Guignard J P, Gouyon J B, John E G
Department of Paediatrics, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland.
Pediatr Nephrol. 1991 Jul;5(4):443-6. doi: 10.1007/BF01453678.
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.
足月新生儿处于肾功能不全状态，其肾小球滤过率（GFR）低至每1.73平方米20毫升/分钟，妊娠28周时为每1.73平方米10毫升/分钟。虽然未成熟的“功能不全”肾脏能够应对大多数正常需求，但其储备有限，常常被常见的新生儿应激所压垮。各种血管活性系统，如肾素 - 血管紧张素系统、肾内腺苷、前列腺素和心房利钠肽，在新生儿期都处于活跃状态。其中一些系统似乎对维持肾小球滤过率至关重要。低氧应激对血管紧张素II和腺苷的过度刺激会进一步损害肾小球滤过率，最终导致肾衰竭。另一方面，通过给予血管紧张素转换酶抑制剂抑制血管紧张素II的形成也会导致肾衰竭。预防这些肾脏风险需要精确了解新生儿肾脏生理学、病理生理学和药理学。
