629 MECHANISM OF HYPOCHLOREMIC METABOLIC ALKALOSIS(HMA) IN DOGS FED A CHLORIDE-DEFICIENT FORMULA(CDF)

Abstract

HMA, failure to thrive(FTT), deceleration of head growth and a Bartter-like syndrome was observed in 200 infants in the USA unintentionally fed a CDF([Na⁺,K⁺,Cl^-] of 17,25,<2mEq/L). HMA was corrected by adding chloride to the CDF. Suggested causes for the metabolic abnormalities include chloride depletion, alkali excess ([citrate^-]25mEq/L) and/or increased PGE₂. To better define pathophysiologic mechanisms, metabolic balance studies were performed in 3 mongrel puppies(A,B,C) fed the CDF(150ml/kg/day) for 11 wks. During 3 additional weeks, A was fed CDF, B received CDF+chloride ([Cl-]14.4mEq/L) and C was fed another soy formula([C1^-]11mEq/L). Mean laboratory values obtained before CDF(I-A,B,C), after 11 wks of CDF(II-A,B,C) and after 3 final weeks (III) were:

(^ang/ml/hr);(^bng/ml);(^cml/kg);(^dng/kg/24hr);(U=urinary excretion) Each puppy exhibited FTT. These findings support the hypothesis that CDF and not chloride loss, alkali administration or increased PGE₂ resulted in hypochloremia, ECFV depletion with increased PRA and PA, increased renal conservation of NaHCO₃ and increased urinary potassium excretion.

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