She also developed new-onset diabetes after

She also developed new-onset diabetes after PD0325901 molecular weight transplantation (NODAT) that resolved after her corticosteroid dose was lowered. Although asymptomatic bacteriuria was documented on at least one occasion over the next year, she remained well until July 2011, when she presented with dysuria, fevers and pain over the allograft. A fully susceptible Escherichia coli was isolated from blood and urine cultures and a small collection at the antero-inferior pole of the allograft was noted on ultrasonography. She was treated with intravenous ceftriaxone and

discharged with a 21-day course of oral cephalexin. She was admitted again 18 days later with similar symptoms. Multiple blood cultures did not reveal a pathogen and Pseudomonas aeruginosa was isolated from urine. The lymphocoele was aspirated and the fluid had a few mononuclear cells seen on microscopy, but was sterile on culture. She was treated initially with ceftriaxone and changed to a 2-week course of oral ciprofloxacin after the P. aeruginosa was identified. Further episodes of pyrexia in August 2011 were investigated extensively with negative blood and urine cultures. Quantiferon testing showed low mitogen response with no evidence of active tuberculosis,

reflecting subnormal immune response. Mycobacterial urine cultures were also negative. A gallium scan revealed mild asymmetrical activity in left iliac fossa that localized to the perinephric lymphocoele. Each febrile episode responded to antibiotics Romidepsin purchase directed against common urinary pathogens. E. coli, P. aeruginosa and mixed coliforms were detected on five occasions over the next 6 months. During

this period she Immune system received a 2-week course of parenteral piperacillin/tazobactam as an outpatient, followed by a 4-week course of ciprofloxacin. The latter isolates were now resistant to ciprofloxacin. From March 2012 onwards, the only organism isolated was Klebsiella pneumoniae that was resistant to all commonly available oral antibiotics. She received a further 4-week course of intravenous piperacillin/tazobactam. The diagnosis of malakoplakia was made in May 2012, following biopsy of a allograft parenchymal lesion seen on computed tomography (CT) that consisted of oedematous, multi-focal, septated high-attenuation foci measuring 5.4 × 3.4 cm and 4.7 × 4.6 cm. The bladder lining was also noted to be abnormal, with a trabeculated appearance with high attenuation signal. An urgent biopsy of the lesion excluded active malignancy and confirmed parenchymal malakoplakia with CD68+ histiocytic response and intracytoplasmic basophilic microcalcifications, with typical targetoid/owl’s eye appearances characteristic of Michaelis–Gutmann (MG) bodies (see Fig. 1).

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