Monitoring of the renal function in Indometacin treated patients with rheumatoid arthritis

Drita Yzeiri Havziu; М. Hiljadnikova-Bajro; Т. Kadifkova Panovska

Drita Yzeiri Havziu Faculty of Medical Sciences-State University of Tetovo, Macedonia
М. Hiljadnikova-Bajro Faculty of Pharmacy, Ss. Cyril and Methodius University, Skopje, Macedonia
Т. Kadifkova Panovska Faculty of Pharmacy, Ss. Cyril and Methodius University, Skopje, Macedonia

Abstract

Abstract

Nonsteroidal antiinflamatory drugs (NSAIDs) are considered as one of the most nephrotoxic drugs and their use in chronic rheumatic treatment is frequently accompanied by renal impairments of various pathophysiology and severity. The aim of this study was to evaluate the kidney performance among Indometacin treated patients with rheumatoid arthritis (RA).

A total of 20 patients (14-RA^sero+,6-RA^sero-) with an average age of 46,57 ±7,51,suffering from chronic rheumatic pain were evaluated quarterly for one year and once more one month after discontinuation of treatment. The results were compared to the reference interval and a control group of 80 healthy individuals. A panel of 5 urinary specific nephrotoxicity biomarkers including N-Acetyl-β-(D)-Glucosaminidase (NAG), Alanine Aminopeptidase (AAP), γ-glutamyl transferase (γ–GT),α1 Microgloglobulin (α1M) and microalbuminuria,was used to monitor glomerular and tubular functioning. Present or past history of kidney disease was considered an exclusion criteria for enrollment in the study.

After a 12 month treatment with Indometacin (2x25mg) a significant increase of the evaluated markers was evident among all patients, except for microalbuminuria and α1M which were insignificantly increased among RA^sero- patients and did not exit the reference interval. These findings suggest a renal impairment resulting from Indometacin nephrotoxicity but might also be affected by the rheumatic complications. Fortunately, the damage is reversible at this stage and the evaluated parameters normalize within one month after the cessation of treatment indicating that the detected impairment is predominantly caused by the toxicity of Indometacin. Further studies are needed to precisely differentiate the level of impairment caused by the NSAIDs and the rheumatic pathology itself but we strongly recommend regular monitoring of the renal performance in patients undergoing continuous Indometacin treatment for rheumatic pain.

Keywords: Biomarkers, Nephrotoxicity, Nonsteroidal antiinflamatory drugs, rheumatoid arthritis.