Acute Renal Failure is NOT an "Acute Renal Success"
Acute Renal Failure is NOT an "Acute Renal Success"
Objectives: Acute kidney injury occurs frequently after cardiac or major vascular surgery and is believed to be predominantly a consequence of impaired renal oxygenation. However, in patients with acute kidney injury, data on renal oxygen consumption (RVO2), renal blood flow, glomerular filtration, and renal oxygenation, i.e., the renal oxygen supply/demand relationship, are lacking and current views on renal oxygenation in the clinical situation of acute kidney injury are presumptive and largely based on experimental studies.
Design: Prospective, two-group comparative study.
Setting: Cardiothoracic intensive care unit of a tertiary center.
Patients: Postcardiac surgery patients with (n = 12) and without (n = 37) acute kidney injury were compared with respect to renal blood flow, glomerular filtration, RVO2, and renal oxygenation.
Interventions: None
Measurements and Main Results: Data on systemic hemodynamics (pulmonary artery catheter) and renal variables were obtained during two 30-min periods. Renal blood flow was measured using two independent techniques: the renal vein thermodilution technique and the infusion clearance of paraaminohippuric acid, corrected for renal extraction of paraaminohippuric acid. The filtration fraction was measured by the renal extraction of Cr-EDTA and the renal sodium resorption was measured as the difference between filtered and excreted sodium. Renal oxygenation was estimated from the renal oxygen extraction. Cardiac index and mean arterial pressure did not differ between the two groups. In the acute kidney injury group, glomerular filtration (−57%), renal blood flow (−40%), filtration fraction (−26%), and sodium resorption (−59%) were lower, renal vascular resistance (52%) and renal oxygen extraction (68%) were higher, whereas there was no difference in renal oxygen consumption between groups. Renal oxygen consumption for one unit of reabsorbed sodium was 2.4 times higher in acute kidney injury.
Conclusions: Renal oxygenation is severely impaired in acute kidney injury after cardiac surgery, despite the decrease in glomerular filtration and tubular workload. This was caused by a combination of renal vasoconstriction and tubular sodium resorption at a high oxygen demand.
Acute kidney injury (AKI) develops in 5–25% of patients after cardiac and major vascular surgery. Dialysis-dependent AKI in these patients is associated with a mortality of up to 80% and even a minimal increase in serum creatinine after cardiac surgery is associated with a nearly three-fold increase in mortality. The pathogenesis of postoperative AKI is believed to be predominantly a consequence of renal ischemia. The outer portion of the medulla is particularly sensitive to ischemia, as medullary tissue oxygen tension is low because of the high oxygen utilization of the medullary thick ascending limbs of the renal medulla.
It is well known that tubular sodium resorption is a major determinant of renal oxygen consumption (RVO2) and it has been shown that there is a close correlation between glomerular filtration rate (GFR), renal sodium resorption, and RVO2 in postoperative patients. The filtered load of sodium is, thus, an important determinant of RVO2 in man, and maneuvers that decrease GFR and the sodium load to the distal tubules act to decrease medullary sodium resorption and O2 consumption, thereby increasing medullary oxygenation and vice versa. It has provocatively been stated that "acute renal failure is acute renal success", as a reduction in GFR in AKI should lead to a reduction of the renal reabsorptive workload, thus preserving medullary oxygenation with a reduced risk of further aggravation of ischemia.
In patients with AKI, data on RVO2, renal blood flow (RBF), GFR, and renal oxygenation, i.e., the renal oxygen supply-demand relationship, are lacking, and current views on renal oxygenation in the clinical situation of AKI are presumptive and largely based on experimental studies.
We have, therefore, studied patients with AKI after complicated cardiac surgery with respect to their RVO2, RBF, GFR, and renal oxygenation. RBF was assessed by two independent techniques, the retrograde renal vein thermodilution (TD) technique and by infusion clearance (IC) of paraaminohippuric acid (PAH), with correction for renal extraction of PAH. Patients undergoing cardiac surgery with no postoperative renal impairment served as controls. Our null hypothesis was that renal oxygenation is normal in AKI due to proportional reductions in GFR, RBF, and RVO2.
Abstract and Introduction
Abstract
Objectives: Acute kidney injury occurs frequently after cardiac or major vascular surgery and is believed to be predominantly a consequence of impaired renal oxygenation. However, in patients with acute kidney injury, data on renal oxygen consumption (RVO2), renal blood flow, glomerular filtration, and renal oxygenation, i.e., the renal oxygen supply/demand relationship, are lacking and current views on renal oxygenation in the clinical situation of acute kidney injury are presumptive and largely based on experimental studies.
Design: Prospective, two-group comparative study.
Setting: Cardiothoracic intensive care unit of a tertiary center.
Patients: Postcardiac surgery patients with (n = 12) and without (n = 37) acute kidney injury were compared with respect to renal blood flow, glomerular filtration, RVO2, and renal oxygenation.
Interventions: None
Measurements and Main Results: Data on systemic hemodynamics (pulmonary artery catheter) and renal variables were obtained during two 30-min periods. Renal blood flow was measured using two independent techniques: the renal vein thermodilution technique and the infusion clearance of paraaminohippuric acid, corrected for renal extraction of paraaminohippuric acid. The filtration fraction was measured by the renal extraction of Cr-EDTA and the renal sodium resorption was measured as the difference between filtered and excreted sodium. Renal oxygenation was estimated from the renal oxygen extraction. Cardiac index and mean arterial pressure did not differ between the two groups. In the acute kidney injury group, glomerular filtration (−57%), renal blood flow (−40%), filtration fraction (−26%), and sodium resorption (−59%) were lower, renal vascular resistance (52%) and renal oxygen extraction (68%) were higher, whereas there was no difference in renal oxygen consumption between groups. Renal oxygen consumption for one unit of reabsorbed sodium was 2.4 times higher in acute kidney injury.
Conclusions: Renal oxygenation is severely impaired in acute kidney injury after cardiac surgery, despite the decrease in glomerular filtration and tubular workload. This was caused by a combination of renal vasoconstriction and tubular sodium resorption at a high oxygen demand.
Introduction
Acute kidney injury (AKI) develops in 5–25% of patients after cardiac and major vascular surgery. Dialysis-dependent AKI in these patients is associated with a mortality of up to 80% and even a minimal increase in serum creatinine after cardiac surgery is associated with a nearly three-fold increase in mortality. The pathogenesis of postoperative AKI is believed to be predominantly a consequence of renal ischemia. The outer portion of the medulla is particularly sensitive to ischemia, as medullary tissue oxygen tension is low because of the high oxygen utilization of the medullary thick ascending limbs of the renal medulla.
It is well known that tubular sodium resorption is a major determinant of renal oxygen consumption (RVO2) and it has been shown that there is a close correlation between glomerular filtration rate (GFR), renal sodium resorption, and RVO2 in postoperative patients. The filtered load of sodium is, thus, an important determinant of RVO2 in man, and maneuvers that decrease GFR and the sodium load to the distal tubules act to decrease medullary sodium resorption and O2 consumption, thereby increasing medullary oxygenation and vice versa. It has provocatively been stated that "acute renal failure is acute renal success", as a reduction in GFR in AKI should lead to a reduction of the renal reabsorptive workload, thus preserving medullary oxygenation with a reduced risk of further aggravation of ischemia.
In patients with AKI, data on RVO2, renal blood flow (RBF), GFR, and renal oxygenation, i.e., the renal oxygen supply-demand relationship, are lacking, and current views on renal oxygenation in the clinical situation of AKI are presumptive and largely based on experimental studies.
We have, therefore, studied patients with AKI after complicated cardiac surgery with respect to their RVO2, RBF, GFR, and renal oxygenation. RBF was assessed by two independent techniques, the retrograde renal vein thermodilution (TD) technique and by infusion clearance (IC) of paraaminohippuric acid (PAH), with correction for renal extraction of PAH. Patients undergoing cardiac surgery with no postoperative renal impairment served as controls. Our null hypothesis was that renal oxygenation is normal in AKI due to proportional reductions in GFR, RBF, and RVO2.
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