Loratadina y nefritis intersticial aguda / Acute interstitial nephritis induced by loratadine

RESUMEN

La loratadina en un antagonista de segunda generación de los receptores H1 de la histamina con mayor potencia antialergénica y asociada a menos efectos adversos que otros antihistamínicos. La nefritis intersticial es una causa de insuficiencia renal aguda generalmente inducida por drogas, y con menor frecuencia asociada a infecciones o sarcoidosis. Aunque el número de fármacos asociados a nefritis intersticial aguda es inmenso, nunca anteriormente había sido descrita la loratadina. Presentamos un caso de nefritis intersticial en un paciente que había recibido loratadina (10 mg/día) durante los diez días previos a su ingreso en nuestro hospital, por un cuadro de prurito diseminado. La sospecha inicial fue de glomerulonefritis rápidamente progresiva, por lo que se practicó biopsia renal y se inició tratamiento esteroideo (tres bolos de 500 mg, seguidos de 1 mg/kg/día de prednisona). La loratadina fue suspendida. Asistimos a una lenta aunque progresiva mejoría de función renal, y un mes más tarde la analítica (urea y creatinina) era normal y la hematuria y proteinuria habían desaparecido. Se inició pauta descendente de tratamiento esteroideo. Pensamos que se trata de un caso interesante dada su presentación clínica y la particularidad de no estar descrito con anterioridad

ABSTRACT

Loratadine is a second generation histamine H1 receptor antagonist, that has high potency antiallergic properties and is associated with low adverse effects compared with other antihistamines. Acute interstitial nephritis is a cause of acute renal failure that is most often induced by drugs or, less frequently, infection or sarcoidosis. Although the number of drugs associated with acute intersticial nephritis is too large, the antihistaminic loratadine have never been reported before. We report a case of an interstitial nephritis with acute renal failure that suggesting hypersensitivity reaction in a 77 old man who had received loratadine (10 mg/day) during ten days before his assesment to our hospital by diseminated pruritic syndrome. The initial suspect was rapidly progressive glomerulonephitis and renal biopsy was practice and treatment with corticosteroids were initiated (prednisone bolus of 500 mg three days and 1 mg/kg/day/later). The loratadine therapy was cessation. He exhibiting a slow and progressive improvement on renal function and one month later, urea and creatinine levels was normal and hematuria and proteinuria had disapeared. The corticosteroids therapy were progressive decreased until withdrawal. We think that this is an interesting case, basing in its clinical presentation and that it had never been reported before