Objective To observe the changes of renal tubular injury and the extent of interstitial fibrosis in the C57BL/6 mouse models of chronic kidney disease(CKD),and provide experimental animal evidence for study of the pro-gression of acute kidney injury(AKI)to chronic kidney disease as well as its mechanisms. Methods Twenty-four 8-week-old male C57BL/6 mice were randomly and equally divided into control group, low-dose, medium-dose, and high-dose cisplatin groups,6 mice in each group. Mice in the cisplatin groups were administrated with 5,7 or 10 mg/kg cispla-tin by intraperitoneal injection once a week for 4 weeks. Plasma creatinine and 24-hour urinary protein were detected to as-sess the renal function. The mice were sacrificed, and plasma and kidney samples were collected for subsequent tests. Pathological changes were observed using periodic acid-Schiff(PAS)staining. To evaluate renal tubules injury, the ex-pression of kidney injury molecule 1(KIM-1)was examined by immunohistochemistry and the level of urinary N-Acetyl-β-D-glucosaminidase was detected with a commercial kit. The infiltration of CD3-positive T cells and F4/80-positive macro-phages was observed by immunohistochemistry(IHC)and immunofluorescence. The expression of collagen I and α-smooth muscle actin(α-SMA)were tested by immunohistochemistry to assess the renal fibrosis, while total kidney collagen was detected by Picrosirius red staining. Results In contrast to the normal control group,the kidney injury became more seri-ous in the cisplatin-treated mice as cisplatin concentration increased. Particularly,significant kidney damage was observed in the high-dose cisplatin group. Compared with the control group,the plasma creatinine and 24-hour urinary protein were significantly increased in the high-dose cisplatin group(P<0.05 and P<0.001)indicating impaired renal function. Mor-phologically,numerous clear vacuoles and necrosis were present in renal tubule epithelial cells in the high-dose cisplatin group. The expression of KIM-1 was markedly up-regulated and the level of urinary NAG was elevated. Infiltration of CD3-positive T cells and F4/80-positive macrophages was enhanced in the mice of high-dose cisplatin group. Data from immuno-histochemistry and picrosirius red staining showed that mice of the high-dose cisplatin group developed renal fibrosis evi-denced by markedly up-regulated expression of collagen I and α-SMA. Conclusions Repeated administration of 10 mg /kg cisplatin for 4 weeks can induce chronic renal insufficiency in mice,which may serve as a novel model for the research on underlying mechanisms of progression from acute kidney injury to chronic kidney disease.

Lung transplantation is the only effective treatment of end-stage lung diseases. Nevertheless, shortage of donor lungs has become increasingly prominent worldwide. A large quantity of patients died while waiting for lung transplantation. Urgent lung transplantation is a prioritized allocation strategy for donor lung transplantation according to the urgency of diseases, aiming to shorten the waiting time for donor lungs and reduce the fatality of patients on the waiting list for lung transplantation. However, no consensus has been reached worldwide on the definition, criteria and application of the terminology of urgent lung transplantation. In addition, the survival and net benefits of lung transplant recipients based on this allocation system are still controversial. On the basis of previous clinical research on urgent lung transplantation, the definition criteria, risk factors, survival outcomes, limitations and optimization measures were explicitly elucidated in this article, aiming to provide theoretical reference for comprehensive evaluation of the feasibility of urgent lung transplantation and further optimizing the allocation system of donor lungs.

Lung transplantation has become the most effective treatment of end-stage lung diseases. Along with persistent optimization of lung transplantation technique and perioperative management, the short-term clinical efficacy after lung transplantation has been significantly improved, whereas the long-term clinical prognosis remains unoptimistic. Besides chronic lung allograft dysfunction, postoperative malignant tumors also threaten the long-term survival of the recipients. Common malignant tumors following lung transplantation include nonmelanoma skin cancer, posttransplant lymphoproliferative disease and lung cancer. After solid organ transplantation, a large majority of the recipients require lifelong immunosuppressive therapy. The intensity of immunosuppressive therapy for the lung transplant recipients is generally higher than other organ transplant recipients. Immunosuppression is the main factor which leads to the impairment of anti-tumor immune monitoring function and promotes the incidence and development of malignant tumors. In this article, the risk factors, prevention and treatment of the most common malignant tumors after lung transplantation were reviewed, aiming to provide reference for comprehensive diagnosis and treatment of malignant tumors following lung transplantation.