Chest
Volume 114, Issue 4, October 1998, Pages 1220-1223
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Selected Reports
Tubulointerstitial Nephritis Induced by the Leukotriene Receptor Antagonist Pranlukast

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A 7-year-old boy with asthma was receiving the leukotriene receptor antagonist pranlukast (Ultair; SmithKline Beecham; Pittsburgh) as part of an open-label clinical trial. The patient's asthma improved, and he remained asymptomatic; but routine study evaluations 9 to 12 months into therapy showed microhematuria, proteinuria, glucosuria, anemia, and renal insufficiency. Renal biopsy demonstrated changes classic for acute allergic tubulointerstitial nephritis (ATIN), with mixed interstitial inflammatory infiltrate including eosinophils. Within 6 months of pranlukast withdrawal, anemia resolved and urinary sediment and renal function normalized. The case demonstrates that hypersensitivity reaction to pranlukast and resultant ATIN is possible, and that periodic urine testing in patients receiving pranlukast should be considered.

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CASE REPORT

A 7-year-old white boy with a 4-year history of moderate persistent asthma was enrolled via the University of South Florida (Tampa) division of Allergy and Immunology in a double-blind, placebo-controlled clinical trial of pranlukast. Prior to study enrollment, therapy for asthma included nebulized albuterol 2 to 4 times daily. Acute exacerbations 1 and 18 months prior to enrollment required 5 days of pulse therapy with oral prednisolone, but he was not receiving other corticosteroid therapy.

DISCUSSION

Binding of the single leukotriene receptor present in human bronchial smooth muscle by the cysteinyl-leukotrienes (LTC4, LTD4, and LTE4) contributes to the immediate and long-term bronchoconstriction, microvascular permeability, mucus secretion, and eosinophil influx that mediates the airway obstruction present in patients with asthma.1 Experimental evidence in animals and humans indicates that pranlukast significantly reduces these responses, and clinical trials have demonstrated that

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