Cyclooxygenase-2 Inhibitor-Associated Acute Renal Failure
Cyclooxygenase-2 Inhibitor-Associated Acute Renal Failure
Cyclooxygenase (COX)-2 inhibitors are widely prescribed for their antiinflammatory and analgesic effects. The potential for COX-2 inhibitors to exert deleterious effects on renal function similar to those of traditional nonsteroidal antiinflammatory drugs is not well defined. Until recently, COX-1 was considered responsible for the synthesis of renal prostaglandins. However, COX-2 is also constitutively expressed in the human kidney. Clinical studies have reported a significant decrease in glomerular filtration rate in young and elderly sodium-depleted volunteers given COX-2 inhibitors. We describe the case of a 71-year-old woman who developed acute renal failure after receiving a 50-mg dose of the selective COX-2 inhibitor rofecoxib.
Traditional nonsteroidal antiinflammatory drugs (NSAIDs) inhibit both isoforms of the enzyme cyclooxygenase (COX). The first, COX-1, is constitutively expressed in most cells throughout the body, and its inhibition has been associated with gastrointestinal bleeding and ulceration. In contrast, COX-2 expression is induced in the presence of inflammation and its inhibition results in the therapeutic effects of NSAIDs. Thus, the development of selective COX-2 inhibitors brought about a new way to produce potent antiinflammatory actions with a decreased risk of significant gastrointestinal adverse effects.
In addition to the gastrointestinal side effects of NSAIDs, renal toxicity, including acute renal failure, is described in the literature. These agents can be particularly harmful to renal function in patients relying on the vasodilatory actions of prostaglandins in the kidney. However, the potential for COX-2 inhibitors to have effects on renal function similar to those of NSAIDs is not well defined, and the role of COX-2 in the human kidney is not fully understood. Several in vitro and clinical studies have begun to elucidate the role of this enzyme and the effects of its inhibition on renal function. Case reports of selective COX-2 inhibitor-associated acute renal failure are emerging.
Cyclooxygenase (COX)-2 inhibitors are widely prescribed for their antiinflammatory and analgesic effects. The potential for COX-2 inhibitors to exert deleterious effects on renal function similar to those of traditional nonsteroidal antiinflammatory drugs is not well defined. Until recently, COX-1 was considered responsible for the synthesis of renal prostaglandins. However, COX-2 is also constitutively expressed in the human kidney. Clinical studies have reported a significant decrease in glomerular filtration rate in young and elderly sodium-depleted volunteers given COX-2 inhibitors. We describe the case of a 71-year-old woman who developed acute renal failure after receiving a 50-mg dose of the selective COX-2 inhibitor rofecoxib.
Traditional nonsteroidal antiinflammatory drugs (NSAIDs) inhibit both isoforms of the enzyme cyclooxygenase (COX). The first, COX-1, is constitutively expressed in most cells throughout the body, and its inhibition has been associated with gastrointestinal bleeding and ulceration. In contrast, COX-2 expression is induced in the presence of inflammation and its inhibition results in the therapeutic effects of NSAIDs. Thus, the development of selective COX-2 inhibitors brought about a new way to produce potent antiinflammatory actions with a decreased risk of significant gastrointestinal adverse effects.
In addition to the gastrointestinal side effects of NSAIDs, renal toxicity, including acute renal failure, is described in the literature. These agents can be particularly harmful to renal function in patients relying on the vasodilatory actions of prostaglandins in the kidney. However, the potential for COX-2 inhibitors to have effects on renal function similar to those of NSAIDs is not well defined, and the role of COX-2 in the human kidney is not fully understood. Several in vitro and clinical studies have begun to elucidate the role of this enzyme and the effects of its inhibition on renal function. Case reports of selective COX-2 inhibitor-associated acute renal failure are emerging.
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