A comparison between the acute effects of coxis on renal function with that of diclofenac sodium in patients with rheumatological disorders

Abstract EN

The aim of this study was identify the effect of (coxibs) on renal function in comparison to the traditional (NSAIDs) to provide more insight on this issue.

Particular emphasis has been paid to the possible acute renal toxicities such as acute decline in renal function, hyperkalaemia, hypertension and sodium and water retension, the study was conducted during the period from (February –August) 2018 , Rheumatological out-patient clinic in Ibn-Sina Teaching Hospital in Mosul.

patients and methods : Eighty patients with different rheumatological disorders who have no history of pre-existing renal disease.

They were divided into 2 groups: Group A (40 patients): Treated with diclofenac sodium and Group B (40 patients): Who were treated with celeecoxib.

Twenty healthy subjects, group C were taken as a control group.

They have all undergone clinical examination including measurement of their body weights and blood pressure at the start of the study and repeated a month later.

Certain Biochemical markers including urea, creatinine, serum sodium and potassium have been measured at the start and repeated a month later following the commencement of treatment.

Results: Patients in group B had decrease in renal function manifested as arise in blood urea, (P <0.001), and both group had increase in serum creatinine group A (P<0.05) group B (P<0.001), and decline in creatinine clearance group A (P <0.001), group B (P <0.001), compared with the control group.

There was also significant sodium and potassium retention in both groups.

Group A (sodium P<0.05 potassium P <0.001), group B (sodium P<0.001 potassium P <0.001).

Conclusion: The effects celecoxib ( COX-2 inhibitors) on renal function are similar to those observed with diclofenac (non-selective NSAID’s) and, consequently, standard precautions to avoid renal toxicity with the use of non-selective NSAID’s apply to coxibs.