Abstract

Premature female triplets were noted to have poor weight gain, end hyponatremia at age one week. Renal function, cortisols, sweat electrolytes and physical exam were normal. Urinary Na+ losses were initially high despite high plasma aldosterone(A). Hypernatremia, induced by p.o. Na+ supplementation, suppressed (A) and renin(R) transiently in only one of the triplets. They hove maintained normal growth and normonatremia on a normal Na+ diet for the past two months, in the presence of high (A) and (R). (Bee table below): The non-suppressabllity of (A) and (R) suggests two mechanisms: 1. Primary proximal tubular Na+ loss with compensatory hyperaldosteronism, unlikely alone in the absence of hypokalemia. 2. Partial distal tubular unresponsiveness to (A) which may improve with age and renal maturation. Measurements of (A) and (R) in infants with hyponatrenia ate necessary to distinguish pseudohypoaldosteronism from other electrolyte imbalances found in infants of low birth weight.

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