in a large number of infants fed soy protein isolate (1–3) which was deficient in chloride has prompted a renewed interest in this pathophysiological state. These infants were characterized by having an elevated blood pH, increased serum bicarbonate concentration, and a slight compensatory increase in pCO2. Under experimental (4, 5) and clinical conditions, metabolic alkalosis can result from either the gain of base or the loss of acid from extracellular fluid associated with chloride and potassium deficits. Thus, two phases of this disorder can be considered: 1) the mechanisms which produce the metabolic alkalosis, i.e. increased alkali intake, or acid loss through vomiting, and 2) the processes responsible for subsequent maintenance of the alkalosis, i.e. hypochloremia, sodium avid state, etc. The clinical and laboratory evaluation of the infants fed soy formula failed to show the first phase in the development of metabolic alkalosis. Therefore, the composition of the formula itself was considered, namely, the low chloride, high citrate, phytate phosphorus, soy bean protein as well as the hypothetical consideration of prostaglandin precursors or enhancers.


Metabolic Alkalosis Phytate Phosphorus Chloride Depletion Prostaglandin Precursor Potassium Deficit 
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  1. 1.
    Roy S, III, Arant BS Jr: Alkalosis from chloride-deficient Neo-mullsoy, Letter to the Editor. N. Eng. J. Med. 301: 615, 1979.Google Scholar
  2. 2.
    Infant Metabolic alkalosis and soy based formula - United States. Morbidity and Mortality Weekly Rep. 28: 358, 1979.Google Scholar
  3. 3.
    Grossman H, Dugan E, McCamman, et al: The dietary chloride deficiency syndrome. Pediatr. 66: 366, 1980.Google Scholar
  4. 4.
    Kassirer JP and Schwartz WB. The response of normal man to selective depletion of hydrochloric acid. Amer. J. of Med. 40: 10, 1966.CrossRefGoogle Scholar
  5. 5.
    Schwartz WB, Ypersele deStrihou CV, Kassirer JP: Role of anions in metabolic alkalosis. N. Eng. J. Med. 279: 630, 1968.CrossRefGoogle Scholar
  6. 6.
    O’Dell BL, Savage JE: Effect of phytic acid on zinc availability. Proc. Soc. Exp. Biol. Med. 103: 304, 1960.PubMedGoogle Scholar
  7. 7.
    Fung WP: Effect of soyabean milk on the healing of gastric ulcers, a controlled endoscopic study. Med. J. of Aust. 1: 717, 1975.Google Scholar
  8. 8.
    Fung WP, Tye CY: Evaluation of soya bean milk as an antacid. Sing. Med. J. 14: 515, 1973.Google Scholar
  9. 9.
    Gardiner EE, Dewar WA: Dietary chloride requirement of broiler chicks fed on a wheat-soyabean diet. Br. Poult. Sci. 17: 337, 1976.PubMedCrossRefGoogle Scholar
  10. 10.
    Weber PC: Renal prostaglandins in the control of renin. Contr. Nephrol. Vol. 12, p 92, Karher Basel, 1978.Google Scholar
  11. 11.
    McGiff JC, Crowshaw K, Itskowitz HA: Prostaglandins and renal function. Fed. Proc. Fed. Am. Soc. Exp. Biol. 33: 39, 1974.Google Scholar
  12. 12.
    Horton R, Zipser R: Prostaglandins: Renin release and renal function. Contr. Nephrol. Vol. 14, p 87, Karher Basel, 1978.Google Scholar
  13. 13.
    Weming C, Vetter W, Weidmann P, et al: Effect of prostaglandin El on renin in the dog. Am. J. Physiol. 220: 852, 1971.Google Scholar

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© Martinus Nijhoff Publishers, The Hague 1981

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  • Jose R. Salcedo

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