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In the perinatal period, kidney function, as it relates to fluid and electrolyte homeostasis in the premature and full-term neonate, is predominantly influenced by (1) anatomical kidney development at the time of birth, (2) physiologic adaptations that occur during the transition from intrauterine to extrauterine environment, and (3) diminished capacity of the newborn kidney to respond to increased fluid, electrolyte, or acid load. Their combined effects on renal function in the newborn infant are in indirect proportion to gestational age such that premature infants are most vulnerable to effects of anatomical immaturity, changes in renal blood flow, and limited functionality of hormonal regulatory mechanisms. Consequently, a clear understanding of changes in glomerular and tubular function and renal hemodynamics in the perinatal period is crucial for appropriate management of fluid and electrolyte problems in the sick neonate. In this chapter, general and specific aspects of renal function as they relate to the antenatal and postnatal periods are reviewed to provide a framework for evaluating renal function in the healthy and sick newborn infant. Diagnostic and therapeutic aspects regarding normal and abnormal renal function are discussed elsewhere.

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Morphologic aspects of human kidney development are discussed in detail in Chapter 464. Here, attention is given to spatiotemporal relationships between anatomical and functional development of renal structures. Table 465-1 provides a summary of relationships between anatomical and functional kidney development.

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Table Graphic Jump Location
Table 465-1. Relationships between Anatomical Kidney Development and Functional Kidney Development
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Human kidney development begins at the fifth week of gestation (Fig. 465-1).1,2 The first functioning nephrons are formed by week 9 and excrete urine by week 12. By 32 to 34 weeks, nephrogenesis is completed, following which no new nephron units are formed.3,4 In humans who suffer fetal or perinatal renal injury, the developing kidney is incapable of compensating for irreversible nephron loss by either accelerating the rate of nephron formation ex utero in infants born prematurely, or by de novo generation of nephrons once nephrogenesis is completed.3,5

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Figure 465-1.
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Schematic representation of the relationship between nephron formation and gestational age during human fetal renal development. Renal branching morphogenesis, a principal determinant of nephron number (solid line), is complete by midgestation. Renal mass (dashed line) increases exponentially in the latter half of gestation ...

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