[The immature kidney]

Abstract

In humans, urine formation starts with the metanephros at the 10th week of gestation. Nephrogenesis progresses during gestation and is achieved around the 35th week. Clamping of the cord is the signal for a striking increase in renal function which reaches mature levels at the end of the first year of life. The integrity of several hormonal systems (the renin-angiotensin system, the prostaglandins) is mandatory for kidney growth and the development of renal function. The mechanisms underlying renal homeostasis are fragile and can easily be disturbed during respiratory and cardiovascular distress, or be affected by the administration of vasoactive agents. Thus, perinatal asphyxia or hypoxemia, as seen in respiratory distress syndrome or neonatal pulmonary hypertension induces intense renal vasoconstriction, with consequent oligoanuria. Congestive heart failure also results in renal hypoperfusion and sodium retention. Vasoactive agents and diuretics (indomethacin, tolazoline, furosemide) used to threat these conditions can result in renal vasoconstriction, renal hypoperfusion and failure. The pathogenesis and pathophysiology of neonatal renal disturbances being now better defined, a rational approach to the treatment of renal functional abnormalities during the neonatal period is possible.