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Renal oxygenation in clinical acute kidney injury.

Ricksten SE, Bragadottir G, Redfors B - Crit Care (2013)

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An increase in renal O2Ex means that renal DO2 has decreased in relation to renal VO2, i. e., renal oxygenation is impaired, and vice versa... Prasad et al. demonstrated in conscious volunteers that 20 mg of furosemide increased medullary oxygenation, using the blood oxygen level-dependent magnetic resonance imaging technique (BOLD MRI)... In contrast, acetazolamide, which inhibits tubular reabsorption of the proximal tubules in the cortex and which does not affect medullary PO2 in experimental studies, did not affect medullary oxygenation... Furosemide increased fractional excretion of sodium (excreted sodium/filtered sodium) from 2% to 25% and caused a 10-fold increase in urine flow because of a 28% decrease in tubular sodium reabsorption... These changes were in turn associated with a 23% decrease in renal VO2... Thus, furosemide decreased renal O2Ex and improved renal oxygenation as renal blood flow was not significantly affected by the diuretic... Redfors et al. recently studied the effects of low-dose (2-4 μg/kg/min) dopamine on renal blood flow, GFR, tubular sodium reabsorption, renal VO2 and the renal oxygen demand/supply relationship in post-cardiac surgery patients... Postoperative AKI in this group of patients is considered a consequence of impaired renal DO2, in turn caused by intra-operative hypotension and hemodilution-induced anemia, as well as perioperative low cardiac output... In spite of a normalization of cardiac index (CI) with inotropic treatment with or without intra-aortic balloon pump (IABP), renal oxygenation was severely impaired in patients with early AKI, as demonstrated by a 70% relative increase in renal O2Ex, compared to uncomplicated post-cardiac surgery patients with normal renal function This was, in turn, caused by a pronounced renal vasoconstriction and a 40% lower renal blood flow, in combination with a renal VO2 that was not significantly different from the control group, despite the 60% decrease in GFR and renal tubular sodium reabsorption (Table 3)... Figure 4 shows the close correlation between GFR and renal VO2 in patients with early AKI after cardiac surgery versus those undergoing uncomplicated surgery with no renal impairment... At a target MAP of 75 mm Hg, renal DO2 (13%), GFR (27%) and urine flow were higher and renal O2Ex was lower (7.4%) compared with a target MAP of 60 mm Hg... However, the renal variables did not differ when compared at target MAPs of 75 and 90 mm Hg (Figure 8)... ANP is ideally suited for treatment of ischemic AKI, as it preferentially dilates the preglomerular resistance vessels; this will increase GFR but also renal blood flow, meeting the increased oxygen demand of the medulla by an increase in renal DO2... Mannitol increases renal blood flow and GFR in clinical ischemic AKI most likely by endothelial and epithelial de-swelling effects.

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Effects of mannitol (M1, M2) on renal vascular resistance (RVR), renal blood flow (RBF), glomerular filtration rate (GFR) and renal filtration fraction (FF) in patients with early acute kidney injury after cardiac surgery. * p < 0.05 Modified from [44].
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Figure 7: Effects of mannitol (M1, M2) on renal vascular resistance (RVR), renal blood flow (RBF), glomerular filtration rate (GFR) and renal filtration fraction (FF) in patients with early acute kidney injury after cardiac surgery. * p < 0.05 Modified from [44].

Mentions: Another approach for the treatment of clinical ischemic AKI would be to target the vascular endothelium and tubular epithelium. Experimental studies have shown that mannitol may decrease ischemia-induced swelling of tubular cells, which might obstruct the tubular lumen [41]. Mannitol treatment has been shown to increase GFR in patients after severe trauma or surgery [42]. In addition, our group has shown that mannitol increases GFR in postoperative cardiac surgery patients possibly by a de-swelling effect on tubular cells [6]. Furthermore, it has been suggested that outer medullary hypoxia may cause endothelial ischemic injury and endothelial cell swelling contributing to congestion and impaired perfusion of this region [43], which could, at least to some extent, explain the high renal vascular resistance seen in clinical early AKI [2]. The effects of mannitol treatment on renal perfusion, filtration and oxygenation were recently studied in patients with normal preoperative creatinine, who developed early AKI after complicated cardiac surgery, requiring inotropic support with or without IABP [44]. Mannitol induced a 60% increase in diuresis, which was accompanied by decrease in renal vascular resistance and a 12-15% increase in renal blood flow, while no effects were seen on cardiac index or cardiac filling pressures. Mannitol did not affect filtration fraction or renal oxygenation, suggestive of balanced increases in perfusion/filtration and renal oxygen demand/supply (Figure 7).


Renal oxygenation in clinical acute kidney injury.

Ricksten SE, Bragadottir G, Redfors B - Crit Care (2013)

Effects of mannitol (M1, M2) on renal vascular resistance (RVR), renal blood flow (RBF), glomerular filtration rate (GFR) and renal filtration fraction (FF) in patients with early acute kidney injury after cardiac surgery. * p < 0.05 Modified from [44].
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3672481&req=5

Figure 7: Effects of mannitol (M1, M2) on renal vascular resistance (RVR), renal blood flow (RBF), glomerular filtration rate (GFR) and renal filtration fraction (FF) in patients with early acute kidney injury after cardiac surgery. * p < 0.05 Modified from [44].
Mentions: Another approach for the treatment of clinical ischemic AKI would be to target the vascular endothelium and tubular epithelium. Experimental studies have shown that mannitol may decrease ischemia-induced swelling of tubular cells, which might obstruct the tubular lumen [41]. Mannitol treatment has been shown to increase GFR in patients after severe trauma or surgery [42]. In addition, our group has shown that mannitol increases GFR in postoperative cardiac surgery patients possibly by a de-swelling effect on tubular cells [6]. Furthermore, it has been suggested that outer medullary hypoxia may cause endothelial ischemic injury and endothelial cell swelling contributing to congestion and impaired perfusion of this region [43], which could, at least to some extent, explain the high renal vascular resistance seen in clinical early AKI [2]. The effects of mannitol treatment on renal perfusion, filtration and oxygenation were recently studied in patients with normal preoperative creatinine, who developed early AKI after complicated cardiac surgery, requiring inotropic support with or without IABP [44]. Mannitol induced a 60% increase in diuresis, which was accompanied by decrease in renal vascular resistance and a 12-15% increase in renal blood flow, while no effects were seen on cardiac index or cardiac filling pressures. Mannitol did not affect filtration fraction or renal oxygenation, suggestive of balanced increases in perfusion/filtration and renal oxygen demand/supply (Figure 7).

View Article: PubMed Central - HTML - PubMed

AUTOMATICALLY GENERATED EXCERPT
Please rate it.

An increase in renal O2Ex means that renal DO2 has decreased in relation to renal VO2, i. e., renal oxygenation is impaired, and vice versa... Prasad et al. demonstrated in conscious volunteers that 20 mg of furosemide increased medullary oxygenation, using the blood oxygen level-dependent magnetic resonance imaging technique (BOLD MRI)... In contrast, acetazolamide, which inhibits tubular reabsorption of the proximal tubules in the cortex and which does not affect medullary PO2 in experimental studies, did not affect medullary oxygenation... Furosemide increased fractional excretion of sodium (excreted sodium/filtered sodium) from 2% to 25% and caused a 10-fold increase in urine flow because of a 28% decrease in tubular sodium reabsorption... These changes were in turn associated with a 23% decrease in renal VO2... Thus, furosemide decreased renal O2Ex and improved renal oxygenation as renal blood flow was not significantly affected by the diuretic... Redfors et al. recently studied the effects of low-dose (2-4 μg/kg/min) dopamine on renal blood flow, GFR, tubular sodium reabsorption, renal VO2 and the renal oxygen demand/supply relationship in post-cardiac surgery patients... Postoperative AKI in this group of patients is considered a consequence of impaired renal DO2, in turn caused by intra-operative hypotension and hemodilution-induced anemia, as well as perioperative low cardiac output... In spite of a normalization of cardiac index (CI) with inotropic treatment with or without intra-aortic balloon pump (IABP), renal oxygenation was severely impaired in patients with early AKI, as demonstrated by a 70% relative increase in renal O2Ex, compared to uncomplicated post-cardiac surgery patients with normal renal function This was, in turn, caused by a pronounced renal vasoconstriction and a 40% lower renal blood flow, in combination with a renal VO2 that was not significantly different from the control group, despite the 60% decrease in GFR and renal tubular sodium reabsorption (Table 3)... Figure 4 shows the close correlation between GFR and renal VO2 in patients with early AKI after cardiac surgery versus those undergoing uncomplicated surgery with no renal impairment... At a target MAP of 75 mm Hg, renal DO2 (13%), GFR (27%) and urine flow were higher and renal O2Ex was lower (7.4%) compared with a target MAP of 60 mm Hg... However, the renal variables did not differ when compared at target MAPs of 75 and 90 mm Hg (Figure 8)... ANP is ideally suited for treatment of ischemic AKI, as it preferentially dilates the preglomerular resistance vessels; this will increase GFR but also renal blood flow, meeting the increased oxygen demand of the medulla by an increase in renal DO2... Mannitol increases renal blood flow and GFR in clinical ischemic AKI most likely by endothelial and epithelial de-swelling effects.

Show MeSH
Related in: MedlinePlus