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Contribution of hemodilution to renal hypoxia following cardiopulmonary bypass surgery (890.12)
Journal article   Peer reviewed

Contribution of hemodilution to renal hypoxia following cardiopulmonary bypass surgery (890.12)

I. Sgouralis, R. Evans, B. Gardiner and A. Layton
The FASEB Journal, Vol.28(Supp. 1)
2014
DOI: https://doi.org/10.1096/fasebj.28.1_supplement.890.12
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Abstract

Acute kidney injury (AKI) is a prevalent complication of surgical procedures that require cardiopulmonary bypass (CPB). We have used a mathematical model of the rat kidney to simulate renal hemodynamics during CPB and to study the pathways that can lead to AKI. The model represents vascular blood flow, glomerular filtration, and metabolically driven salt reabsorption along the nephron. Autoregulation is provided by active afferent arteriole constriction initiated by the myogenic response and tubuloglomerular feedback. The model simulates the effects of (i) reduced renal perfusion pressure, which reduces blood flow and glomerular filtration rate (GFR); (ii) hemodilution, which increases GFR; and (iii) hypothermia, which reduces sodium reabsorption and oxygen consumption. Medullary oxygenation is determined by the balance between oxygen consumption, which is increased by hemodilution but decreased due to low perfusion pressure and temperature, and medullary blood supply, which is reduced by hemodilution and the low perfusion pressure. Model simulations suggest that the rise in body temperature following the surgery increases medullary oxygen consumption and drives the kidney into a hypoxic state which may result in AKI. This research was supported in part by NIH grant DK-89066.

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