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

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 characterize...

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Published in:American journal of physiology. Renal physiology 2016-04, Vol.310 (8), p.F785-F795
Main Authors: Mulay, Shrikant R, Eberhard, Jonathan N, Pfann, Victoria, Marschner, Julian A, Darisipudi, Murthy N, Daniel, Christoph, Romoli, Simone, Desai, Jyaysi, Grigorescu, Melissa, Kumar, Santhosh V, Rathkolb, Birgit, Wolf, Eckhard, Hrabě de Angelis, Martin, Bäuerle, Tobias, Dietel, Barbara, Wagner, Carsten A, Amann, Kerstin, Eckardt, Kai-Uwe, Aronson, Peter S, Anders, Hans Joachim, Knauf, Felix
Format: Article
Language:English
Subjects:
Animals
Disease Models, Animal
Fibrosis
Hypertension - etiology
Hypertension - pathology
Innovative Methodology
Kidney diseases
Mice
Mice, Inbred C57BL
Myocardium - pathology
NMR
Nuclear magnetic resonance
Oxalic Acid
Renal Insufficiency, Chronic - chemically induced
Renal Insufficiency, Chronic - complications
Renal Insufficiency, Chronic - pathology
Rodents
Tissues
Uremia - etiology
Uremia - pathology
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Summary: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 wk, 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.
ISSN:1931-857X
1522-1466
DOI:10.1152/ajprenal.00488.2015