RENAL TOXICITY COMPARISON BY NSAIDS DEPENDING ON THE MECHANISM OF ACTION IN PATIENTS WITH HEADACHES

Drita Yzeiri Havziu, Biljana Gjoegjeska, Arlinda Haxhiu Zaimi, Edita Alili Idrizi, Gjylaj Alija, Merita Dauti, Sihana Ameti Lika, Lulzime Balazhi

Abstract

Non-selective COX inhibitors are the most widely prescribed NSAID treatment for headaches. Celecoxib is another NSAID therapy that has been approved in the last several years, with different mechanisms of action. Nonsteroidal anti-inflammatory drugs (NSAIDs) cause renal toxicity following the inhibition of cyclooxygenases. Relatively little is known about the comparative nephrotoxicity of NSAIDs in patients with a chronic headache based on COX inhibition. Therefore, this study was designed to compare the nephrotoxic effects of nonselective COX inhibitors, relatively selective inhibitors, and selective inhibitors based on the mechanism of action. Besides conventional markers of renal function (serum/urine creatinine determined by Jaffe's methods of enzymatic assay for urea in serum, uric acid in serum, and glutamyl transferase [?-GT] in serum). We used nephelometry by ß2 microglobulin (ß2M) and photoelectric colorimetry for microalbuminuria in urine, as well as ion selective electrode (ISE) for electrolyte detection in serum, to evaluate glomerular and tubular functioning. Kidney disease history was a requirement to be excluded from the study. The results showed increased values of microalbuminuria in patients treated with NSAIDs as non-selective COX inhibitors compared with patients treated with NSAIDs as relatively selective and highly selective COX-2 inhibitors - 52.8% (19), 16.7% (2), 16.7% (4), consequently and in ß2 microglobulin 97.2% (35), 91.7% (11), 54.2% (13), consequently. The renoprotective properties of highly selective COX-2 inhibitors have been confirmed with non-selective COX inhibitors that are less nephrotoxic agents.

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