Celecoxib-Induced Nephrotoxicity in A Renal Transplant Recipient
A 47-year-old renal transplant recipient came to the transplant clinic with a serum creatinine level that was elevated above her baseline value. She had been taking celecoxib for arthritic pain. She was told to discontinue the drug, and shortly after, her serum creatinine level returned to baseline. Several case reports describe nephrotoxicity with cyclooxygenase (COX)-2 inhibitors. However, only two of these reports involved renal transplant recipients, and in both, rofecoxib was the COX-2 inhibitor of concern. To our knowledge, this is the first case report of a renal transplant recipient who developed nephrotoxicity while taking celecoxib. The potential renal effects of COX-2 inhibitors have received little attention, even though nonsteroidal anti-inflammatory drugs are considered to carry the risk of nephrotoxicity in patients with comorbidities such as diabetes mellitus and hypertension. Further studies are necessary to determine the safety of COX-2 inhibitors in transplant recipients and other patient groups that may be at heightened risk of nephrotoxicity.
Nonsteroidal antiinflammatory drugs (NSAIDs) are widely used for a variety of indications, including acute pain, menstrual pain, arthritic pain, and headache. The long-term use of these agents is often limited by unwanted adverse effects, such as gastritis and renal dysfunction. In an effort to decrease gastrointestinal adverse effects while retaining pain-relieving properties, the selective cyclooxygenase (COX)-2 inhibitors were developed. The popularity of this class produced retail sales in excess of $4.7 billion in the United States for 2003.
The COX-2 inhibitors inhibit only the COX-2 isoenzyme, whereas traditional NSAIDs inhibit both COX-1 and COX-2. Inhibition of COX-1 has been associated with gastrointestinal adverse effects. Inhibition of COX-2 has been targeted to decrease inflammatory mediators that cause pain (Figure 1). It is this pathway that gives COX-2 inhibitors a potential advantage over the older NSAIDs.
(Enlarge Image)
Differentiation of the effects of cyclooxygenase (COX)-1 and COX-2 isoenzymes. NSAID = nonsteroidal antiinflammatory drug.
With widespread use and an aging population in the United States, growing numbers of case reports and adverse events associated with COX-2 inhibitors are being reported in the literature. Adverse outcomes ranging from acute renal failure to gastrointestinal bleeding have been described. Even patients with otherwise normal renal function may be at risk for interstitial nephritis as a result of these agents. Thus patients with underlying renal or cardiovascular disease may be at even greater risk. In most reported cases, the event improved or resolved completely with discontinuation of the drug.
A 47-year-old renal transplant recipient came to the transplant clinic with a serum creatinine level that was elevated above her baseline value. She had been taking celecoxib for arthritic pain. She was told to discontinue the drug, and shortly after, her serum creatinine level returned to baseline. Several case reports describe nephrotoxicity with cyclooxygenase (COX)-2 inhibitors. However, only two of these reports involved renal transplant recipients, and in both, rofecoxib was the COX-2 inhibitor of concern. To our knowledge, this is the first case report of a renal transplant recipient who developed nephrotoxicity while taking celecoxib. The potential renal effects of COX-2 inhibitors have received little attention, even though nonsteroidal anti-inflammatory drugs are considered to carry the risk of nephrotoxicity in patients with comorbidities such as diabetes mellitus and hypertension. Further studies are necessary to determine the safety of COX-2 inhibitors in transplant recipients and other patient groups that may be at heightened risk of nephrotoxicity.
Nonsteroidal antiinflammatory drugs (NSAIDs) are widely used for a variety of indications, including acute pain, menstrual pain, arthritic pain, and headache. The long-term use of these agents is often limited by unwanted adverse effects, such as gastritis and renal dysfunction. In an effort to decrease gastrointestinal adverse effects while retaining pain-relieving properties, the selective cyclooxygenase (COX)-2 inhibitors were developed. The popularity of this class produced retail sales in excess of $4.7 billion in the United States for 2003.
The COX-2 inhibitors inhibit only the COX-2 isoenzyme, whereas traditional NSAIDs inhibit both COX-1 and COX-2. Inhibition of COX-1 has been associated with gastrointestinal adverse effects. Inhibition of COX-2 has been targeted to decrease inflammatory mediators that cause pain (Figure 1). It is this pathway that gives COX-2 inhibitors a potential advantage over the older NSAIDs.
(Enlarge Image)
Differentiation of the effects of cyclooxygenase (COX)-1 and COX-2 isoenzymes. NSAID = nonsteroidal antiinflammatory drug.
With widespread use and an aging population in the United States, growing numbers of case reports and adverse events associated with COX-2 inhibitors are being reported in the literature. Adverse outcomes ranging from acute renal failure to gastrointestinal bleeding have been described. Even patients with otherwise normal renal function may be at risk for interstitial nephritis as a result of these agents. Thus patients with underlying renal or cardiovascular disease may be at even greater risk. In most reported cases, the event improved or resolved completely with discontinuation of the drug.