Clinical data and risk factors for diabetic nephropathy in Brazilian central population

Silva, Elisângela Gomes da; Anjos, Laura Raniere Borges dos; Lima, Rayane Mendes de; Alves, Thales Biffe; Pedrino, Gustavo Rodrigues; Cruz, Aldo Alfonso Alván De la; Santos, Rodrigo da Silva; Freiria-Oliveira, André Henrique; Reis, Ângela Adamski da Silva

doi:10.1016/j.dib.2018.10.115

Cited by 4 publications

(2 citation statements)

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“…Diabetic nephropathy is a chronic kidney disease caused by diabetes-related complications, including proteinuria and glomerulosclerosis. It is known to affect ~30% of patients with type 1 diabetes and ~10% of patients with type 2 diabetes ( 1 ). Numerous studies have reported the use of metformin in the treatment of various medical conditions in humans such as diabetes ( 22 , 23 ).…”

Section: Discussionmentioning

confidence: 99%

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Metformin attenuates diabetic renal injury via the AMPK‑autophagy axis

et al. 2021

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Diabetic nephropathy (DN) is a clinical condition characterized by kidney damage that is observed in patients with diabetes. DN is the main cause of end-stage renal disease (ESRD), which is the final stage of chronic kidney disease. Increasing evidence suggests that metformin, a characteristic oral hypoglycemic drug used for treating diabetes, exerts beneficial effects on various medical conditions and diseases, including cancer, cardiovascular diseases and thyroid-related disorders. However, the impact of metformin on DN remains unknown. The present study investigated whether metformin could attenuate the inflammatory response, fibrosis and increased oxidative stress observed during DN in diabetic/dyslipidemic (db/db) mice. The kidneys of the mice (12-16 weeks) were isolated for immunohistochemistry and western blotting. The results demonstrated that metformin significantly reduced the oxidative damage and fibrosis in the kidneys of db/db mice. Furthermore, metformin treatment significantly inhibited the generation of inflammatory cytokines, including TNF-α and IL-1β in db/db mice. These effects were induced by the activation of the AMP-activated protein kinase (AMPK) pathway, which was mediated by increased phosphorylation of AMPK and mammalian target of rapamycin (mTOR), resulting in autophagy and the simultaneous decrease in reactive oxygen species production, cell apoptosis and inflammatory response. These findings suggested that metformin may reduce DN damage via regulation of the AMPK-mTOR-autophagy axis and indicated that metformin may be considered as a potential target in the treatment of DN.

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Section: Discussionmentioning

confidence: 99%

“…Diabetic nephropathy (DN) is the leading cause of end-stage renal disease (ESRD) worldwide ( 1 ). The development of DN is associated with hypertension, elevated urinary albumin levels, glomerulosclerosis and a decline in the glomerular filtration rate, ultimately resulting in ESRD ( 2 ).…”

Section: Introductionmentioning

confidence: 99%