000009558 001__ 9558
000009558 005__ 20240328093853.0
000009558 0247_ $$2DOI$$a10.6083/pr76f424d
000009558 037__ $$aIR
000009558 041__ $$aeng
000009558 245__ $$aCardiac arrest induced systemic ischemia alters phenotype of renal ischemia reperfusion injury
000009558 260__ $$bOregon Health and Science University
000009558 269__ $$a2022-04-08
000009558 336__ $$aAbstract
000009558 520__ $$aCardiorenal syndrome type 1 (CRS1) is acute kidney injury (AKI) due to rapid worsening of cardiac function, and is a common cause of AKI. Ischemic AKI and subsequent chronic kidney disease (CKD) is mainly investigated by using the model of renal pedicle clamp (ischemia-reperfusion injury: IRI) which models renal transplant warm ischemia. However, results from IRI do not mimic clinical CRS1. We have previously identified a cardiac-derived soluble factor, cardiac LIM protein (CSRP3), which mediates renal function. We hypothesized that the phenotype of AKI-CKD transition differs between animal models of systemic ischemia and renal-limited ischemia.
000009558 540__ $$fCC BY
000009558 542__ $$fIn copyright - joint owners
000009558 650__ $$aAcute Kidney Injury$$039113
000009558 6531_ $$aaki-ckd transition
000009558 6531_ $$acardiorenal syndrome type 1
000009558 6531_ $$achronic kidney disease
000009558 691__ $$aSchool of Medicine$$041369
000009558 692__ $$aDepartment of Anesthesiology and Perioperative Medicine$$041393
000009558 7001_ $$aFunahashi, Yoshio$$uOregon Health and Science University$$041354
000009558 7001_ $$aGroat, Tahnee$$uOregon Health and Science University$$041354
000009558 7001_ $$aHutchens, Michael$$uOregon Health and Science University$$041354
000009558 711__ $$aResearch Week$$uOregon Health and Science University$$d2022
000009558 8564_ $$9856ccfa0-f841-4134-8e47-4b4916691d55$$s171734$$uhttps://digitalcollections.ohsu.edu/record/9558/files/ResearchWeek2022-Abstract_funahashi.pdf
000009558 905__ $$a/rest/prod/pr/76/f4/24/pr76f424d
000009558 980__ $$aResearch Week