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Volume 21, Issue 1
January – February 2001

Article Navigation
Review Articles| March 12 2001


RENAL EFFECTS OF COX-2-SELECTIVE INHIBITORS

Subject Area: Nephrology
D. Craig Brater;
D. Craig Brater
aDepartment of Medicine, Indiana University School of Medicine, Indianapolis,
Ind., and
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Cynthia Harris;
Cynthia Harris
aDepartment of Medicine, Indiana University School of Medicine, Indianapolis,
Ind., and
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Jan S. Redfern;
Jan S. Redfern
bMerck & Co., Inc., Rahway, N.J., USA
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Barry J. Gertz
Barry J. Gertz
bMerck & Co., Inc., Rahway, N.J., USA
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Am J Nephrol (2001) 21 (1): 1–15.
https://doi.org/10.1159/000046212
Article history
Published Online:
March 12 2001

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Citation

D. Craig Brater, Cynthia Harris, Jan S. Redfern, Barry J. Gertz; Renal Effects
of COX-2-Selective Inhibitors. Am J Nephrol 1 February 2001; 21 (1): 1–15.
https://doi.org/10.1159/000046212

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ABSTRACT

Although nonsteroidal anti-inflammatory drugs (NSAIDs) effectively treat a
variety of inflammatory diseases, these agents may cause deleterious effects on
kidney function, especially with respect to solute homeostasis and maintenance
of renal perfusion and glomerular filtration. NSAIDs act by reducing
prostaglandin biosynthesis through inhibition of cyclooxygenase (COX) which
exists as two isoforms (COX-1 and COX-2). NSAID-induced gastrointestinal
toxicity is generally believed to occur through blockade of COX-1 activity,
whereas the anti-inflammatory effects of NSAIDs are thought to occur primarily
through inhibition of the inducible isoform, COX-2. However, the situation in
the kidney may be somewhat different. Recent studies have demonstrated that
COX-2 is constitutively expressed in renal tissues of all species; this isoform
may, therefore, be intimately involved in prostaglandin-dependent renal
homeostatic processes. Drugs that selectively inhibit COX-2 might, therefore, be
expected to produce effects on renal function similar to nonselective NSAIDs
which inhibit both COX-1 and COX-2. This assertion is borne out by recent
clinical studies showing that the COX-2 inhibitors rofecoxib and celecoxib
procedure qualitative changes in urinary prostaglandin excretion, glomerular
filtration rate, sodium retention, and their consequences similar to
nonselective NSAIDs. It, therefore, seems unlikely that these COX-2 inhibitors
(and perhaps their successors) will offer renal safety benefits over
nonselective NSAID therapies, and, at this juncture, it is reasonable to assume
that all NSAIDs, including COX-2-selective inhibitors, share a similar risk for
adverse renal effects.

Keywords:
Rofecoxib, Celecoxib, COX-2 inhibitors, Nonsteroidal anti-inflammatory drugs,
Nephrotoxicity, Glomerular filtration, Hypertension, Acute renal failure

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© 2001 S. Karger AG, Basel
2001
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the publisher.
Drug Dosage: The authors and the publisher have exerted every effort to ensure
that drug selection and dosage set forth in this text are in accord with current
recommendations and practice at the time of publication. However, in view of
ongoing research, changes in government regulations, and the constant flow of
information relating to drug therapy and drug reactions, the reader is urged to
check the package insert for each drug for any changes in indications and dosage
and for added warnings and precautions. This is particularly important when the
recommended agent is a new and/or infrequently employed drug.
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