Non steroidal antiinflammatory drugs may be harmful to normal kidneys: experimental surgery model*

The exact effect of analgesics on normal kidneys is not known yet. We aimed to evaluate the impression of non steroidal antiinflammatory drugs (NSAID) used post-operatively on kidneys, in rat (tracheotomy) model.

Twenty-five non-uremic male wistar albino rats were included. For 18 rats, tracheotomy was performed and divided into two groups. First group, NSAID (diclofenac 10 mg/kg/day intramuscular (im)) (NSAID, n=8); second group isotonic (im)(Control, n=10) were administered for a week. For third group (Histological control,n=7) in order to evaluate normal histology neither surgery nor medication were applied. At the end (7th day), 24 hours urine collected then, blood samples were taken by intracardiac punction and were sacrified. One of the kidneys fixed for histological evaluation, the other was preserved for the measurements of tissue enzyme levels. Lipid peroxidation products and antioxidant enzyme levels were measured both from plasma and renal tissues. Histologically inflammation, regeneration, degeneration assessed semiquatitativelly and immunohistochemical dyes were applied.

Hemoglobin thiobarbituric acid reactive substance level indicating the increase of lipid peroxidation in NSAID group was higher than control group (673±204 vs.373±27nmol/gHb respectively, p>0.05). Superoxide dismutase (one of the antioxidant enzymes responsible for reduction of reactive oxygen substances) and serum nitrate levels were lower in NSAID groups (700±68 vs.1371±164U/gHb and 26±4.4 vs.50.8±6.8 µmol/mL respectively, p<0.05).Although tissue levels were parallel to plasma levels but the difference wasn't significant. In histological assessment degeneration was present only in NSAID group (1.3±0.6 vs.0.0±0, p<0.05). Inflammation were lower than the control group (0.8±0.4 vs.1.2±0.2, p>0.05). Cyclooxygenase-2 expression was disappeared in NSAID group.

NSAIDs mostly used post-operatively for analgesia, may cause unfavorable effects on kidneys by oxidative stress.