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May aid in identifying patients with delayed methotrexate clearance; toxicity appears to be related at least as much to the length of time that methotrexate concentrations are elevated as to the peak concentrations achieved. Methotrexate elimination is reduced in patients with impaired renal function, ascites, or pleural effusions. Such patients require especially careful monitoring for toxicity, and require dose reduction or, in some cases, discontinuation of methotrexate administration. Leucovorin given at the appropriate time rescues bone marrow and gastrointestinal cells from methotrexate but has no apparent effect on pre-existing methotrexate nephrotoxicity. It is recommended that duration of leucovorin administration in these patients be based on determination of plasma methotrexate concentrations. Methotrexate, especially at higher doses or with prolonged treatment, has been associated with hepatotoxicity including acute hepatitis, chronic fibrosis, necrosis, cirrhosis, and liver enzyme elevations. It works like folic acid in the body, which helps to reduce the action and toxic effects of folic acid antagonists (eg, methotrexate). His only other medications were amlodipine (5 mg per day) and methotrexate (15 mg per week). This indicates that NSAIDs may enhance the toxicity of methotrexate. He was treated for RA with infliximab (3 mg/kg) for 3 years, as well as methotrexate (20 mg/week), and corticosteroids. Alkalinization of urine (with bicarbonate and/or acetazolamide) and intravenous hydration (1000 mL per square meter of body surface area over six hours prior to beginning the methotrexate infusion and 3000 mL per square meter of body surface area per day during the methotrexate infusion and for two days after the infusion is completed) are also important to prevent renal toxicity caused by methotrexate and/or its metabolites.

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