first case of amyloidosis secondary to IPT reported in the literature. IPT is a well-recognized benign lesion that can occur in patients from early childhood to old age, but predominantly affects young adults [3]. Since the first description of IPT in the lung in 1939 [4], numerous cases have been reported in various organs and deep soft tissues [5]. A 9-year-old girl was admitted to our pediatric ne- phrology department with weakness and edema in De- cember 1994. She had previously been admitted to our pediatric surgery department in 1991 for a laparoscopic examination: a large infiltrating and inoperable tumor was found and a biopsy was performed. The histopathological diagnosis was fibromatosis and she received chemotherapy in the pediatric oncology department between 1991 and 1992. In December 1992, another biopsy was performed and histological examination showed a lesion characterized by inflammatory cells, especially plasma cells, in a pre- dominantly fibrotic process typical of IPT (Fig. 1). She was followed without any medication and was doing well until December 1994. On admission in December 1994, physical examination revealed failure to thrive, periorbital and pretibial edema, ascites, and a firm abdominal mass 10x12 cm in size. Laboratory investigations revealed: hematocrit 36%, leu- cocyte count 12,600/mm 3, erythrocyte sedimentation rate 80 ram/h, blood urea nitrogen 8 mg/dl, serum creatinine 0.7 mg/dl, total serum protein 4.3 g/dl, serum albumin 1.9 g/ dl, total serum lipids 690 mg/dl, serum cholesterol 291 rag/ dl, serum C3 40 mg/dl and serum C4 4 mg/dl. Serum electrolytes, serum glutamic oxaloacetic transaminase, serum glutamic pyruvic transaminase, antinuclear factor, and rheumatoid factor were within normal ranges. Urinal- ysis revealed proteinuria 266 mg/m 2 per hour. Abdominal ultrasonography showed that the liver, spleen, and kidneys were normal. There was ascites and an abdominal mass, localized between the right kidney and urinary bladder, 793 with calcifications. A renal biopsy was performed. By light microscopy, 15 glomeruli were present and Congo red- positive birefringent material was seen in 50% of the glo- merular tuft and along the peripheral capillary loops. Per- manganate digestion studies suggested the diagnosis of an AA type amyloidosis in the renal biopsy. Colchicine was started at a dose of 0.5 mg twice a day. The prognosis of IPT is generally excellent. Surgery is the main therapy and complete removal of the lesion results in disease-free survival even in angioinvasive cases [3, 5]. However, we would like to emphasize the importance of early diagnosis and treatment, because amyloidosis may be a complication of IPT. Aytiil NoyanJ, Ali AnaraP, Aysun Karabay 1, Biilent Antmen2, Atilla Tanyeli2, and Nurdan TunalP Depm'tments of ~Pediatric Nephrology, 2pediatric Oncology, and 3Pathology School of Medicine ~ukurova University TR-01330 Adana, Turkey References 1. Boichis H, Pross M (1992) The renal amyloidosis. In: Edelmann JM (ed) Pediatric kidney disease. Little Brown, Boston, p 1535 2. Noyan A, Duman N, G6nliJ~en G, Anarat A, Tuncer I (1995) Amyloidosis secondary to xanthogranulomatous pyelonephritis: an unusal case. Pediatr Nephrol 9:251 3. Vujonic GM, Milovanovic D, Aleksandrovic S (1992) Aggressive inflammatory pseudotumor of the abdomen 9 years after the therapy for Wilms tumor. Cancer 70:2362-2366 4. Brunn H (1939) Two interesting benign lung tumors of contra- dictory histopathology: remarks on the necessity for maintaining chest tumor registry. J Thorac Surg 9:119-131 5. Scott L, Blair G, Taylor G, Dimmick J, Fraser G (1988) In- flammatory pseudotumor in children. J Pediatr Surg 23:755-758 Inefficacy of pefloxacin in steroid-responsive nephrotic syndrome Key words: Pefloxacin - Nephrotic syndrome Sirs, Treatment with pefloxacin has been reported to cause re- duction of proteinuria in idiopathic nephrotic syndrome (NS) [1]. The immunomodulatory effect of fluorinated quinolones is thought to be due to increased production of interleukin-2 [2]. This effect is distinct from that of cy- closporine A, which blocks the production and release of interleukin-2 from T lymphocytes [3], and which has been widely used to treat both steroid-sensitive and resistant NS in children. Pefloxacin has been mainly used in patients with ste- roid-resistant NS [1, 4, 5]. In a single report, which ap- peared in an abstract form, pefloxacin was administered along with prednisolone to six patients with steroid-de- pendent NS and induced remission [6]. We have used pe- floxacin to treat relapses in ten patients (5 boys, 5 girls) with steroid-responsive NS and found it to be ineffective. The mean (SD) age at onset of NS was 2.9 (1.9) years and at the time of pefloxacin therapy 7.3 (4.7) years. The mean (SD) blood levels of urea were 22.3 (5.6) mg/dl and creatinine 0.4 (0.1) mg/dl. Five patients were steroid de- pendent, 3 had frequent relapses and 2 were infrequent relapsers. Seven patients (5 with steroid dependence, 2 with frequent relapses) had previously been treated with one or more courses of cyclophosphamide, chlorambucil, leva- misole or long-term alteruate-day steroids. Renal biopsy in five patients had shown minimal change.