title: [Renal tolerance of selective inhibitors of cyclooxygenase type 2].
abstract: ANTIINFLAMMATORY DRUGS: Non-steroidal antiinflammatory drugs (NSAID) constitute one of the most widely prescribed drug classes. Selective inhibitors of cyclooxygenase type 2 (Cox-2) can have antiinflammatory and antialgesic activities without affecting prostaglandin synthesis at sites where classical NSAID have known toxicity. This fact has led to the development of celebrex and rofecoxib, the leading selective inhibitors of Cox-2. We review here the renal effects of steroidal antiinflammatory drugs. RENAL EFFECTS OF NSAID: The renal effects of NSAID are, in decreasing order: electrolyte imbalance (hyperkaliemia, edema, hypertension), acute renal failure, nephrotic syndrome associated with interstitial nephropathy, papillary necrosis. Electrolyte disorders and acute renal failure are observed more frequently in patients with risk factors. INTRARENAL LOCALIZATION OF CYCLOOXYGENASE: Cox-1 is present in endothelial and smooth muscle cells of pre- and postglomerular vessels as well as in the cortex, the medullary tubes and in interstitial cells. Cox-2 expression has been identified in the interstitium, medullary tubes and intercalate cells, and in the deep medulla. The regulatory role of Cox-2 on renin production has been demonstrated in the macula densa. RENAL EFFECTS OF COX-2 INHIBITORS: Several studies have demonstrated that Cox-2 inhibitors inhibit prostaglandin synthesis much like conventional NSAID. The long-term effects of selective inhibitors of Cox-2 on blood pressure, edema, kaliemia and renal function have also been described. All these studies point to the strictly identical renal effects of these new drugs and conventional NSAID.
authors.affiliation: Service de Néphrologie, Groupe Hospitalier Pitié-Salpêtrière, 83, bd de l'Hôpital, F75013 Paris.
authors.forename: G
authors.initials: G
authors.lastname: Deray
mesh_terms: D058186:Acute Kidney Injury / Q000139:chemically induced; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects / Q000494:pharmacology* / Q000627:therapeutic use; D001168:Arthritis / Q000188:drug therapy; D001172:Arthritis, Rheumatoid / Q000188:drug therapy; D000068579:Celecoxib; D002986:Clinical Trials as Topic; D016861:Cyclooxygenase Inhibitors / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use; D004008:Diclofenac / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use; D006801:Humans; D007668:Kidney / Q000187:drug effects* / Q000378:metabolism; D007674:Kidney Diseases / Q000139:chemically induced; D007783:Lactones / Q000494:pharmacology / Q000627:therapeutic use; D009288:Naproxen / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism; D011453:Prostaglandins / Q000096:biosynthesis; D011720:Pyrazoles; D051381:Rats; D012307:Risk Factors; D013449:Sulfonamides / Q000494:pharmacology / Q000627:therapeutic use; D013450:Sulfones; D014883:Water-Electrolyte Imbalance
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D016861:Cyclooxygenase Inhibitors; D007783:Lactones; D011453:Prostaglandins; D011720:Pyrazoles; D013449:Sulfonamides; D013450:Sulfones; C116926:rofecoxib; D004008:Diclofenac; D009288:Naproxen; D011451:Prostaglandin-Endoperoxide Synthases; D000068579:Celecoxib