Focal Segmental Glomerulosclerosis (FSGS) is one of the most frequent glomerulopathies, and is considered a public health problem worldwide. FSGS is characterized by glomerular loss mainly due to in ammation and collagen bers deposition. STAT-3 is a transcription factor associated with cell differentiation, migration and proliferation. Its activation occurs in response to several growth factors and cytokines. In renal cells, STAT-3 has been related with disease progression. Considering this perspective, the present study evaluated the involvement of STAT-3 in an experimental model of FSGS induced by Doxorubicin (DOX). First, we described a novel FSGS model in Swiss mice that after DOX administration showed typical signs of kidney dysfunction like higher proteinuria. Since there were no studies of ADM nephropathy model in heterogeneous mice, we were the rst to evaluate the model in this lineage. Control animals treated with STAT-3 inhibitor (STATTIC) presented lower levels of albumin/creatinine ratio, glycosuria e proteinuria while DOX-injected mice showed higher levels. After analyzing some molecules involved in the STAT-3 signaling pathway, it was observed that STAT-3 blockade decreased levels of STAT-3, IL-6 and IL-6R, which remained elevated in DOX-administrated mice. Moreover, we detected that SOCS-3 (a regulator of STAT family) was up-regulated only in STATTIC-treated mice. Finally, histopathological analyzes showed that DOX-treated group had a signi cant increase in a tubulointerstitial brosis and tubular necrosis, which were not identi ed in both control and STATTIC groups. Thus, our results indicate that STAT-3 can have an important role in experimental FSGS induced by DOX and further studies are encouraged.

Focal Segmental Glomerulosclerosis (FSGS) is one of the most frequent glomerulopathies, and is considered a public health problem worldwide. FSGS is characterized by glomerular loss mainly due to inflammation and collagen fibers deposition. STAT-3 is a transcription factor associated with cell differentiation, migration and proliferation. Its activation occurs in response to several growth factors and cytokines. In renal cells, STAT-3 has been related with disease progression. Considering this perspective, the present study evaluated the involvement of STAT-3 in an experimental model of FSGS induced by Doxorubicin (DOX). First, we described a novel FSGS model in Swiss mice that after DOX administration showed typical signs of kidney dysfunction like higher proteinuria. Since there were no studies of ADM nephropathy model in heterogeneous mice, we were the first to evaluate the model in this lineage. Control animals treated with STAT-3 inhibitor (STATTIC) presented lower levels of albumin/creatinine ratio, glycosuria e proteinuria while DOX-injected mice showed higher levels. After analyzing some molecules involved in the STAT-3 signaling pathway, it was observed that STAT-3 blockade decreased levels of STAT-3, IL-6 and IL-6R, which remained elevated in DOX-administrated mice. Moreover, we detected that SOCS-3 (a regulator of STAT family) was up-regulated only in STATTIC-treated mice. Finally, histopathological analyzes showed that DOX-treated group had a significant increase in a tubulointerstitial fibrosis and tubular necrosis, which were not identified in both control and STATTIC groups. Thus, our results indicate that STAT-3 can have an important role in experimental FSGS induced by DOX and further studies are encouraged.

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The aim of this study was to conduct a systematic review in order to evaluate the main effects of intradialytic physical exercise on different parameters of functional capacity in dialytic patients. The clinical question that guided the objective of this study was developed using the PICO method (Population, Intervention, Comparation and Outcome)." Where i) population: patients on hemodialysis; ii) intervention: physical exercise; iii) comparison: active vs sedentary patients; and iv) outcome: functional capacity. The combinations of the following keywords were used: CKD, physical exercise, exercise, physical training and hemodialysis. The selection of studies was performed using the PubMed database and only studies dating from 2011 to 2021 were selected. The search results led to 53 studies. The following steps were carefully analyzed, such as the title, abstract and the full paper description to evaluate whether they met the following inclusion criteria: i) target audience of the studies should be patients on hemodialysis; ii) outcomes that analyze different parameters of functional capacity; iii) Intervention using physical exercise; and iii) intradialytic exercise. The final results indicate that intradialytic physical exercise can cause significant changes in the evaluated outcomes of functional capacity, such as increased strength, improvement of cardiorespiratory function, and improvement of locomotor activity. It was concluded that intradialytic training protocols should be encouraged in clinical practices because they are responsible for causing beneficial changes in the functional capacity of hemodialytic patients.