In April 2011, a 54-year-old male from Southern Italy presented with multiple asymptomatic nodular lesions involving the lower limbs. He reported some of these nodules had appeared 5 months earlier, while others, of which many had resolved, dated back in time 3–4 years. Treatment with topical antibiotics and corticosteroids repeatedly failed to cause any evident improvement of these lesions. Patient’s history revealed the presence of arterial hypertension, ulcerative colitis since 1981, and nephrotic syndrome secondary to mesangial glomerulonephritis, since 1976, which led him to hemodialysis at first and eventually to bilateral kidney transplantation in 2001. Consequently, the patient took the following medications mesalazine, methylprednisolone, azathioprine, tacrolimus, propranolol and amlodipine. On physical examination, there were a solitary pinkcolored nodule on the right ankle area and a few discrete lesions on the left knee, presenting as violaceous, indurated nodules and spreading across the area in an arciform pattern, some of which showed signs of ulceration (Fig. 1). The lower limbs showed also a few hyperchromic and atrophic changes resulting from lesions previously occurred. Bilateral inguinal lymphadenopathy was present, with enlarged, non-tender, mobile and firm discrete elements. A series of examinations were carried out consisting of blood count, hematochemistry, urinalysis, serum IgE, ECG, chest radiography, urine and stool cultures, tuberculin skin test, QuantiFERON-TB Gold test, VDRL, TPHA, cutaneous swab from ulcerative lesions for microscopic examination, skin biopsies and microbiological tissue cultures for mycobacteria, fungi, and Leishmania, as well as real-time polymerase chain reaction (PCR) and PCR microarray detection of Mycobacterium tuberculosis and atypical mycobacteria. Microbiological assessments were negative, and laboratory examinations disclosed no abnormal findings, except for mild proteinuria, microhematuria and high creatinine serum levels. Pathological study of a skin specimen showed foci of granulomatous inflammation with lymphocytes, plasma cells and abundant eosinophils, with the formation of numerous eosinophilic abscesses. Several vessels with flattened endothelial cells were also visible (Fig. 2). Many of the clinical and histopathological findings were consistent with the diagnosis of Kimura’s disease (KD). Based on such findings, a lymph node biopsy was taken into consideration to better define the nature of concomitant lymphadenopathy in our patient, who, however, refused this procedure. After consultation with nephrologists, treatment already received by the patient was not changed and a wait-and-see approach was chosen. At a follow-up assessment 6 months later, nodular lesions had regressed spontaneously without the development of any new lesions. The immunosuppressive therapy was not modified, and the only relevant event in the patient’s history was an episode of deep vein thrombosis of the left leg. KD is a benign chronic inflammatory disease with unknown etiology, which is endemic in Asia [1, 2]. Long considered synonym to angiolymphoid hyperplasia with eosinophilia (AHLE) is now regarded as a distinct entity. D. Bonamonte (&) C. Foti N. Cassano M. Vestita P. Greco G. A. Vena Unit of Dermatology and Venereology, Department of Biomedical Sciences and Human Oncology, University of Bari, Bari, Italy e-mail: d.bonamonte@dermatologia.uniba.it