This article reviews the role of prostaglandins (PG) in maintaining renal function in the face of vasoconstrictive substances and decreased renal blood flow. Inhibition of the synthesis of renal PG by nonsteroidal antiinflammatory drugs (NSAID) may lead to the development of hemodynamically induced renal dysfunction in patients with a decreased effective plasma volume or chronic renal insufficiency. The importance of stimulation of renal PG activity to the action of diuretics and a pharmacodynamic mechanism for NSAID-induced diuretic resistance are presented. Evidence for the relative selectivity of sulindac in inhibiting systemic PG without inhibiting renal PG is also reviewed. Inhibition of renal PG synthesis has been postulated to be a contributing factor for other forms of NSAID-induced renal dysfunction (interstitial nephritis, analgesic-associated nephropathy). The relationship between renal PG inhibition by NSAID and these syndromes is briefly discussed. Considering the frequent use of NSAID, it is important that practitioners are aware of the mechanisms whereby patients may develop NSAID-induced renal dysfunction and that they are able to identify patients at risk.
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