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1.
International Eye Science ; (12): 731-736, 2024.
Artigo em Chinês | WPRIM | ID: wpr-1016586

RESUMO

Diabetic retinopathy(DR)represents the primary cause of blindness among the global working-age population, and the disruption of the blood-retinal barrier is a crucial factor. Research in recent years has elucidated that DR transcends the scope of a mere microvascular disorder into a complex interplay of retinal glial cells and neurodegeneration microvascular pathology. Neuronal damage may precede vascular endothelial changes in the retinal neurovascular unit(RNVU)in the early stage of DR, and glial cell activation further exacerbates vascular barrier dysfunction. Retinal microglia are immune cells that reside in the retina and are involved in chronic inflammatory responses induced by long-term exposure to high glucose levels. Microglia secrete various inflammatory factors in response to high glucose levels, which can lead to the destruction of the blood-retinal barrier structure, increased neuronal apoptosis, and altered gliosis of Muller cells, thus affecting the retina's homeostatic balance. The RNVU has received increasing attention in recent years as a unitary structural study, and the mechanism of microglia in the RNVU and the progress of the study are reviewed.

2.
Chinese Journal of Organ Transplantation ; (12): 183-186, 2023.
Artigo em Chinês | WPRIM | ID: wpr-994650

RESUMO

This review summarizes the clinical data of one pediatric liver transplant recipient and two adult kidney transplant recipients with posterior reversible encephalopathy syndrome(PRES)at Tongji Hospital of Huazhong University of Science & Technology.The relevant clinical characteristics of recipients are discussed for providing reference for clinical diagnoses and treatments.

3.
Organ Transplantation ; (6): 389-2023.
Artigo em Chinês | WPRIM | ID: wpr-972929

RESUMO

Objective To analyze the clinicopathological features and prognosis of polyomavirus nephropathy (PyVN) after kidney transplantation. Methods Clinical data of 44 patients who were diagnosed with PyVN after kidney transplantation were retrospectively analyzed. The causes of puncture and the time of pathological diagnosis were analyzed. Histological grading was carried out according to Banff 2018 classification. Clinical data and pathological characteristics of patients at all grades were statistically compared. BK viral DNA loads in the blood and urine were measured and renal allograft function were assessed. Clinical prognosis of all patients was compared among different groups and the risk factors affecting clinical prognosis were also analyzed. Results The time interval between pathological diagnosis of PyVN and kidney transplantation was 16(8, 29) months, and the increase of serum creatinine level was the main cause for puncture. Among 44 patients, 19 cases were classified as grade ⅠPyVN, 21 cases of grade Ⅱ PyVN and 4 cases of grade Ⅲ PyVN, respectively. Under optical microscope, there was no significant difference in the positive rate of virus inclusion bodies among different groups (P=0.148). Inflammatory cell infiltration, interstitial fibrosis and polyomavirus load in grade Ⅱ PyVN patients were all more or higher than those in grade Ⅰ counterparts. Inflammatory cell infiltration and polyomavirus load in grade Ⅲ patients were more or higher than those in grade Ⅰ counterparts. Polyomavirus load in grade Ⅲ patients was more or higher than that in grade Ⅱ counterparts. The differences were statistically significant (all P < 0.05/3). Upon diagnosis, BK viral DNA load was detected in the blood and urine of 39 patients. Among them, 38 patients were positive for BK virus in the urine and 30 patients were positive for BK virus in the blood. The serum creatinine level upon diagnosis was higher compared with that at postoperative 1 month. The serum creatinine level at the final follow-up was significantly higher than that upon diagnosis. The differences were statistically significant (P < 0.001, P=0.049). There was no significant difference in the serum creatinine level among patients with different grades of PyVN at postoperative 1 month (P=0.554). The serum creatinine level of patients with grade Ⅱ PyVN upon diagnosis was significantly higher than that of those with grade Ⅰ PyVN (P=0.007). The 1-, 3- and 5-year cumulative survival rates of renal allografts were 95%, 69% and 62%, respectively. The survival rates of renal allografts significantly differed among patients with different grades of PyVN. The higher the grade, the lower the survival rate (P=0.014). Univariate and multivariate Cox's regression analyses prompted that intrarenal polyomavirus load and serum creatinine level upon diagnosis were the independent risk factors for renal allograft dysfunction (all P < 0.05). Conclusions PyVN mainly occurs within 2 years after kidney transplantation. Clinical manifestations mainly consist of increased serum creatinine level, BK viremia and BK viruria. Postoperative routine monitoring of BK virus contributes to early diagnosis and protection of renal allografts. Banff 2018 classification may effectively predict the prognosis of renal allografts.

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