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Mulay, S.R.* ; Eberhard, J.N.* ; Pfann, V.* ; Marschner, J.A.* ; Darisipudi, M.N.* ; Daniel, C.* ; Romoli, S.* ; Desai, J.* ; Grigorescu, M.* ; Kumar, S.V.* ; Rathkolb, B.* ; Wolf, E.* ; Hrabě de Angelis, M. ; Bäuerle, T.* ; Dietel, B.* ; Wagner, C.A.* ; Amann, K.* ; Eckardt, K.U.* ; Aronson, P.S.* ; Anders, H.J.* ; Knauf, F.*

Oxalate-induced chronic kidney disease with its uremic and cardiovascular complications in C57BL/6 mice.

Am. J. Physiol.-Renal Physiol. 310, F785-F795 (2016)
Verlagsversion DOI
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Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Chronic kidney disease (CKD) research is limited by the lack of convenient inducible models mimicking human CKD and its complications in experimental animals. We demonstrate that a soluble oxalate-rich diet induces stable stages of CKD in male and female C57BL/6 mice. Renal histology is characterized by tubular damage, remnant atubular glomeruli, interstitial inflammation, and fibrosis with the extent of tissue involvement depending on the duration of oxalate feeding. Expression profiling of markers and magnetic resonance imaging findings established to reflect inflammation and fibrosis parallel the histological changes. Within 3 weeks the mice reproducibly develop normochromic anemia, metabolic acidosis, hyperkalemia, FGF23 activation, hyperphosphatemia and hyperparathyroidism. In addition, the model is characterized by profound arterial hypertension as well as cardiac fibrosis that persist following the switch to a control diet. Together, this new model of inducible CKD overcomes a number of previous experimental limitations and should serve useful in research related to CKD and its complications.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Ckd-mbd ; Cardiovascular ; Hypertension ; Oxalate ; Renal Failure; Unilateral Ureteral Obstruction; Chronic-renal-failure; Acid Nephropathy; Mouse Model; Inflammation; Fibrosis; Progression; Mechanisms; Ckd; Sex
ISSN (print) / ISBN 0002-9513
e-ISSN 1522-1466
Quellenangaben Band: 310, Heft: 8, Seiten: F785-F795 Artikelnummer: , Supplement: ,
Verlag American Physiological Society
Verlagsort Bethesda
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Experimental Genetics (IEG)
German Center for Diabetes Reseach (DZD)