sorption occurs with much lower FENa values. It should be remembered, however, that many low birth weight babies are obligatory sodium losers, and will most probably receive oral sodium supplementation. These premature infants may under normal conditions have FENa values >3%. We caution against using spot urine samples for the determination of urinary solute/creatinine ratios at this very young age. We have recently shown that under normal conditions there is a great variability in urinary creatinine excretion, even when the urine creatinine values are corrected for urine osmolality .
With the diagnosis of prerenal ARF, immediate treatment is essential. Without waiting for the results of a variety of laboratory investigations, rapid volume replacement should be undertaken. This can serve both as a diagnostic trial and therapeutic tool. Crystalloid solution (20 ml/kg normal saline or 5% glucose) is given to most newborns, over a 2-h period. In tiny premature infants smaller amounts should be given (10-20 ml/kg). When hypovolemia is the sole cause for the observed oligo-anuria, urinary flow rate is expected to normalize within a few hours. When no diuresis ensues, fluid administration should be repeated, using either plasma or 5% albumin in the same dose and an identical time sequence as before, unless the neonate develops signs of CHF. Colloid administration is not recommended, as crystalloid infusion appears a safer, certainly cheaper, and equally effective alternative . The administration of dopami-nergic agents and/or diuretics may be beneficial. At this young age treatment with mannitol is not recommended. When volume trials are unsuccessful in inducing diuresis and/or improving renal function, temporary dialysis treatment (preferably peritoneal dialysis) may have to be considered.
Babies with hypotension or CHF will probably need ino-tropic and systemic vasoactive support. This can be achieved with dopaminergic agents, which also cause renal vasodilation. DA is a naturally occurring catechol-amine, which exerts its effects via dopaminergic and ad-renergic receptors. DA increases RBF via both the DA,-and DA2-receptor subtypes. Low-dose i.v. DA treatment of human preterm infants with RDS has been shown to improve renal function . In experimental animals, however, the renal circulation of the developing animal benefits only slightly from administration of dopaminergic agents [79, 80]. The a- and p-adrenergic actions of DA therapy result in an increase in cardiac output and a rise in MAP. DA also has a direct tubular effect, via tubular dopaminergic receptors . DA is ideal for the prevention and treatment of neonatal ARF: it supports the systemic circulation and at the same time may im-
prove renal perfusion. However, it is important to bear in mind that the effects of DA are dose-dependent. The renal vasodilator and diuretic response to DA result from stimulation of dopaminergic receptors and are seen only with low i.v. doses of the drug (0.5-2 ug/kg per min). Medium (2-6 ug/kg per min) or high doses of DA (6-10 ug/kg per min), often needed to sustain systemic cardiovascular effects via a- and (3-adrenergic receptors,
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