mobic and Nephritis--Interstitial

Nonsteroidal anti-inflammatory drugs (NSAIDs) can affect renal function in a variety of ways. The most important clinical effects are decreased sodium excretion, decreased potassium excretion, and declines in renal perfusion. Decreased sodium excretion can result in weight gain, peripheral edema, attenuation of the effects of antihypertensive agents, and rarely precipitation of chronic heart failure. Hyperkalemia can occur to a degree sufficient to cause cardiac arrhythmias. Renal function can decline sufficiently enough to cause acute renal failure. Risk factors for all of these effects have been identified, allowing prospective identification of patients at risk with institution of appropriate precautionary measure. All NSAIDs seem to share these adverse effects. Preliminary data from cyclooxygenase-2-selective inhibitors suggest that they also affect renal prostaglandins. Therefore, the same cautions should be exercised with their use as with traditional NSAIDs.

Topics: Anti-Inflammatory Agents, Non-Steroidal; Butanones; Celecoxib; Cyclooxygenase 2; Cyclooxygenase 2 Inhibitors; Cyclooxygenase Inhibitors; Humans; Isoenzymes; Kidney; Lactones; Meloxicam; Membrane Proteins; Nabumetone; Natriuresis; Nephritis, Interstitial; Potassium; Prostaglandin-Endoperoxide Synthases; Pyrazoles; Renal Circulation; Sodium; Sulfonamides; Sulfones; Thiazines; Thiazoles

To observe the effect of selective cyclooxygenase-2 (COX-2) inhibitor-meloxicam on the progression of tubulointerstitial fibrosis in rats with unilateral ureteral obstruction (UUO).. UUO rats were treated with meloxicam (M), indomethacin (I) or vehicle alone (U) for 4 weeks. Using reverse transcription-polymerase chain reaction (RT-PCR), we examined the mRNA expressions of transforming growth factor (TGF)-beta receptor-1 and 2 in left kidney from rats with UUO. Immuno-precipitation and immunohistochemistry analysis were carried out to investigate the protein level of TGF-beta(1). Tubulointerstitial fibrosis was quantified by Masson's staining. Similar studies were performed in another group of rats with sham operation (C).. mRNA expressions of TGF-beta receptor-1 and 2 were markedly increased in Group U compared with those in Group C. Both meloxicam and indomethacin inhibited their expressions to a different degree (P < 0.01), but the effect of meloxicam was more significant. Meloxicam decreased the protein level of TGF-beta(1) (P < 0.01), while indomethacin had no such effect. Compared with Group C, there appeared tubulointerstitial fibrosis in the kidney of rats with UUO. The lesion was aggravated by indomethacin, but remarkably attenuated by meloxicam.. In summary, selective COX-2 inhibitor-meloxicam has a salutary effect on the tubular and interstitial response to UUO. TGF-beta and its receptor approaches partly explain some of the mechanism.

Topics: Animals; Cyclooxygenase 2; Cyclooxygenase 2 Inhibitors; Cyclooxygenase Inhibitors; Disease Models, Animal; Indomethacin; Isoenzymes; Male; Meloxicam; Nephritis, Interstitial; Prostaglandin-Endoperoxide Synthases; Protective Agents; Rats; Rats, Sprague-Dawley; Thiazines; Thiazoles; Ureteral Obstruction