| Abstrakt: |
The newborn infant is in a state of renal insufficiency with a glomerular filtration rate (GFR) as low as 20 ml/min per 1.73 m2 at term, and 10 ml/min per 1.73 m2 at 28 weeks of gestation. While the immature “insufficient” kidney can cope with most of the normal demands, its reserve is limited, and often overwhelmed by commonly occurring neonatal stresses. Various vasoactive systems such as the renin-angiotensin system, intrarenal adenosine, the prostaglandins and the atrial natriuretic peptide, are hyperactive in the neonatal period. Some of these systems appear crucial for the maintenance of GFR. Overstimulation of both angiotensin II and adenosine by an hypoxaemic stress can further impair the GFR, eventually leading to established renal failure. Inhibition of angiotensin II formation by the administration of angiotensin converting enzyme inhibitors can, on the other hand, also lead to renal failure. Prevention of these renal risks requires a precise knowledge of the newborn kidney physiology, physiopathology and pharmacology. |
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