Author: Leo
Keywords: eNOS | CNIN | TGF | transforming growth factor | nitric oxide
synthase
 |
| From google images |
Calcineurin Inhibitor (CNIS) is an effective immunosuppressive agent for the successful treatment of children with hormone-resistant nephrotic syndrome (SRNS). Oxidative stress (nitrotyrosine [NT]), fibrosis cytokines (transforming growth factor β1 [TGF-β1]), and endothelial injury (endothelial nitric oxide synthase [eNOS]) Be evaluated. To evaluate the ultrastructure of mitochondrial damage in endothelial cells and renal tubular epithelial cells has been completed.
The same time as the above-
Calcineurin Inhibitor (CNIS) is an effective immunosuppressive agent for the successful treatment of children with hormone-resistant nephrotic syndrome (SRNS). Because these patients require long-term treatment, CNI's early identification of renal toxicity (CNIN) is essential. CNI bottom level monitoring - serum creatinine and glomerular filtration rate are not accurate markers of CNIN.
Studies have been conducted to identify early markers of CNIN in patients with SRNS (steroid-responsive nephrotic syndrome). 24 SRNS pediatric patients were treated with renal biopsy, and CNI treatment (zero time biopsy) was compared with at least 1 year (protocol agreed renal biopsy) as a control standard.
A semi-quantitative morphological classification of CNIN histological features has been completed. Oxidative stress (nitrotyrosine [NT]), fibrosis cytokines (transforming growth factor β1 [TGF-β1]), and endothelial injury (endothelial nitric oxide synthase [eNOS]) Be evaluated.
In addition, the study of ultrastructure of mitochondrial damage in endothelial cells and renal tubular epithelial cells has been completed. The agreement between the renal biopsy group and the zero-time biopsy group showed a significant increase in glomerular sclerosis, glomerular cell hyperplasia, tubular atrophy, interstitial fibrosis, arterial transparency and smooth muscle vacuoles (P <0.05 - P <.001).
The expression of eNOS (91.6%), NT (71%) and TGF-β1 (87.5%) were significantly increased after biopsy. In the CNI cases, the mean mitochondrial damage levels in endothelial cells and renal tubular epithelial cells were 2.28 and 1.4, respectively, whereas the pre-CNIs were 0.28 and 0.27, respectively.
The results showed that NT, eNOS, and TGF-β1 immunohistochemistry could be used as early markers of CNIN. Mitochondrial damage in endothelial cells and renal tubular cells may play an important role in the pathogenesis of CNIN.
Email:kdtinchina@yahoo.com
whatsapp:008615931093124
