Limits...
Renal oxygenation in clinical acute kidney injury.

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

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

Effects of incremental infusion rates of vasopressin (1.2, 2.4 and 4.8 units/hour) on renal blood flow (RBF), glomerular filtration rate (GFR), renal oxygen consumption (RVO2) and renal oxygen extraction (RO2Ex) in post-cardiac surgery patients. Vasopressin causes a constriction of renal efferent arterioles with a decrease in RBF and an increase in GFR and RVO2.Vasopressin impairs the renal oxygen demand/supply relationship as reflected by the increase in RO2 Ex. From [7] with permission.
© Copyright Policy
Related In: Results  -  Collection


getmorefigures.php?uid=PMC3672481&req=5

Figure 9: Effects of incremental infusion rates of vasopressin (1.2, 2.4 and 4.8 units/hour) on renal blood flow (RBF), glomerular filtration rate (GFR), renal oxygen consumption (RVO2) and renal oxygen extraction (RO2Ex) in post-cardiac surgery patients. Vasopressin causes a constriction of renal efferent arterioles with a decrease in RBF and an increase in GFR and RVO2.Vasopressin impairs the renal oxygen demand/supply relationship as reflected by the increase in RO2 Ex. From [7] with permission.

Mentions: Bragadottir et al. evaluated the renal effects of low-doses (1.2, 2.4, 4.8 U/h) of vasopressin in post-cardiac surgery patients, doses that did not affect systemic blood pressure [7]. Vasopressin exerted a dose-dependent increase in GFR, sodium reabsorption, renal VO2, renal O2Ex and renal vascular resistance, whereas renal blood flow decreased. Thus, vasopressin considerably impaired renal oxygenation by postglomerular vasoconstriction, which induced a decrease in renal blood flow and an increase in both GFR and renal VO2 (Figure 9). From a renal point of view, vasopressin should be used with caution in the treatment of vasodilatory shock, because it has the potential to cause considerable renal oxygen supply/demand mismatch.


Renal oxygenation in clinical acute kidney injury.

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

Effects of incremental infusion rates of vasopressin (1.2, 2.4 and 4.8 units/hour) on renal blood flow (RBF), glomerular filtration rate (GFR), renal oxygen consumption (RVO2) and renal oxygen extraction (RO2Ex) in post-cardiac surgery patients. Vasopressin causes a constriction of renal efferent arterioles with a decrease in RBF and an increase in GFR and RVO2.Vasopressin impairs the renal oxygen demand/supply relationship as reflected by the increase in RO2 Ex. From [7] with permission.
© Copyright Policy
Related In: Results  -  Collection

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

Figure 9: Effects of incremental infusion rates of vasopressin (1.2, 2.4 and 4.8 units/hour) on renal blood flow (RBF), glomerular filtration rate (GFR), renal oxygen consumption (RVO2) and renal oxygen extraction (RO2Ex) in post-cardiac surgery patients. Vasopressin causes a constriction of renal efferent arterioles with a decrease in RBF and an increase in GFR and RVO2.Vasopressin impairs the renal oxygen demand/supply relationship as reflected by the increase in RO2 Ex. From [7] with permission.
Mentions: Bragadottir et al. evaluated the renal effects of low-doses (1.2, 2.4, 4.8 U/h) of vasopressin in post-cardiac surgery patients, doses that did not affect systemic blood pressure [7]. Vasopressin exerted a dose-dependent increase in GFR, sodium reabsorption, renal VO2, renal O2Ex and renal vascular resistance, whereas renal blood flow decreased. Thus, vasopressin considerably impaired renal oxygenation by postglomerular vasoconstriction, which induced a decrease in renal blood flow and an increase in both GFR and renal VO2 (Figure 9). From a renal point of view, vasopressin should be used with caution in the treatment of vasodilatory shock, because it has the potential to cause considerable renal oxygen supply/demand mismatch.

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