Renal tissue hypoxia in a rat model of polycystic kidney disease

C. P. C. Ow, A. Abdelkader, Jacqueline Phillips, R. G. Evans

    Research output: Contribution to journalMeeting abstract


    Background: Polycystic kidney disease (PKD) is characterized by the development of numerous fluid-filled cysts. Hypoxia has been identified as a final common pathway in the progression of chronic kidney disease. Histological analysis of kidney sections from animals with PKD have provided qualitative evidence of tissue hypoxia. To date, no direct measurements of tissue PO2 have been made.

    Aim: To directly measure renal tissue PO2 in the Lewis rat model of PKD (LPK) and to determine the relative contributions of altered renal oxygen delivery and oxygen consumption in driving tissue hypoxia.

    Methods: Experiments were performed in 11–13 week-old Lewis and LPK rats. Rats were anesthetized with sodium thiobarbital and artificially ventilated. Renal tissue oxygenation was measured using the Clark electrode (10 μm diameter). Tissue PO2 was determined within multiple sites in the renal parenchyma and in cysts in the superficial cortex (n=12 Lewis; n=11 LPK). Arterial and renal venous oxygen content were determined by direct blood oximetry.

    Results: In LPK rats, tissue PO2 was higher within the cysts (32.8 ± 4.0 mmHg) than in the superficial cortical tissue itself (18.3 ± 3.5 mmHg), but still lower than the tissue PO2 of the superficial cortex of Lewis rats (46.0 ± 3.1 mmHg). Renal tissue oxygen delivery was 78.5% lower in LPK rats than Lewis rats. Total sodium reabsorption was 98.0% less in LPK rats than Lewis rats, but renal oxygen consumption did not differ significantly between LPK and Lewis rats.

    Conclusion: In this model of PKD, the superficial renal cortex is severely hypoxic. Tissue hypoxia in the kidney of LPK rats is driven in part by the compromised tissue oxygen delivery. Our inability to detect a significant deficit in renal oxygen consumption in LPK rats, despite a marked deficit in sodium reabsorption, suggests that inefficient utilization of oxygen for sodium reabsorption may also contribute to the development of renal hypoxia in PKD.
    Original languageEnglish
    Article numberH-063
    Pages (from-to)E155-E155
    Number of pages1
    Issue number6
    Publication statusPublished - Jun 2014
    EventAnnual Scientific Meeting of the High Blood Pressure Research Council of Australia (HBPRCA) (35th : 2013) / Annual Scientific Meeting of the Australian Atherosclerosis Society (AAS) (39th : 2013) - Melbourne, Australia, Australia
    Duration: 5 Dec 20137 Dec 2013


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