Buylaert, Mirabel A.

Franz, Stefan E.

Moll, Solange

Schifferli, Jürg A.

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Teaching Point(Section Editor: K. Ku¨hn)A well-meant present from a friendStefan E. Franz1, Mirabel A. Buylaert1, Solange Moll2 and Ju¨rg A. Schifferli11Department of Internal Medicine and 2Department of Pathology, University Hospital Basel, Basel, SwitzerlandKeywords: diclofenac; nephrotoxicity; nonsteroidalanti-inflammatory drugs; over-the-counter medicines;topical applicationCaseA 70-year-old female was admitted to hospital becauseof a general weakness and a high creatinine level. Onadmission she was hypotensive (105u55 mmHg) andcomplained of chronic back pains. During the weekspreceding the hospitalization she was taking fosinopril10 mg qd, amitryptiline 50 mg qd and paracetamolas required (not )1000 mg per day). She had raisedurea (35.1 mmolul), creatinine (889 mmolul), potassium(6.1 mmolul) and C-reactive protein (CRP; 72 mgul)and she had a metabolic acidosis (pH 7.17, bicarbo-nate 14.6 mmolul). Urinalysis revealed albuminuria qq,10–15 WBCuhigh-power field, 3–5 RBC, no casts.An urgent abdominal ultrasound showed normal sizekidneys.Remarkably, her past medical history included anepisode of acute renal failure 2 years before the presenthospitalization, at which time she presented witholiguria and a high creatinine (1187 mmolul) requiringimmediate dialysis. Because of back pain she had beenstarted on mefenamic acid 6 weeks earlier. The renalbiopsy had showed a severe interstitial nephritis witha dense mononuclear cell infiltrate and minimaltubular destruction. The administration of prednisone(1 mgukg body weight) had allowed rapid recovery ofrenal function: dialysis was discontinued after 5 daysand her creatinine level dropped to 155 mmolul at day14 and stabilized around 90 mmolul after 2 months.The steroids had been rapidly reduced and stoppedafter 2 months. The patient was strongly advised notto take any nonsteroidal anti-inflammatory drugs(NSAIDs) and was prescribed only paracetamol.Because of this past medical history, the patientwas directly questioned about NSAIDs. She was wellaware of her allergy and despite the recent flare-upof back pain she denied ingestion of NSAIDs orover-the-counter medication.Initially the patient was given 1 l NaCl 0.9% andlisinopril was discontinued. Renal biopsy revealed anacute interstitial nephritis similar to that seen 2 yearspreviously, but this time with granulomatous lesions(Figure 1). Prednisone 1 mgukg body weight wasadministered and renal function improved over thenext days. Creatinine dropped to 140 mmolul after2 weeks and CRP returned to normal. During recoverythe patient recalled having received from her goodfriend a ‘helpful’ topical gel (Voltaren gel1: diclofenac)that she had applied on her back during 10 dayspreceding the hospitalization.NSAIDs are well known to induce renal failure involume-depleted patients by inhibition of prostaglan-din synthesis [1]. In addition, NSAIDs, including theselective COX-2 inhibitors [2], have been reported toproduce allergic reactions in the kidney; most often anephrotic syndrome due to a membranous glomerulo-nephritis or an acute interstitial nephritis. Althoughthese latter reactions are rare complications ofNSAIDs, they are not seen uncommonly, simplybecause of the very wide application of these drugs.Fig. 1. Second biopsy: granuloma and a diffuse interstitial infiltrateof mononuclear cells. (Haemotoxylin and eosin, 3350.)Correspondence and offprint requests to: Stefan E. Franz,Kantonsspital Aarau, CH-5001 Aarau, Switzerland.Email: stefan.franz@ksa.chNephrol Dial Transplant (2003) 18: 613–614# 2003 European Renal Association–European Dialysis and Transplant AssociationIn several countries, NSAIDs can be bought freelyover the counter. Although only rarely documented, are-exposure to the same or another NSAID mayproduce a relapse of the glomerular or interstitialnephritis and all authors advise against it [3]. Thepatient presented here illustrates this point and inaddition shows that topical administration of aNSAID leads to systemic levels sufficient to reactivatean allergy [4]. A long duration of exposure to theallergen, a pronounced interstitial cell infiltration,interstitial granuloma, the presence of tubular atrophyand a shrinking kidney on ultrasound are all indicatorsfor a more severe outcome [5]. The offending drugshould be stopped immediately and although no goodevidence is available, most clinicians treat the acuteinterstitial nephritis with a short course of steroids.Teaching points(i) Even topical rechallenge with an allergeniccompound may re-induce interstitial nephritis.(ii) Patients often do not realize that topical sub-stances are absorbed and do not mention them.Also, doctors forget to ask [6].(iii) A ‘wonderful gel’ that is fine for a friend is notautomatically good for you.References1. Nephrotoxicity of non-steroidal anti-inflammatory drugs. Lancet1994; 344: 515–5182. Demke D, Zhao S, Arellano FM. Interstitial nephritis associatedwith celecoxib. Lancet 2001; 358: 1726–17273. Andrews PA, Sampson SA. Topical non-steroidal drugs aresystemically absorbed and may cause renal disease. Nephrol DialTransplant 1999; 14: 187–1894. Radermacher J, Jentsch D, Scholl MA, Lustinetz T, Frolich JC.Diclofenac concentrations in synovial fluid and plasma aftercutaneous application in inflammatory and degenerative jointdisease. Br J Clin Pharmacol 1991; 5: 537–5415. Schwarz A, Krause PH, Kunzendorf U, Keller F, Distler A.The outcome of acute interstitial nephritis: risk factors forthe transition from acute to chronic interstitial nephritis.Clin Nephrol 2000; 54: 179–1906. O’Callaghan CA, Andrews PA, Ogg CS. Renal disease and useof topical non-steroidal anti-inflammatory drugs. BMJ 1994;308: 110–111614 S. E. Franz et al.

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