NSAIDs Tacrolimus

Concurrent nephrotoxin use (e.g., aminoglycosides, polymixins, amphotericin B, foscamet, cyclosporine, tacrolimus, and NSAIDs)... 

Determine if drug therapy may be contributing to ARF. Consider not only drugs that can directly cause ARF (e.g., aminoglycosides, amphotericin B, NSAIDs, cyclosporine, tacrolimus, ACE inhibitors, and ARBs), but also drugs that can predispose a patient to nephrotoxicity or prerenal ARF (i.e., diuretics and anti hypertensive agents). 

TACROLIMUS ANALGESICS-NSAIDs t risk of nephrotoxicity Additive effect Monitor renal function closely... 

Additive renal toxic effects may occur with immunosuppressants (e.g. azathioprine, ciclosporin, tacrolimus), ACE inhibitors, penicillamine, irinotecan and aminoglycoside antibiotics. A deterioration of renal function may even occur after the topical use of NSAIDs. Guidelines are variable for the use of NSAIDs with differing degrees of renal function, as assessed by creatinine clearance measurements. 

NSAIDs, ACE-inhibitors, cyclosporine, norepinephrine, angiotensin receptor blockers, diuretics, interieukins, cocaine, mitomycin C, Tacrolimus, Estrogen, quinine. ... 

Clinically important, potentially hazardous interactions with amiloride, aminoglycosides, amphotericin B, ampicillin, anisindione, anticoagulants, armodafinil, atorvastatin, azathioprine, azithromycin, bacampicillin, basiliximab, bezafibrate, bosentan, bupropion, carbenicillin, caspofungin, cholestyramine, clarithromycin, cloxacillin, co-trimoxazole, corticosteroids, cyclophosphamide, daclizumab, danazol, dicloxacillin, dicumarol, digoxin, diltiazem, disulfiram, echinacea, erythromycin, ethotoin, etoposide, ezetimibe, flunisolide, fluoxymesterone, fluvastatin, foscarnet, fosphenytoin, gemfibrozil, hemophilus B vaccine, HMG-CoA reductase inhibitors, imatinib, imipenem/cilastatin, influenza vaccines, ketoconazole, lanreotide, lopinavir, lovastatin, mephenytoin, methicillin, methoxsalen, methylphenidate, methylprednisolone, methyltestosterone, mezlocillin, mizolastine, mycophenolate, nafcillin, nisoldipine, NSAIDs, orlistat, oxacillin, penicillins, phellodendron, phenytoin, pravastatin, prednisolone, prednisone, pristinamycin, ranolazine, red rice yeast, rifabutin, rifampin, rifapentine, ritonavir, rosuvastatin, simvastatin, sirolimus, spironolactone, St John s wort, sulfacetamide, sulfadiazine, sulfamethoxazole, sulfisoxazole, sulfonamides, tacrolimus, telithromycin, tenoxicam, testosterone, ticarcillin, tolvaptan, trabectedin, triamterene, troleandomycin, ursodeoxycholic acid, vaccines, vecuronium, warfarin, zofenopril... 

Clinically important, potentially hazardous interactions with aspirin, boswellia, ciprofibrate, diuretics, methotrexate, NSAIDs, oxycodone hydrochloride, salicylates, tacrine, tacrolimus, urokinase... 

In the U.S. double-blind study in which NSAID use was unrestricted, a dose-dependent increase in serum creatinine from baseline was observed. In contrast, although slight increases were seen in the Japanese study, most patients creatinine levels remained within the normal range. Whether the concomitant use of NSAIDs was a confounding factor in the development of increased creatinine is not clear. It is important to note that the antirheumatic effect of tacrolimus becomes clear within the first 4 weeks after treatment initiation and, therefore, the potential exists to reduce the dose of NSAIDs at that time. Further clinical studies are currently under way to confirm these results in a larger cohort of patients who have failed at least one DMARD in the United States and Japan, using a double-blind, placebo-controlled paradigm. This study should also better define the safety profile of tacrolimus in this patient population. 

Other predicted interactions of tacrolimus include additive neuro- or nephrotoxicity with aciclovir, aminoglycosides, co-trimoxazole, ganciclovir, gyrase inhibitors, NSAIDs (see NSAIDs , (p.1081)) or vancomycin (nephrotoxicity has been seen with amphotericin B and tacrolimus). ... 

NSAIDs are known to inhibit prostaglandin synthesis and as a result may decrease renal blood flow, which in certain circumstances can lead to renal failure. Renal impairment is more likely to occur in the presence of renal vasoconstrictors. Tacrolimus is known to cause renal vasoconstriction and thus the combined effects of ibuprofen and tacrolimus may have led to acute renal failure. Both patients also had a degree of liver impairment, which the authors suggest may have potentiated the toxicity of tacrolimus with ibuprofen. 

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