Renocardiac Effects of p-Cresyl Sulfate Administration in Acute Kidney Injury Induced by Unilateral Ischemia and Reperfusion Injury In Vivo
The precise mechanisms underlying the cardiovascular complications due to acute kidney injury (AKI) and the retention of uremic toxins like p-cresyl sulfate (PCS) remain incompletely understood. The objective of this study was to evaluate the renocardiac effects of PCS administration in animals subjected to AKI induced by ischemia and reperfusion (IR) injury. C57BL6 mice were subjected to distinct protocols: (i) administration with PCS (20, 40, or 60 mg/L/day) for 15 days and (ii) AKI due to unilateral IR injury associated with PCS administration for 15 days. The 20 mg/L dose of PCS led to a decrease in renal mass, an increase in the gene expression of Cystatin C and kidney injury molecule 1 (KIM-1), and a decrease in the α-actin in the heart. During AKI, PCS increased the renal injury biomarkers compared to control; however, it did not exacerbate these markers. Furthermore, PCS did not enhance the cardiac hypertrophy observed after 15 days of IR. An increase, but not potentialized, in the cardiac levels of interleukin (IL)-1β and IL-6 in the IR group treated with PCS, as well as in the injured kidney, was also noticed. In short, PCS administration did not intensify kidney injury, inflammation, and cardiac outcomes after AKI.
Citação
@online{carlos_alexandre2023,
author = {Carlos Alexandre , Falconi and Fernanda , Fogaça-Ruiz and
Silva, Jéssica Verônica, Da and Raquel Silva , Neres-Santos and
Carmen Lucía , Sanz and Lia Sumie , Nakao and Andréa Emília Marques
, Stinghen and Carolina Victoria Cruz , Junho and Marcela Sorelli ,
Carneiro-Ramos},
title = {Renocardiac Effects of p-Cresyl Sulfate Administration in
Acute Kidney Injury Induced by Unilateral Ischemia and Reperfusion
Injury In Vivo},
volume = {15},
number = {11},
date = {2023-11-10},
doi = {10.3390/toxins15110649},
langid = {pt-BR},
abstract = {The precise mechanisms underlying the cardiovascular
complications due to acute kidney injury (AKI) and the retention of
uremic toxins like p-cresyl sulfate (PCS) remain incompletely
understood. The objective of this study was to evaluate the
renocardiac effects of PCS administration in animals subjected to
AKI induced by ischemia and reperfusion (IR) injury. C57BL6 mice
were subjected to distinct protocols: (i) administration with PCS
(20, 40, or 60 mg/L/day) for 15 days and (ii) AKI due to unilateral
IR injury associated with PCS administration for 15 days. The 20
mg/L dose of PCS led to a decrease in renal mass, an increase in the
gene expression of Cystatin C and kidney injury molecule 1 (KIM-1),
and a decrease in the α-actin in the heart. During AKI, PCS
increased the renal injury biomarkers compared to control; however,
it did not exacerbate these markers. Furthermore, PCS did not
enhance the cardiac hypertrophy observed after 15 days of IR. An
increase, but not potentialized, in the cardiac levels of
interleukin (IL)-1β and IL-6 in the IR group treated with PCS, as
well as in the injured kidney, was also noticed. In short, PCS
administration did not intensify kidney injury, inflammation, and
cardiac outcomes after AKI.}
}