Secondary renal artery stenosis
Secondary renal artery stenosis is not rare in sick babies treated in neonatal intensive care units. It is thought to be due to the administration of (high osmotic) fluids via the umbilical artery, causing systemic hypertension as well as neonatal renal failure [50]. Arterial occlusion and secondary activation of the RAAS are responsible for the renal hypoperfusion. Umbilical arterial catheters should be used with caution, without too many manipulations. They should be removed as soon as possible and certainly in case of (repeated) clotting [51].
ACE inhibitors
ACE inhibitors (captopril or enalapril) have been used in the past as antihypertensive agents during pregnancy. These drugs rapidly cross the placenta, also blocking fetal ACE activity. This is especially worrying since in the fetus and the newborn All is mandatory for the maintenance of an effective GFR [7]. During pregnancy the administration of ACE inhibitors may also interfere with normal renal development, causing nephron dysgenesis [52, 53], eventually leading to neonatal renal failure. It is now well established that the maternal ingestion of ACE
inhibitors leads to acute and chronic neonatal ARF [54, 55]. The use of these drugs is therefore contraindicated during pregnancy [56J. Postnatal treatment of hypertensive premature babies with captopril has led to a dramatic fall in MAP, accompanied by persistent oliguria [57]. This exaggerated response is not surprising because of the hyperactivity of the RAAS during the entire neonatal period, particularly in preterm infants. The initial dose of ACE inhibitors in newborn babies should therefore be considerably lower than in older individuals. In new-borns and particularly preterm infants, other antihyper-tensive drugs should be used if possible [58, 59].
PG synthesis inhibitors
High PG activity is a physiological phenomenon during the first days of life. This increased vasodilatory activity is probably needed to maintain sufficient perfusion of the newborn kidney [7]. Serum PG levels are also high in CHF, PDA, and all instances of hypotension and/or hypo-volemia. PG inhibitors, such as indomethacin, have been used prenatally to prevent the premature onset of labor and postnatally to promote the closure of the hemody-namically active PDA. In the course of such treatment, a transient reduction of RBF and GFR has been observed [25, 46, 60, 61]. This is not surprising since PG inhibitors are only effective when the basic PG activity is elevated. In premature infants the plasma half-life of indomethacin is prolonged due to hepatic immaturity. This increases the renal effects of PG synthesis inhibition in these babies [45]. Indomethacin should therefore be given with utmost caution or avoided altogether in neonates who already have or are prone to renal functional disturbances.
Tolazoline
Tolazoline is an a-adrenergic blocking agent that is used as a pulmonary vasodilator in persistent pulmonary hypertension of the newborn [62]. The reported renal side effects of the drug include hypotension and oliguric ARF [63, 64]. In newborn animal models tolazoline induced renal dysfunction only under hypoxemic conditions [65, 66]. The renal effect of tolazoline has been ascribed to a partial a-adrenergic agonist action [65]. To prevent tol-azoline-induced impairment of renal function a test dose is recommended (0.5 mg/kg) before giving the full dose (1-2 mg/kg) of the drag; control of blood pressure is mandatory. In conditions of decreased cardiac output, a combination therapy of tolazoline with dopamine (DA) may be indicated.
Tolazoline - a-adrenergic блокирование агента, который используется как легочный vasodilator в постоянной легочной гипертонии новорожденного [62]. Сообщенные почечные побочные эффекты препарата включают hypotension и oliguric ARF
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