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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Early type 1 diabetes aggravates renal ischemia/reperfusion-induced acute kidney injury

Full text
Author(s):
de Ponte, Mariana Charleaux [1] ; Cardoso, Vanessa Gerolde [1] ; Goncalves, Guilherme Lopes [1] ; Costa-Pessoa, Juliana Martins [1] ; Oliveira-Souza, Maria [1]
Total Authors: 5
Affiliation:
[1] Univ Sao Paulo, Inst Biomed Sci, Dept Physiol & Biophys, Lab Renal Physiol, BR-05508900 Sao Paulo, SP - Brazil
Total Affiliations: 1
Document type: Journal article
Source: SCIENTIFIC REPORTS; v. 11, n. 1 SEP 24 2021.
Web of Science Citations: 0
Abstract

The present study aimed to investigate the interaction between early diabetes and renal IR-induced AKI and to clarify the mechanisms involved. C57BL/6J mice were assigned to the following groups: (1) sham-operated; (2) renal IR; (3) streptozotocin (STZ-55 mg/kg/day) and sham operation; and (4) STZ and renal IR. On the 12th day after treatments, the animals were subjected to bilateral IR for 30 min followed by reperfusion for 48 h, at which time the animals were euthanized. Renal function was assessed by plasma creatinine and urea levels, as well urinary protein contents. Kidney morphology and gene and protein expression were also evaluated. Compared to the sham group, renal IR increased plasma creatinine, urea and albuminuria levels and decreased Nphs1 mRNA expression and nephrin and WT1 protein staining. Tubular injury was observed with increased Havcr1 and Mki67 mRNA expression accompanied by reduced megalin staining. Renal IR also resulted in increased SQSTM1 protein expression and increased proinflammatory and profibrotic factors mRNA expression. Although STZ treatment resulted in hyperglycemia, it did not induce significant changes in renal function. On the other hand, STZ treatment aggravated renal IR-induced AKI by exacerbating renal dysfunction, glomerular and tubular injury, inflammation, and profibrotic responses. Thus, early diabetes constitutes a relevant risk factor for renal IR-induced AKI. (AU)

FAPESP's process: 17/02020-0 - Mechanisms involved in the transition from post-ischemic acute kidney injury to chronic kidney disease: contribution of angiotensin II and albumin
Grantee:Maria Oliveira de Souza
Support Opportunities: Regular Research Grants
FAPESP's process: 16/12354-0 - Analysis of the transition from acute ischemic renal injury to chronic kidney disease and the contribution of diabetes mellitus in this process
Grantee:Mariana Charleaux de Ponte
Support Opportunities: Scholarships in Brazil - Doctorate
FAPESP's process: 18/26528-5 - Adaptive mechanisms of renal function in a model of adriamycin-induced nephrotoxicity: participation of sirtuin 1 and claudin-1
Grantee:Guilherme Lopes Gonçalves
Support Opportunities: Scholarships in Brazil - Doctorate
FAPESP's process: 19/13584-7 - Mechanisms involved in the progression of renal diseases in experimental models of the adriamycin-induced nephrotoxicity or of the ischemia/reperfusion and Diabetes
Grantee:Maria Oliveira de Souza
Support Opportunities: Regular Research Grants