To evaluate the efficacy and safety of leflunomide in the treatment of proliferative lupus nephritis, a prospective multi-centre observational study was conducted. Patients with biopsy proven proliferative lupus nephritis were assigned to receive either leflunomide or cyclophosphamide with concomitant prednisone. Leflunomide was given orally with a loading dose of 1 mg/kg/day for 3 days followed by 30 mg/day. Intravenous cyclophosphamide was administered monthly at a dose of 0.5 g/m2 of body-surface area. A total of 110 patients were enrolled, 70 in the leflunomide group and 40 in the cyclophosphamide group. The complete remission rate in the leflunomide group was 21% and partial remission rate 52%, as compared with 18% and 55%, respectively, in the cyclophosphamide group. Renal parameters and systemic lupus erythematosus disease activity index improved significantly and similarly in both groups. Serum creatinine decreased or stabilized in both treatment groups. No significant difference was noted with respect to clinical outcome between groups. Repeat biopsy also showed a significant reduction of active lesions in kidney pathology after 6 months of leflunomide treatment. Major adverse events, similar in both treatment groups, included infection, alopecia and hypertension. Leflunomide, compared with cyclophosphamide, in combination with prednisone was effective in the induction therapy of proliferative lupus nephritis and was generally well-tolerated.

Prostate cancer (PCa) remains a leading cause of mortality among men in the United States and Western Europe. The molecular mechanism of PCa pathogenesis has not been fully elucidated. In the present study, the expression profile of E2F transcription factor 7 (E2F7) in PCa was examined using immunohistochemistry and reverse transcription-quantitative PCR, whilst cell cycle progression and apoptosis were determined using fluorescent cell activated sorting techniques. Cell viability was measured using Cell Counting Kit-8 in loss-and gain-of-function studies. Dual-luciferase reporter assay was used to verify if E2F7 was one of the potential targets of miR-30c. The staining score of E2F7 of PCa tissues was found to be notably higher compared with that of adjacent normal tissues. Suppression of E2F7 expression in PCa cell lines led to significantly reduced proliferation rates, increased proportion of cells in the G 1 phase of the cell cycle and higher apoptotic rates compared with those in negative control groups. Dual-luciferase reporter assay revealed E2F7 to be one of the binding targets of microRNA (miR)-30c. In addition, transfection of miR-30c mimics into PCa cells resulted in reduced cell viability, increased proportion of cells in the G 1 phase and higher apoptotic rates. By contrast, transfection with the miR-30c inhibitor led to lower apoptosis rates of PCa cells compared with negative control groups, whilst E2F7 siRNA co-transfection reversed stimulatory effects of miR-30c inhibitors on cell viability. In addition, the expression of cyclin-dependent kinase inhibitor p21 were found to be upregulated by transfection with either E2F7 siRNA or miR-30c mimics into PCa cells. In conclusion, the present study suggested that E2F7 may be positively associated with PCa cell proliferation by inhibiting p21, whereas E2F7 is in turn under regulation by miR-30c. These observations suggest the miR-30c/E2F7/p21 axis to be a viable therapeutic target for PCa.

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<b><i>Background:</i></b> Kimura disease (KD) is a chronic benign inflammatory disorder that is usually manifested as a deep, subcutaneous mass with or without regional lymphadenopathy in the head and neck region. Various types of glomerulonephritis are associated with KD, including minimal change disease (MCD), membranous glomerulopathy (MN), and immunoglobulin (Ig)A-nephropathy. Kidney interstitial lesion associated with KD is rarely reported. The aim of this study was to expand the spectrum of kidney lesions associated with KD. <b><i>Methods:</i></b> From 2007 to 2016, 12 cases of KD with kidney lesions were retrospectively reviewed. Pathological examinations included hematoxylin and eosin staining, periodic acid-schiff staining, periodic acid-methenamine silver staining, and Masson staining, immunofluorescence, and electron microscope analyses. <b><i>Results:</i></b> Anatomic sites of subcutaneous involvement included head and neck area, arm, and groin. Most cases had elevated IgE level and peripheral eosinophilia. Nephrotic syndrome was the most common kidney manifestation. Pathological results showed 3 types of glomerulonephritis, including 9 cases of MCD, 2 cases of IgA nephropathy, and 1 case of MN. Of note, 4 MCD cases showed concurrent glomerular and interstitial lesions associated with KD, including 2 distinct patterns: (1) a diffusely eosinophilic and lymphatic infiltration similar to KD lesion developed elsewhere and (2) exclusively eosinophilic infiltration in the interstitium. Eight out of 10 patients were responsive to steroid treatment and had complete remission of proteinuria and recovery of kidney function. <b><i>Conclusion:</i></b> Our report suggested that, in addition to glomerulonephritis, interstitial lesions may also be associated with KD. Pathologist should pay special attention to differentiated diagnosis when such pathological changes are identified in patients with subcutaneous mass or cervical lymphadenopathy with concurrent kidney manifestation.

Background. Reports about prognosis of adults receiving small pediatric-donor kidneys (PDK) as compared to those receiving elder pediatric or adult donor kidneys (ADKs) are controversial. This study aimed to examine the outcomes of adults receiving small PDK and possible prognostic factors. Methods. The records of adults who received kidneys from donors < 10 years old at our center from July 1, 2011 to June 30, 2018 were reviewed. Results. A total of 121 adults were small PDK recipients. Twenty-three patients received 29 biopsies or nephrectomy between 6 and 896 days posttransplantation days. Seven patients (30.4%) had pediatric donor glomerulopathy (PDG), which developed from 113 to 615 days posttransplantation. The incidence of proteinuria and hematuria was significantly higher in the PDG group. The characteristic pathological finding in PDG was irregular lamination and splintering of the glomerular basement membrane (GBM). Donor age, donor weight, and donor kidney volume were significantly less in PDG cases compared with the non-PDG cases. For the risk factors of PDG, increasing urinary RBC count during follow-up was an independent predictor, while increasing donor age and body weight were protective factors. PDG was not a significant risk factor for Scr increasing of PDKs. Conclusions. PDG is a potential cause of abnormal urinalysis in adults receiving small PDKs. The pathological characteristic change of PDG is splitting and lamination of GBM. Persistent hematuria after transplantation in recipients of PDK is a predictor of PDG development.