NSAIDs, prostaglandins and the neonatal kidney

Abstract

Renal prostaglandins, particularly PGE(2), play a homeostatic role in the immature kidney through their hemodynamic and tubular effects, and this role may be crucial under conditions of renal stress. Nonsteroidal anti-inflammatory drugs (NSAIDs) are commonly used in the neonatal period to treat or prevent patent ductus arteriosus (PDA) in preterm infants. The nephrotoxic effects induced by NSAIDs result from the inhibition of renal cyclooxygenase activity and prostaglandin synthesis. NSAID-induced prostaglandin inhibition may result in renal hypoperfusion and acute renal failure which are clinically relevant, but usually reversible, adverse effects in the newborn. Currently, ibuprofen appears to be the therapeutic option of choice in the preterm newborn with PDA because of its better renal tolerability compared to other NSAIDs. Nevertheless, the use of this drug is not free from adverse renal effects, particularly in circumstances when renal prostaglandin activation is maximal. The implementation of measures to prevent or minimise nephrotoxicity and close monitoring of renal function are mandatory in the newborn treated with NSAIDs. The measurement of urinary PGE(2) may represent a non-invasive and sensitive tool to evaluate renal function, and thus should be implemented in the clinical management of newborns exposed to nephrotoxic insults.