Abstract
The remarkable growth of the kidney and the rapid changes in renal function in the second half of gestation and early postnatal period are discussed. Adaptation to the extrauterine environment involves immediate postnatal natriuresis that is prolonged in the pre-term neonate, followed by the sodium retention necessary for growth. Glomerular filtration rate increases throughout the postnatal period, and it is modulated by the renin-angiotensin system and prostaglandins. Because of this, the fetus and neonate are particularly susceptible to renal injury following the administration of angiotensin converting enzyme inhibitors or nonsteroidal anti-inflammatory drugs. Renal tubular function in the neonate is characterized by reduced renal concentration and acidification ability, which can be further compromised by obstructive uropathy. Urine calcium excretion is high in the neonate, which can be aggravated by calciuric drugs, such as furosemide and glucocorticoids. Reduced renal mass results in compensatory renal growth even in the fetus, a response that could prove maladaptive later in life through excessive glomerular hyperfiltration and progressive interstitial fibrosis. These factors underscore the importance of attempting to maximize functional renal mass in the neonate or infant with renal impairment of any etiology.
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