Background: Selective cyclo-oxygenase (COX)-2 inhibitors (coxibs) produce the beneficial effects of nonsteroidal anti-inflammatory drugs (NSAIDs) while sparing the COX-1-mediated adverse effects on platelets and the gastrointestinal system. However, due to the presence of constitutive COX-2 in the human kidney, coxibs have the same potential for adverse renal effects as traditional NSAIDs.
Objective: To provide evidence-based guidelines for the use of traditional NSAIDs and coxibs in patients potentially at risk for renal and associated hemodynamic blood pressure effects.
Methods: All pertinent peer-reviewed papers were retrieved with the usual electronic search tools.
Results: Both traditional NSAIDs and coxibs compromise the glomerular filtration rate in patients at increased risk. If there are differences in the blood pressure-raising potential of these drugs, these differences do not appear to be clinically significant.
Conclusions: The blood pressure should be monitored for all patients taking chronic NSAID or coxib therapy. If a clinically significant (4 to 5 mmHg or more) increase in blood pressure is detected, the NSAID or the coxib should be discontinued and replaced with acetaminophen, to which codeine might be added. If the NSAID or the coxib is considered necessary, the increase in blood pressure should be treated. In addition, if the glomerular filtration rate reserve is compromised, all patients (including those taking short term therapy) should be closely monitored for the early detection of signs and symptoms of renal failure.