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      Podocyte Involvement in Renal Thrombotic Microangiopathy: A Clinicopathological Study

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          Background: The current study aimed to evaluate the associations between podocyte injury and clinicopathological features in renal thrombotic microangiopathy (TMA) based on a Chinese cohort, which might be underscored in this disease. Methods: The clinical, laboratory, and renal histopathological data of patients with renal biopsy-proven TMA from 2000 to 2015 in our institute were collected. Foot process effacement (FPE) was quantified by foot process width (FPW) by electron microscopy. Podocytes in the renal specimens were also detected by stainings for podocyte-specific markers, including Wilms tumor 1 (WT-1), synaptopodin, and podocalyxin. The associations between FPW and clinico-histopathological data were further analyzed. A composite end-point was defined by all-cause death or end-stage renal disease to address the predictive value of FPW. Results: Sixty-three patients with renal biopsy-proven TMA were enrolled. The FPW of renal TMA patients was 1,090 ± 637 nm (range, 572–4,748 nm), which was significantly higher than the normal range in our center ( p = 0.005). By immunohistochemistry and immunofluorescence assays, we found decreased expressions of synaptopodin, podocalyxin, and WT-1 and continued stainings of WT-1 in some podocytes without detectable synaptopodin stainings in the areas of sclerotic tufts and cellular crescents. The FPW value was correlated with the serum albumin concentration ( r<sub>s</sub> = −0.281, p = 0.026), proteinuria amount ( r<sub>s</sub> = 0.255, p = 0.047), serum creatinine levels ( r<sub>s</sub> = 0.339, p = 0.007), and eGFR ( r<sub>s</sub> = −0.335, p = 0.007). According to ROC curve analysis, the optimal cutoff level of FPW for predicting the composite end-point was 869 nm. In patients with FPW ≥ 869 nm, FPW levels were further correlated with the severity of mesangiolysis ( r<sub>s</sub> = 0.351, p = 0.033) and glomerulosclerosis ( r<sub>s</sub> = 0.369, p = 0.025) in pathological evaluations. Patients without clinical remission also had higher FPW than those with remission (1,240 ± 793 vs. 925 ± 344 nm, p = 0.013). The multivariate Cox hazard model showed that FPW ≥ 869 nm was an independent risk factor for the composite end-point (hazard ratio: 3.64, 95% CI: 1.37–9.66, p = 0.009). Conclusion: The podocyte injury was prevalent and the FPW levels were closely associated with clinicopathological features, especially prognosis, in renal TMA patients.

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          Most cited references 27

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          Thrombotic microangiopathies.

           Joel L. Moake (2002)
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            Atypical hemolytic uremic syndrome and C3 glomerulopathy: conclusions from a "Kidney Disease: Improving Global Outcomes" (KDIGO) Controversies Conference.

            In both atypical hemolytic uremic syndrome (aHUS) and C3 glomerulopathy (C3G) complement plays a primary role in disease pathogenesis. Herein we report the outcome of a 2015 Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference where key issues in the management of these 2 diseases were considered by a global panel of experts. Areas addressed included renal pathology, clinical phenotype and assessment, genetic drivers of disease, acquired drivers of disease, and treatment strategies. In order to help guide clinicians who are caring for such patients, recommendations for best treatment strategies were discussed at length, providing the evidence base underpinning current treatment options. Knowledge gaps were identified and a prioritized research agenda was proposed to resolve outstanding controversial issues.
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              Haemolytic uraemic syndrome


                Author and article information

                Am J Nephrol
                American Journal of Nephrology
                S. Karger AG
                September 2020
                28 August 2020
                : 51
                : 9
                : 752-760
                aRenal Division, Department of Medicine, Peking University First Hospital, Beijing, China
                bInstitute of Nephrology, Peking University, Beijing, China
                cKey Laboratory of Renal Disease, Ministry of Health of China, Beijing, China
                dKey Laboratory of CKD Prevention and Treatment, Ministry of Education of China, Beijing, China
                eResearch Units of Diagnosis and Treatment of Immune-Mediated Kidney Diseases, Chinese Academy of Medical Sciences, Beijing, China
                fDepartment of Electron Microscopy, Peking University First Hospital, Beijing, China
                gDepartment of Nephrology, Peking University International Hospital, Beijing, China
                hPeking-Tsinghua Center for Life Sciences, Beijing, China
                Author notes
                *Feng Yu, Renal Division, Department of Medicine, Peking University First Hospital, No. 8, Xishiku Street, Beijing 100034 (PR China), yufengevert1@sina.com
                510141 Am J Nephrol 2020;51:752–760
                © 2020 S. Karger AG, Basel

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                Page count
                Figures: 3, Tables: 1, Pages: 9
                Novel Research Findings


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