Nitrofurantoin is used to treat acute and chronic UTIs. It isn’tuseful in treating pyelonephritis or perinephric (around the kid-ney) diseases.
After oral administration, nitrofurantoin is absorbed rapidly and well from the GI tract. Taking the drug with food enhances its bioavailability. It’s available in a microcrystalline form and a macrocrystalline form. The microcrystalline form is absorbed more slowly because of slower dissolution and thus causes less GI distress.
The drug is 20% to 60% protein-bound. Nitrofurantoin crosses the placental barrier and is secreted in breast milk. It’s also distrib-uted in bile.
Nitrofurantoin is partially metabolized by the liver, and 30% to 50% is excreted unchanged in urine.
Usually bacteriostatic, nitrofurantoin may become bactericidal, depending on its urinary concentration and the susceptibility of the infecting organism.
Although its exact mechanism of action is unknown, nitrofuran-toin appears to inhibit formation of acetyl coenzyme A from pyru-vic acid, thereby inhibiting the energy production of the infecting organism. Nitrofurantoin may also disrupt bacterial cell-wall for-mation.
Because the absorbed drug concentrates in urine, nitrofurantoin is used to treat UTIs. It has a higher antibacterial activity in acid urine. Nitrofurantoin isn’t effective against systemic bacterial in-fections.
Nitrofurantoin has few significant interactions.
§ Probenecid and sulfinpyrazone inhibit the excretion of nitrofu-rantoin by the kidneys, reducing its efficacy and increasing its tox-ic potential.
§ Magnesium salts and magnesium-containing antacids can de-crease the extent and rate of nitrofurantoin absorption.
§ Nitrofurantoin may decrease the antibacterial activity of nor-floxacin and nalidixic acid. (See Adverse reactions to nitrofuran-toin.)