000140946 001__ 140946 000140946 005__ 20240321220915.0 000140946 0247_ $$2doi$$a10.1371/journal.pone.0218308 000140946 0247_ $$2pmid$$apmid:31206554 000140946 0247_ $$2pmc$$apmc:PMC6576776 000140946 037__ $$aDZNE-2020-07268 000140946 041__ $$aEnglish 000140946 082__ $$a610 000140946 1001_ $$0P:(DE-HGF)0$$aRuss, Martin$$b0$$eCorresponding author 000140946 245__ $$aIncreased compensatory kidney workload results in cellular damage in a short time porcine model of mixed acidemia - Is acidemia a 'first hit' in acute kidney injury? 000140946 260__ $$aSan Francisco, California, US$$bPLOS$$c2019 000140946 264_1 $$2Crossref$$3online$$bPublic Library of Science (PLoS)$$c2019-06-17 000140946 3367_ $$2DRIVER$$aarticle 000140946 3367_ $$2DataCite$$aOutput Types/Journal article 000140946 3367_ $$0PUB:(DE-HGF)16$$2PUB:(DE-HGF)$$aJournal Article$$bjournal$$mjournal$$s1604651774_15308 000140946 3367_ $$2BibTeX$$aARTICLE 000140946 3367_ $$2ORCID$$aJOURNAL_ARTICLE 000140946 3367_ $$00$$2EndNote$$aJournal Article 000140946 520__ $$aAcute kidney injury (AKI) corrupts the outcome of about 50% of all critically ill patients. We investigated the possible contribution of the pathology acidemia on the development of AKI. Pigs were exposed to acidemia, acidemia plus hypoxemia or a normal acid-base balance in an experimental setup, which included mechanical ventilation and renal replacement therapy to facilitate biotrauma caused by extracorporeal therapies. Interestingly, extensive histomorphological changes like a tubular loss of cell barriers occurred in the kidneys after just 5 hours exposure to acidemia. The additional exposure to hypoxemia aggravated these findings. These 'early' microscopic pathologies opposed intra vitam data of kidney function. They did not mirror cellular or systemic patterns of proinflammatory molecules (like TNF-α or IL 18) nor were they detectable by new, sensitive markers of AKI like Neutrophil gelatinase-associated lipocalin. Instead, the data suggest that the increased renal proton excretion during acidemia could be an 'early' first hit in the multifactorial pathogenesis of AKI. 000140946 536__ $$0G:(DE-HGF)POF3-342$$a342 - Disease Mechanisms and Model Systems (POF3-342)$$cPOF3-342$$fPOF III$$x0 000140946 542__ $$2Crossref$$i2019-06-17$$uhttp://creativecommons.org/licenses/by/4.0/ 000140946 588__ $$aDataset connected to CrossRef, PubMed, 000140946 650_2 $$2MeSH$$aAcid-Base Imbalance: complications 000140946 650_2 $$2MeSH$$aAcute Kidney Injury: etiology 000140946 650_2 $$2MeSH$$aAnimals 000140946 650_2 $$2MeSH$$aHypoxia 000140946 650_2 $$2MeSH$$aKidney: physiopathology 000140946 650_2 $$2MeSH$$aKidney Tubules: pathology 000140946 650_2 $$2MeSH$$aProtons 000140946 650_2 $$2MeSH$$aSwine 000140946 7001_ $$aOtt, Sascha$$b1 000140946 7001_ $$0P:(DE-2719)2811747$$aBedarf, Janis R$$b2$$udzne 000140946 7001_ $$aKirschfink, Michael$$b3 000140946 7001_ $$aHiebl, Bernhard$$b4 000140946 7001_ $$aUnger, Juliane K$$b5 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