Please use this identifier to cite or link to this item: http://www.repositorio.ufc.br/handle/riufc/16279
Title in Portuguese: Metabolic acidosis aggravates experimental acute kidney injury
Author: Magalhães, Patrícia Andréa da Fonseca
Brito, Teresinha Silva de
Freire, Rosemayre Souza
Silva, Moisés Tolentino Bento da
Santos, Armênio Aguiar dos
Vale, Mariana Lima
Menezes, Dalgimar Beserra de
Martins, Alice Maria Costa
Libório, Alexandre Braga
Keywords: Cetose
Heme Oxigenase (Desciclizante)
Nefropatias
Issue Date: Feb-2016
Publisher: Life Sciences
Citation: MAGALHÃES, P. A. F. et al. Metabolic acidosis aggravates experimental acute kidney injury. Life Sciences, v. 146, p. 58-65, feb. 2016.
Abstract: ims Ischemia/reperfusion (I/R) injury and metabolic acidosis (MA) are two critical conditions that may simultaneously occur in clinical practice. The result of this combination can be harmful to the kidneys, but this issue has not been thoroughly investigated. The present study evaluated the influence of low systemic pH on various parameters of kidney function in rats that were subjected to an experimental model of renal I/R injury. Main methods Metabolic acidosis was induced in male Wistar rats by ingesting ammonium chloride (NH4Cl) in tap water, beginning 2 days before ischemic insult and maintained during the entire study. Ischemia/reperfusion was induced by clamping both renal arteries for 45 min, followed by 48 h of reperfusion. Four groups were studied: control (subjected to sham surgery, n = 8), I/R (n = 8), metabolic acidosis (MA; 0.28 M NH4Cl solution and sham surgery, n = 6), and MA + I/R (0.28 M NH4Cl solution plus I/R, n = 9). Key findings Compared with I/R rats, MA + I/R rats exhibited higher mortality (50 vs. 11%, p = 0.03), significant reductions of blood pH, plasma bicarbonate (pBic), and standard base excess (SBE), with a severe decline in the glomerular filtration rate and tubular function. Microscopic tubular injury signals were detected. Immunofluorescence revealed that the combination of MA and I/R markedly increased nuclear factor κB (NF-κB) and heme-oxygenase 1 (HO-1), but it did not interfere with the decrease in endothelial nitric oxide synthase (eNOS) expression that was caused by I/R injury. Significance Acute ischemic kidney injury is exacerbated by acidic conditions.
URI: 1879-0631 On line
http://www.repositorio.ufc.br/handle/riufc/16279
metadata.dc.type: Artigo
ISSN: 0024-3205 Impresso
Appears in Collections:DFAR - Artigos publicados em revistas científicas

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