Publications by authors named "G Pino-Chavez"
Article Synopsis
- Acute Kidney Injury (AKI) and Chronic Kidney Disease (CKD) are increasingly viewed as part of the same disease continuum, with Ischaemia Reperfusion Injury (IRI) being the leading cause of AKI, often linked to conditions like sepsis.
- The study demonstrated a rat model of kidney IRI, utilizing Ischaemic Preconditioning (IPC) to investigate its protective effects against AKI and renal fibrosis.
- Results showed that IPC significantly reduced renal fibrosis by 66% compared to IRI alone, highlighting a possible transitional point at 14 days when kidneys may either recover or progress to fibrosis, suggesting new targets for treatment.
Background/aim: Acute and chronic kidney diseases are a major contributor to morbidity and mortality worldwide, with no specific treatments currently available for these. To enable understanding the pathophysiology of and testing novel treatments for acute and chronic kidney disease, a suitable in vivo model of kidney disease is essential. In this article, we describe two reliable rodent models (rats and mice) of efficacious kidney injury displaying acute to chronic kidney injury progression, which is also reversible through novel therapeutic strategies such as ischemic preconditioning (IPC).
View Article and Find Full Text PDFIschemic preconditioning (IPC) is effective in limiting subsequent ischemic acute kidney injury in experimental models. MicroRNAs are an important class of post-transcriptional regulator and show promise as biomarkers of kidney injury. We evaluated the time- and dose-dependence of benefit from IPC in a rat model of functional (bilateral) ischemia-reperfusion injury (IRI).
View Article and Find Full Text PDFObjectives: We evaluated a continuous, immediate, localized ischemic preconditioning regimen in a rat model of ischemia-reperfusion injury and assessed whether it attenuated injury at the histologic and molecular levels.
Materials And Methods: Fifteen adult male Lewis rats received sham operation, left unilateral warm ischemia (45 minutes of cross-clamping of the renal pedicle; ischemia-reperfusion injury group), or 15 minutes of ischemia followed by a 20-minute reperfusion period, 45 minutes of ischemia-reperfusion injury, and subsequent reperfusion (ischemic preconditioning/ischemia-reperfusion injury group). Kidney tissue was retrieved 48 hours later, sectioned, stained with hematoxylin and eosin, and examined.
Objective: Ex vivo perfusion model of pig-to-human kidney xenotransplantation to evaluate human antiporcine xenograft rejection once hyperacute rejection (HAR) is avoided.
Methods: Pig kidneys were perfused for 3 hours with pig blood (group 1; n = 5), human blood (group 2; n = 5), complement heat inactivated human blood (group 3; n = 5), platelet-depleted human blood (group 4; n = 5); and xenoreactive natural antibodies (XNA)-depleted human blood (group 5; n = 5). Tissue samples were studied with immunoperoxidase techniques.