ABSTRACT
This chapter describes ibuprofen’s role and risk factors for their development. Nonsteroidal anti-inflammatory drugs (NSAIDs) can produce either acute, reversible or permanent renal toxicity and a variety of effects on electrolyte and water homeostasis. Acute tubular ischemia and necrosis from ibuprofen occurs in some patients administered ibuprofen from a hemodynamic effect upon this vasculature. Renal autacoids produce many physiological effects. Understanding their effects is necessary for understanding the consequences of their depletion when ibuprofen is administered. Accumulation of glucuronide conjugates of both R and S enantiomers could provide more (R)-(-) substrate for conversion to the active (S)-(+) enantiomer and allow a disproportionate increase in cyclooxygenase inhibition. The most common form of ibuprofen-associated renal impairment is acute ischemic renal insufficiency. Acute interventional studies of small groups of preselected subjects demonstrate abrupt reductions in glomerular filtration rate of 9% to 69% following the administration of NSAIDs.
