Most pancreatic enzymes are present by 16 weeks. T rypsin, chymotrypsin, phospholipase A, and lipase are found in the 14-week fetus, and their concentrations increase with gestational age (Wedin, 1992). Amylase has been identiied in amnionic luid at 14 weeks (Davis, 1986). The exocrine function of the fetal pancreas is limited. Physiologically important secretion occurs only after stimulation by a secretagogue such as acetylcholine, which is released locally after vagal stimulation (Werlin, 1992). Cholecystokinin normally is released only after protein ingestion and thus ordinarily would not be found in the fetus.
Renal development involves interaction between pluripotential stem cells, undiferentiated mesenchymal cells, and epithelial components (Fanos, 2015). Two primitive urinary systemsthe pronephros and the mesonephros-precede development of the metanephros, which forms the inal kidney (Chap. 3, p. 33). The pronephros involutes by 2 weeks, and the mesonephros produces urine at 5 weeks and degenerates by 11 to 12 weeks. Failure of these two structures either to form or to regress may result in anomalous urinary system development. Between 9 and 12 weeks, the ureteric bud and the nephrogenic blastema interact to produce the metanephros. he kidney and ureter develop from intermediate mesoderm. The bladder and urethra develop from the urogenital sinus. The bladder also develops in part from the allantois.
By week 14, the loop of Henle is functional and reabsorption occurs (Smith, 1992). New nephrons continue to be formed until 36 weeks. In preterm neonates, their formation continues after birth. Although the fetal kidneys produce urine, their ability to concentrate and modiy the pH is limited even in the mature fetus. Fetal urine is hypotonic with respect to fetal plasma and has low electrolyte concentrations.
Renal vascular resistance is high, and the filtration fraction is low compared with adult values (Smith, 1992). Fetal renal blood low and thus urine production are controlled or inluenced by the renin-angiotensin system, the sympathetic nervous system, prostaglandins, kallikrein, and atrial natriuretic peptide. The glomerular filtration rate increases with gestational age from less than 0.1 mLimin at 12 weeks to 0.3 mLi min at 20 weeks. In later gestation, the rate remains constant when corrected for fetal weight (Smith, 1992). Hemorrhage or hypoxia generally results in a decrease in renal blood flow, glomerular filtration rate, and urine output.
Urine usually is found in the bladder even in small fetuses.
The fetal kidneys start producing urine at 12 weeks. By 18 weeks, they are producing 7 to 14 mLi day, and at term, this increases to 650 mLiday (Wladimirof, 1974). Maternally administered furosemide increases fetal urine formation, whereas uteroplacental insuiciency, fetal growth restriction, and other fetal disorders can lower it. Obstruction of the urethra, bladder, ureters, or renal pelves can damage renal parenchyma and distort fetal anatomy (Muller Brochut, 2014). Kidneys are not essential for survival in utero but inluence control of amnionic luid composition and volume. hus, abnormalities that cause chronic fetal anuria are usually accompanied by oligohydramnios and pulmonary hypoplasia. Pathological correlates and prenatal therapy of urinary tract obstruction are discussed in Chapter 16 (p. 325).