[The significance of renal prostaglandins for kidney function in early childhood].

When comparing iatrogenic inhibition with endogenous stimulation of renal prostaglandin production, the role of this mediator and modulator system for renal function becomes apparent. Renal perfusion and glomerular filtration as well as modulation of tubular function with respect to electrolyte and water excretion is significantly influenced by renal prostaglandin activity. Treatment with the prostaglandin cyclooxygenase inhibitor indomethacin reduces the endogenous creatinine clearance by about fifty percent in a state of a diminished circulatory blood volume, such as may exist during left-to-right shunting across a persistent ductus arteriosus in preterm infants. In addition, urinary electrolyte and water excretion is reduced by increased tubular absorption leading to marked oliguria. In contrast, electrolytes and water are lost in congenital renal tubular disorders associated with increased prostaglandin E2 (PGE2) activity (a so called hyperprostaglandin E syndrome). Patients with this renal disorder require a permanent high dosed indomethacin therapy. After this pharmacotherapy has brought electrolyte and water metabolism into balance, no deterioration of glomerular filtration and renal perfusion was observed. This is in accordance with the general principle that renal function only becomes dependent on the vasodilatory activity of renal prostaglandins in a stress situation resulting in the threat of hypoperfusion. It is essential to bear in mind the physiological and pathophysiological role of renal prostaglandins, when prescribing frequently administered prostaglandin cyclooxygenase inhibitors like aspirin, paracetamol or indomethacin in pediatrics. Otherwise, renal function may deteriorate or the kidney will be irreversibly damaged.