| Full text | |
| Author(s): |
de Araujo, Larissa
;
Costa-Pessoa, Juliana Martins
;
de Ponte, Mariana Charleaux
;
Oliveira-Souza, Maria
Total Authors: 4
|
| Document type: | Journal article |
| Source: | FRONTIERS IN PHYSIOLOGY; v. 11, p. 12-pg., 2020-08-25. |
| Abstract | |
Acute crystalline nephropathy is closely related to tubulointerstitial injury, but few studies have investigated glomerular changes in this condition. Thus, in the current study, we investigated the factors involved in glomerular and tubulointerstitial injury in an experimental model of crystalline-induced acute kidney injury (AKI). We treated male Wistar rats with a single injection of sodium oxalate (NaOx, 7 mg.100 g(-1).day(-1), resuspended in 0.9% NaCl solution, i.p.) or vehicle (control). After 24 h of treatment, food and water intake, urine output, body weight gain, and renal function were evaluated. Renal tissue was used for the morphological studies, quantitative PCR and protein expression studies. Our results revealed that NaOx treatment did not change metabolic or electrolyte and water intake parameters or urine output. However, the treated group exhibited tubular calcium oxalate (CaOx) crystals excretion, followed by a decline in kidney function demonstrated along with glomerular injury, which was confirmed by increased plasma creatinine and urea concentrations, increased glomerular desmin immunostaining, nephrin mRNA expression and decreased WT1 immunofluorescence. Furthermore, NaOx treatment resulted in tubulointerstitial injury, which was confirmed by tubular dilation, albuminuria, increased Kim-1 and Ki67 mRNA expression, decreased megalin and Tamm-Horsfall protein (THP) expression. Finally, the treatment induced increases in CD68 protein staining, MCP-1, IL-1 beta, NFkappaB, and alpha-SMA mRNA expression, which are consistent with proinflammatory and profibrotic signaling, respectively. In conclusion, our findings provide relevant information regarding crystalline-induced AKI, showing strong tubulointerstitial and glomerular injury with a possible loss of podocyte viability. (AU) | |
| 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: | 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: | 19/06358-0 - Contribution of urinary stones in the progression of renal injury in rats |
| Grantee: | Larissa de Araújo |
| Support Opportunities: | Scholarships in Brazil - Scientific Initiation |