Search

Introduction: Urinary oxygen tension (PO2) may provide a useful estimate of renal medullary PO2 and thus risk of acute kidney injury (AKI). However, the relationship between urinary PO2 and medullary PO2 could be confounded by variations in urine flow and arterial PO2. In the current study we exploited data we had previously generated, from experimental studies in ovine septic AKI and in patients undergoing cardiac surgery requiring cardiopulmonary bypass (CPB), to perform a detailed analysis of the influences of urine flow and arterial PO2 on urinary PO2. We also investigated the potential for simultaneous measurement of urine flow and urinary PO2, during CPB, to improve prediction of AKI over that provided by measurement of each variable on its own. Method(s): In ovine septic AKI urine flow, urinary PO2, arterial PO2, and medullary PO2 were measured. In human patients undergoing cardiac surgery requiring CPB urinary PO2 and arterial PO2 were measured continuously and urine flow was estimated every 5 minutes. Result(s): In 28 conscious septic sheep breathing room air, urinary PO2 was more closely correlated with medullary PO2 (r2=0.29) than with arterial PO2 (r2=0.06) or urine flow (r2=0.03). The difference between medullary PO2 and urinary PO2 varied little with urine flow or arterial PO2. In 20 patients, urine flow increased abruptly from 2.81 +/- 0.24 mL/min to 6.53 +/- 0.30 mL/min upon commencement of CPB, usually coincident with a fall in urinary PO2 (Fig. 1). During hyperoxic CPB high values of urinary PO2 were often observed at low urine flow. In 65 patients, low urinary PO2 during CPB (<10 mmHg at any time during CPB) was associated with greater (4.5-fold) risk of AKI. However, the level of urine flow on bypass was not significantly associated with risk of AKI. [Figure presented] Conclusion(s): We developed a method for virtually continuous measurement of urine flow in the operating theatre. We found that urinary PO2 provides a relatively robust estimate of

Introduction: Renal medullary hypoxia may be a pathophysiological factor in cardiac surgery-associated acute kidney injury. However, the effects of cardiopulmonary bypass (CPB) on oxygenation of the renal medulla remain poorly understood. Furthermore, whether increased pump flow or arterial pressure can improve renal medullary oxygenation has not been determined. Therefore, in the current study we tested whether CPB causes medullary hypoxia and whether medullary oxygenation during CPB varies with pump flow and mean arterial pressure. Method(s): Twelve sheep were instrumented to allow measurement of whole kidney, medullary and cortical blood flow and oxygenation. The experiment was performed five days later, under isoflurane anesthesia. Sheep were first placed on CPB at a pump flow of 80 mL/kg/min and a target mean arterial pressure of 70 mmHg. Pump flow was then set at 60 and 100 mL/kg/min while mean arterial pressure was maintained at ~70 mmHg. Mean arterial pressure was then increased by infusion of metaraminol (0.2 mg/min) at a set pump flow of 80 mL/kg/min. Result(s): Transition to CPB at a pump flow of 80 ml/kg/min was associated with reduced total renal blood flow (RBF, -61% less than the conscious state), along with reduced perfusion in the cortex (-44%) and medulla (-40%), and reduced medullary PO2 (from 43 to 21 mmHg; Figure) but not cortical PO2. Changes in pump flow and arterial pressure were associated with changes in medullary PO2 (Figure). That is, decreasing pump flow from 80 to 60 mL/kg/min further decreased RBF (-16%) and medullary PO2 (to 14 mmHg). Increasing pump flow from 80 to 100 mL/kg/min increased RBF (17%) and medullary PO2 (to 29 mmHg). Metaraminol (0.2 mg/min) increased mean arterial pressure (from 63 to 90 mmHg), RBF (47%) and medullary PO2 (from 19 to 39 mmHg). [Figure presented] Conclusion(s): The renal medulla appears to be more susceptible to hypoxia during CPB than the renal cortex. However, medullary oxygenation can be improved by i

Introduction: Continuous measurement of bladder urinary oxygen tension (PO2) may provide a real-time surrogate measure of oxygenation in the renal medulla. Therefore, urinary PO2 may be a useful tool for early prediction of acute kidney injury (AKI) and potentially also the management of renal oxygenation in patients with AKI. We examined the relationship between urinary PO2, measured in the intensive care unit (ICU), and development of AKI in patients who had undergone cardiac surgery requiring cardiopulmonary bypass (CPB). Method(s): In 74 patients undergoing on-pump cardiac surgery, bladder urinary PO2 was measured continuously in the ICU using a fibre optic probe placed in the patient's bladder catheter. AKI was diagnosed by modified 'Kidney Disease: Improving Global Outcomes' (KDIGO) criteria, excluding the urine flow criterion. Result(s): Twenty-eight out of 74 patients (37.8%) developed post-operative AKI (18 Stage 1, 7 Stage 2, and 3 Stage 3). The median time to first diagnosis of AKI, using serum creatinine, was 16.9 hours after entry into the ICU (interquartile range (IQR): 13, 32 h). The median duration of monitoring of urinary PO2 was 37.8 hours (IQR: 24.0, 47.3 h). During the first 3 hours after arrival in the ICU, overall mean urinary PO2 (AKI: 19.4 +/- 9.3 vs. non-AKI: 25.3 +/- 9.7 mmHg, p = 0.01), and the nadir (lowest recorded) urinary PO2 (AKI: 12.1 +/- 6.8 vs. non-AKI: 16.0 +/- 5.7 mmHg, p = 0.01) were lower in patients who developed AKI than those who did not. Furthermore, within the first 3 hours of entry to the ICU, 17 of the 28 patients (61%) who developed AKI had urinary PO2 less than or equal to 15 mmHg while this threshold was only reached in 16 of the 46 patients (35%) who did not develop AKI. Patients who developed AKI also experienced longer periods with urinary PO2 less than or equal to 15 mmHg (median time of 10.9 min per hour of measurement) than those who did not (median 0.0 min per hour), p = 0.01. If urinary PO2 fell to 10 mmHg or

Introduction: Continuous measurement of urinary oxygen tension (PO2) in patients undergoing cardiac surgery may allow prediction of post-operative acute kidney injury (AKI). The predictive efficacy of urinary PO2 may be because it provides a good estimate of renal medullary PO2. Medications given during the perioperative period, particularly diuretics, could potentially alter medullary and/or urinary PO2. Thus, administration of furosemide may reduce the utility of urinary PO2 in predicting AKI. Therefore, we tested the effects of furosemide on urinary PO2 in patients recovering in the intensive care unit (ICU) after open heart surgery requiring cardiopulmonary bypass. Method(s): Bladder urinary PO2 was measured using a fibre optic probe, placed in the patient's bladder catheter at the time of induction of anaesthesia in the operating theatre. Urinary PO2 was measured in the ICU in 66 patients for up to 48 h (mean +/- SEM 38.9 +/- 2.6 h) after admission to the ICU. Of these, 39 patients received a bolus intravenous dose of furosemide (10-80 mg). Result(s): Urine flow in the hour before furosemide administration averaged 0.83 +/- 0.11 mL/min (mean +/- SEM) in the 23 patients who did not develop AKI during the five days after surgery (KDIGO criteria excluding urine flow criterion) and 0.57 +/- 0.11 mL/min in the 16 patients who did develop AKI (Figure 1A). In the two hours following administration of furosemide, urine flow increased to 2.10 +/- 0.37 mL/min in patients who did not develop AKI, and 1.97 +/- 0.44 mL/min in patients who did develop AKI. Urinary PO2 before administration of furosemide was lower in patients who developed AKI (20.2 +/- 2.0 mmHg) than those who did not (26.3 +/- 2.6 mmHg) (Figure 1B). Urinary PO2 did not change significantly in the first two hours following administration of furosemide in patients who did develop AKI (21.9 +/- 2.3 mmHg), or in patients who did not develop AKI (25.9 +/- 1.8 mmHg). There was also no significant relationship bet

Introduction: Renal medullary hypoxia may be a pathophysiological factor in cardiac surgery-associated acute kidney injury. However, the effects of cardiopulmonary bypass (CPB) on oxygenation of the renal medulla remain poorly understood. Furthermore, whether increased pump flow or arterial pressure can improve renal medullary oxygenation has not been determined. Therefore, in the current study we tested whether CPB causes medullary hypoxia and whether medullary oxygenation during CPB varies with pump flow and mean arterial pressure. Method(s): Twelve sheep were instrumented to allow measurement of whole kidney, medullary and cortical blood flow and oxygenation. The experiment was performed five days later, under isoflurane anesthesia. Sheep were first placed on CPB at a pump flow of 80 mL/kg/min and a target mean arterial pressure of 70 mmHg. Pump flow was then set at 60 and 100 mL/kg/min while mean arterial pressure was maintained at ~70 mmHg. Mean arterial pressure was then increased by infusion of metaraminol (0.2 mg/min) at a set pump flow of 80 mL/kg/min. Result(s): Transition to CPB at a pump flow of 80 ml/kg/min was associated with reduced total renal blood flow (RBF, -61% less than the conscious state), along with reduced perfusion in the cortex (-44%) and medulla (-40%), and reduced medullary PO2 (from 43 to 21 mmHg; Figure) but not cortical PO2. Changes in pump flow and arterial pressure were associated with changes in medullary PO2 (Figure). That is, decreasing pump flow from 80 to 60 mL/kg/min further decreased RBF (-16%) and medullary PO2 (to 14 mmHg). Increasing pump flow from 80 to 100 mL/kg/min increased RBF (17%) and medullary PO2 (to 29 mmHg). Metaraminol (0.2 mg/min) increased mean arterial pressure (from 63 to 90 mmHg), RBF (47%) and medullary PO2 (from 19 to 39 mmHg). [Figure presented] Conclusion(s): The renal medulla appears to be more susceptible to hypoxia during CPB than the renal cortex. However, medullary oxygenation can be improved by i

Introduction: Urinary oxygen tension (PO2) may provide a useful estimate of renal medullary PO2 and thus risk of acute kidney injury (AKI). However, the relationship between urinary PO2 and medullary PO2 could be confounded by variations in urine flow and arterial PO2. In the current study we exploited data we had previously generated, from experimental studies in ovine septic AKI and in patients undergoing cardiac surgery requiring cardiopulmonary bypass (CPB), to perform a detailed analysis of the influences of urine flow and arterial PO2 on urinary PO2. We also investigated the potential for simultaneous measurement of urine flow and urinary PO2, during CPB, to improve prediction of AKI over that provided by measurement of each variable on its own. Method(s): In ovine septic AKI urine flow, urinary PO2, arterial PO2, and medullary PO2 were measured. In human patients undergoing cardiac surgery requiring CPB urinary PO2 and arterial PO2 were measured continuously and urine flow was estimated every 5 minutes. Result(s): In 28 conscious septic sheep breathing room air, urinary PO2 was more closely correlated with medullary PO2 (r2=0.29) than with arterial PO2 (r2=0.06) or urine flow (r2=0.03). The difference between medullary PO2 and urinary PO2 varied little with urine flow or arterial PO2. In 20 patients, urine flow increased abruptly from 2.81 +/- 0.24 mL/min to 6.53 +/- 0.30 mL/min upon commencement of CPB, usually coincident with a fall in urinary PO2 (Fig. 1). During hyperoxic CPB high values of urinary PO2 were often observed at low urine flow. In 65 patients, low urinary PO2 during CPB (<10 mmHg at any time during CPB) was associated with greater (4.5-fold) risk of AKI. However, the level of urine flow on bypass was not significantly associated with risk of AKI. [Figure presented] Conclusion(s): We developed a method for virtually continuous measurement of urine flow in the operating theatre. We found that urinary PO2 provides a relatively robust estimate of

Introduction: Continuous measurement of bladder urinary oxygen tension (PO2) may provide a real-time surrogate measure of oxygenation in the renal medulla. Therefore, urinary PO2 may be a useful tool for early prediction of acute kidney injury (AKI) and potentially also the management of renal oxygenation in patients with AKI. We examined the relationship between urinary PO2, measured in the intensive care unit (ICU), and development of AKI in patients who had undergone cardiac surgery requiring cardiopulmonary bypass (CPB). Method(s): In 74 patients undergoing on-pump cardiac surgery, bladder urinary PO2 was measured continuously in the ICU using a fibre optic probe placed in the patient's bladder catheter. AKI was diagnosed by modified 'Kidney Disease: Improving Global Outcomes' (KDIGO) criteria, excluding the urine flow criterion. Result(s): Twenty-eight out of 74 patients (37.8%) developed post-operative AKI (18 Stage 1, 7 Stage 2, and 3 Stage 3). The median time to first diagnosis of AKI, using serum creatinine, was 16.9 hours after entry into the ICU (interquartile range (IQR): 13, 32 h). The median duration of monitoring of urinary PO2 was 37.8 hours (IQR: 24.0, 47.3 h). During the first 3 hours after arrival in the ICU, overall mean urinary PO2 (AKI: 19.4 +/- 9.3 vs. non-AKI: 25.3 +/- 9.7 mmHg, p = 0.01), and the nadir (lowest recorded) urinary PO2 (AKI: 12.1 +/- 6.8 vs. non-AKI: 16.0 +/- 5.7 mmHg, p = 0.01) were lower in patients who developed AKI than those who did not. Furthermore, within the first 3 hours of entry to the ICU, 17 of the 28 patients (61%) who developed AKI had urinary PO2 less than or equal to 15 mmHg while this threshold was only reached in 16 of the 46 patients (35%) who did not develop AKI. Patients who developed AKI also experienced longer periods with urinary PO2 less than or equal to 15 mmHg (median time of 10.9 min per hour of measurement) than those who did not (median 0.0 min per hour), p = 0.01. If urinary PO2 fell to 10 mmHg or

Introduction: Continuous measurement of urinary oxygen tension (PO2) in patients undergoing cardiac surgery may allow prediction of post-operative acute kidney injury (AKI). The predictive efficacy of urinary PO2 may be because it provides a good estimate of renal medullary PO2. Medications given during the perioperative period, particularly diuretics, could potentially alter medullary and/or urinary PO2. Thus, administration of furosemide may reduce the utility of urinary PO2 in predicting AKI. Therefore, we tested the effects of furosemide on urinary PO2 in patients recovering in the intensive care unit (ICU) after open heart surgery requiring cardiopulmonary bypass. Method(s): Bladder urinary PO2 was measured using a fibre optic probe, placed in the patient's bladder catheter at the time of induction of anaesthesia in the operating theatre. Urinary PO2 was measured in the ICU in 66 patients for up to 48 h (mean +/- SEM 38.9 +/- 2.6 h) after admission to the ICU. Of these, 39 patients received a bolus intravenous dose of furosemide (10-80 mg). Result(s): Urine flow in the hour before furosemide administration averaged 0.83 +/- 0.11 mL/min (mean +/- SEM) in the 23 patients who did not develop AKI during the five days after surgery (KDIGO criteria excluding urine flow criterion) and 0.57 +/- 0.11 mL/min in the 16 patients who did develop AKI (Figure 1A). In the two hours following administration of furosemide, urine flow increased to 2.10 +/- 0.37 mL/min in patients who did not develop AKI, and 1.97 +/- 0.44 mL/min in patients who did develop AKI. Urinary PO2 before administration of furosemide was lower in patients who developed AKI (20.2 +/- 2.0 mmHg) than those who did not (26.3 +/- 2.6 mmHg) (Figure 1B). Urinary PO2 did not change significantly in the first two hours following administration of furosemide in patients who did develop AKI (21.9 +/- 2.3 mmHg), or in patients who did not develop AKI (25.9 +/- 1.8 mmHg). There was also no significant relationship bet