Summary Background Results are conflicting with respect to the renal effects of anti‐viral agents used for hepatitis B virus infection. Aim To compare short and long‐term renal effects in real‐life settings and to determine risk factors for renal impairment during treatment. Methods 2221 treatment‐naïve patients were enrolled. Among these, 895 (302 lamivudine, 27 telbivudine, 282 entecavir, 273 tenofovir and 11 adefovir initiated patients) had ‘repeated measures’ of creatinine (baseline, 1st, 6th, 12th and 24th month of treatment). Telbivudine and adefovir groups were excluded from further analysis because of the low number of patients. We calculated the glomerular filtration rate (GFR) using the Modification of Diet in Renal Disease (MDRD) formula at each time point. Hypophosphataemia was also recorded. Risk factors for renal impairment were analysed. Results Tenofovir caused a decline in GFR at each time point when compared to baseline levels. However, lamivudine and entecavir did not change GFR. GFR‐shifting from ≥90 to 60–89 mL/min/1.73 m2 was comparable among groups. The proportion of patients whose baseline creatinine increased more than 25% was comparable among all anti‐virals. GFR showed a decline in patients who switched from entecavir to tenofovir. One patient with compensated cirrhosis needed to change from tenofovir because of renal safety. Seven and three patients developed transient hypophosphataemia in the tenofovir and lamivudine groups, respectively. Conclusions Although tenofovir caused a decline in GFR, differences between the anti‐viral agents do not appear to be so impressive. In patients with and without renal risk factors at baseline, there is no impact of anti‐virals, including tenofovir.

A 41-year-old woman presented with chest pain and a cough. There was a solitary pulmonary nodule in the upper-left lobe. The patient had no history of neoplasm except a hysterectomy for uterine leiomyoma five years before. Six months after the first presentation, the tumor showed a gradual increase in size; an explorative thoracotomy was performed. The histopathologic examination showed a tumor consisting of well-differentiated spindle-shaped cells with intervening collagen. She was readmitted 8 months after the operation because of right-sided spontaneous pneumothorax. Multiple pulmonary nodules appeared when the lung was re-expanded by chest tube drainage. In conclusion, uterine leiomyomas can metastasize to various organs, such as lungs, despite having a benign pathologic appearance.

Intrapulmonary spread of a sarcoma via lymphatics is a rare cause of death in a young adult. A 31-year old man was admitted to our hospital complaining of dyspnea and malaise of 2 months' duration. A chest radiography revealed bilateral hilar enlargement, and reticulonodular infiltrations. Thoracic CT-scans demonstrated mediastinal lymphadenopathy, thickening of interlobular septa, polygonal lines, and thickening of bronchovascular bundles. The diagnosis was made by open-lung biopsy. The patient died within 3 months after diagnosis. Pulmonary lymphangitic sarcomatosis is a rare but important manifestation of an angiosarcoma. Optimal treatment of these patients is not well defined, but a trial of chemotherapy may be warranted.

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