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1.
Mol Med Rep ; 9(4): 1179-84, 2014 Apr.
Article in English | MEDLINE | ID: mdl-24535460

ABSTRACT

The renal allograft survival rates of patients with immunoglobulin A nephropathy (IgAN), and patients with or without other glomerular diseases, have yet to be fully elucidated. In this study, the clinicopathological factors associated with long-term allograft survival for the prognosis of renal allograft recipients with IgAN were examined. All patients enrolled in this study were diagnosed with IgAN following clinical and pathological examinations. Patients underwent renal graft biopsy and were hospitalized at the Fuzhou General Hospital between June, 2004 and December, 2010. Common demographic and clinical indicators were recorded in patients who had graft loss and in those who had functional renal grafts. Forty-two of the 202 biopsy specimens (20.8%) met the diagnostic criteria for IgAN and were divided into two groups, the graft loss group (n=17) and the functional graft group (n=25). Patients were followed up for 1-257 months after kidney transplantation. The mean patient age was 40.6 ± 9.3 years at the time of renal graft biopsy. Examination results indicated concomitant proteinuria and hematuria in 25 patients (59.5%) and proteinuria alone in six patients (14.3%). Graft loss occurred in 17 patients during the follow-up period. Comparison of the graft loss and the functional graft groups indicated that patients in the graft loss group were more likely to have proteinuria (P=0.047), high creatinine levels at the time of biopsy (P=0.009), low glomerular filtration rates (P=0.013), low serum total protein (P=0.01), a high Banff score (P=0.001), extensive glomerulosclerosis (P=0.002), a greater likelihood of crescent formation (P=0.01), severe tubular atrophy (P=0.013) and more extensive interstitial fibrosis (P=0.033). However, the two groups showed no significant differences in blood pressure, hematuria, BUN, UA, Hb, TG and CHO levels. The allograft survival rate of patients with IgAN was identified to be similar to that of patients with and without other glomerular diseases.


Subject(s)
Allografts/pathology , Glomerulonephritis, IGA/pathology , Glomerulonephritis, IGA/therapy , Graft Survival , Kidney Transplantation , Adult , Case-Control Studies , Demography , Female , Glomerulonephritis, IGA/mortality , Humans , Male , Prognosis , Survival Rate
2.
BMC Cell Biol ; 14: 18, 2013 Mar 19.
Article in English | MEDLINE | ID: mdl-23510080

ABSTRACT

BACKGROUND: The objective of this study was to evaluate the effect of bone marrow mesenchymal stem cells (BMSCs) on the apoptosis of granulosa cells (GCs) in rats. RESULTS: Cisplatin increased GC apoptosis from 0.59% to 13.04% in the control and cisplatin treatment groups, respectively, which was significantly reduced upon co-culture with BMSCs to 4.84%. Cisplatin treatment increased p21 and bax and decreased c-myc mRNA expression, which was reversed upon co-culture with BMSCs. As compared to young rats, increased apoptosis was observed in the perimenopausal rats (P < 0.001). After 3 months, the apoptosis rate in the BMSC group was significantly lower than that of the control group (P = 0.007). CONCLUSIONS: BMSC therapy may protect against GC apoptosis induced by cisplatin and perimenopause. Further studies are necessary to evaluate therapeutic efficacy of BMSCs.


Subject(s)
Bone Marrow Cells/drug effects , Cisplatin/administration & dosage , Coculture Techniques/methods , Cyclin-Dependent Kinase Inhibitor p21/metabolism , Granulosa Cells/drug effects , Mesenchymal Stem Cell Transplantation , Mesenchymal Stem Cells/drug effects , Perimenopause/physiology , Animals , Apoptosis/drug effects , Bone Marrow Cells/physiology , Cells, Cultured , Cyclin-Dependent Kinase Inhibitor p21/genetics , Estrogens/administration & dosage , Female , Gene Expression Regulation/drug effects , Granulosa Cells/physiology , Mesenchymal Stem Cells/physiology , Proto-Oncogene Proteins c-myc/genetics , Proto-Oncogene Proteins c-myc/metabolism , Rats , Rats, Sprague-Dawley , bcl-2-Associated X Protein/genetics , bcl-2-Associated X Protein/metabolism
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