Abstract
Citrate complexing of Ca during neonatal “exchange” blood transfusions is associated with stimulation of PTH; theoretically P loading occurs from partially hemolyzed or P buffered blood. During exchange transfusions in 31 neonates (gestation 27-41 wks, postnatal ages 0.1-8d), serum ionized Ca and Mg decreased (paired t, p<.05), P increased from 5.23±.26 (mean+SEM) to 6.64±.29 mg/dl (paired t,p<.01) and PTH (radioimmunoassay, N terminal) increased from 17.5±4.6 to 113.0±21.5 ul-Eq/ml (paired t, p<.05). No significant change in serum CAMP (Gilman) was noted, 51.56±10.29 and 55.03±8.33 pmol/ml, n=9. Following transfusion, n=24, there was an early (2.6±.3 hrs) increase in urinary CAMP (UCAMP) concentration from 962±207 to 1346+208 pmol/ml (paired t, p<.05), and a later (3.9±6 hrs) increase in urinary P (UP) concentration from 14.6±3.6 to 33.7±6.6 mg/dl and UP excretion from .024±.012 to .05±.02 mg/min (paired t, p<.05). Infants<34 wks gestation (n=10) vs ≥ wks (n=10) did not differ in Δ'(maximum minus prestudy value) UP (19.87±.14 vs 17.5±4.07 mg/dl) or ΔUCAMP (43.19± vs 104.8±39.7 pmol/ml). Infants <2 days old (n=10) vs >2d (n=11) did not differ in ΔUP (17.26±6.37 vs 20.65±5.9); ΔUCAMP was lower in older infants (116.3±31.3 vs 26.1±14.6 pmol/ml). Thus, newborn infants, regardless of gestational age or postnatal age, appear to respond to P loading and increased endogenous PTH by increasing UP and UCAMP while serum CAMP remains unchanged.
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