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    Chronic kidney disease with comorbid cardiac dysfunction exacerbates cardiac and renal damage

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    Author
    Liu, S; Wang, BH; Kelly, DJ; Krum, H; Kompa, AR
    Date
    2018-01-01
    Source Title
    Journal of Cellular and Molecular Medicine
    Publisher
    WILEY
    University of Melbourne Author/s
    Kelly, Darren; Kompa, Andrew; KRUM, HENRY
    Affiliation
    Medicine and Radiology
    Metadata
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    Document Type
    Journal Article
    Citations
    Liu, S., Wang, B. H., Kelly, D. J., Krum, H. & Kompa, A. R. (2018). Chronic kidney disease with comorbid cardiac dysfunction exacerbates cardiac and renal damage. JOURNAL OF CELLULAR AND MOLECULAR MEDICINE, 22 (1), pp.628-645. https://doi.org/10.1111/jcmm.13349.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/257386
    DOI
    10.1111/jcmm.13349
    Abstract
    To address the pathophysiological mechanisms underlying chronic kidney disease with comorbid cardiac dysfunction, we investigated renal and cardiac, functional and structural damage when myocardial infarction (MI) was applied in the setting of kidney injury (induced by 5/6 nephrectomy-STNx). STNx or Sham surgery was induced in male Sprague-Dawley rats with MI or Sham surgery performed 4 weeks later. Rats were maintained for a further 8 weeks. Rats (n = 36) were randomized into four groups: Sham+Sham, Sham+MI, STNx+Sham and STNx+MI. Increased renal tubulointerstitial fibrosis (P < 0.01) and kidney injury molecule-1 expression (P < 0.01) was observed in STNx+MI compared to STNx+Sham animals, while there were no further reductions in renal function. Heart weight was increased in STNx+MI compared to STNx+Sham or Sham+MI animals (P < 0.05), despite no difference in blood pressure. STNx+MI rats demonstrated greater cardiomyocyte cross-sectional area and increased cardiac interstitial fibrosis compared to either STNx+Sham (P < 0.01) or Sham+MI (P < 0.01) animals which was accompanied by an increase in diastolic dysfunction. These changes were associated with increases in ANP, cTGF and collagen I gene expression and phospho-p38 MAPK and phospho-p44/42 MAPK protein expression in the left ventricle. Addition of MI accelerated STNx-induced structural damage but failed to significantly exacerbate renal dysfunction. These findings highlight the bidirectional response in this model known to occur in cardiorenal syndrome (CRS) and provide a useful model for examining potential therapies for CRS.

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