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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

Renal medullary hypoxia may contribute to cardiac surgery-associated acute kidney injury (AKI). However, the effects of cardiopulmonary bypass (CPB) on medullary oxygenation are poorly understood. Here we tested whether CPB causes medullary hypoxia and whether medullary oxygenation during CPB can be improved by increasing pump flow or mean arterial pressure (MAP). Twelve sheep were instrumented to measure whole kidney, medullary, and cortical blood flow and oxygenation. Five days later, under isoflurane anesthesia, CPB was initiated at a pump flow of 80 mL kg-1min-1 and target MAP of 70 mm Hg. Pump flow was then set at 60 and 100 mL kg-1min-1, while MAP was maintained at approximately 70 mm Hg. MAP was then increased by vasopressor (metaraminol, 0.2-0.6 mg/min) infusion at a pump flow of 80 mL kg-1min-1. CPB at 80 mL kg-1min-1 reduced renal blood flow (RBF), -61% less than the conscious state, perfusion in the cortex (-44%) and medulla (-40%), and medullary PO2 from 43 to 27 mm Hg. Decreasing pump flow from 80 to 60 mL kg-1min-1 further decreased RBF (-16%) and medullary PO2 from 25 to 14 mm Hg. Increasing pump flow from 80 to 100 mL kg-1min-1 increased RBF (17%) and medullary PO2 from 20 to 29 mm Hg. Metaraminol (0.2 mg/min) increased MAP from 63 to 90 mm Hg, RBF (47%), and medullary PO2 from 19 to 39 mm Hg. Thus, the renal medulla is susceptible to hypoxia during CPB, but medullary oxygenation can be improved by increasing pump flow or increasing target MAP by infusion of metaraminol.Copyright © 2019 International Society of Nephrology

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

Objectives: Acute kidney injury (AKI) develops in ~30% of patients following cardiac surgery on cardiopulmonary bypass (CPB). There are no interventions to prevent post-operative AKI, because its pathophysiology remains unclear. Our aims are (1) to determine the effects of CPB on the renal macro-and micro-circulation and (2) to determine the effects of altering pump flow on global and regional-kidney perfusion and oxygenation during CPB. Method(s): We implanted a flow probe on the renal artery and laser Doppler/oxygen-sensing probes in the cortex and medulla in sheep (N = 10). After baseline recordings in conscious sheep, animals were anesthetized, then placed on CPB with inspired oxygen fraction (FiO2) maintained at 0.6. From a baseline level of 80 mL/kg/min, pump flow was altered to 60, 80 and 100 mL/kg/min in random order. Result(s): During CPB, renal blood flow (RBF; 287 +/- 21 to 109 +/- 19 mL/ min), medullary perfusion (720 +/- 127 to 222 +/- 42 BPU) and medullary oxygenation (48 +/- 5 to 22 +/- 7 mmHg) were all reduced, compared with conscious sheep. Cortical oxygenation increased during CPB (46 +/- 3 to 70 +/- 17 mmHg), despite reduced perfusion (1954 +/- 378 to 872 +/- 112 BPU). Reducing pump flow exacerbated medullary hypoxia (to 11 +/- 3 mmHg), while increasing pump flow tended to improve medullary oxygenation (to 29 +/- 7 mmHg). Conclusion(s): CPB had detrimental effects on RBF, medullary and cortical perfusion and medullary oxygenation. Cortical oxygenation was maintained by the high FiO2. Medullary hypoxia may be a crucial mediator of post-CPB AKI. Thus, avoiding medullary hypoxia, by optimizing perfusion conditions on CPB, may be a feasible strategy to mitigate post-operative AKI.

Renal medullary hypoxia may contribute to cardiac surgery-associated acute kidney injury (AKI). However, the effects of cardiopulmonary bypass (CPB) on medullary oxygenation are poorly understood. Here we tested whether CPB causes medullary hypoxia and whether medullary oxygenation during CPB can be improved by increasing pump flow or mean arterial pressure (MAP). Twelve sheep were instrumented to measure whole kidney, medullary, and cortical blood flow and oxygenation. Five days later, under isoflurane anesthesia, CPB was initiated at a pump flow of 80 mL kg-1min-1 and target MAP of 70 mm Hg. Pump flow was then set at 60 and 100 mL kg-1min-1, while MAP was maintained at approximately 70 mm Hg. MAP was then increased by vasopressor (metaraminol, 0.2-0.6 mg/min) infusion at a pump flow of 80 mL kg-1min-1. CPB at 80 mL kg-1min-1 reduced renal blood flow (RBF), -61% less than the conscious state, perfusion in the cortex (-44%) and medulla (-40%), and medullary PO2 from 43 to 27 mm Hg. Decreasing pump flow from 80 to 60 mL kg-1min-1 further decreased RBF (-16%) and medullary PO2 from 25 to 14 mm Hg. Increasing pump flow from 80 to 100 mL kg-1min-1 increased RBF (17%) and medullary PO2 from 20 to 29 mm Hg. Metaraminol (0.2 mg/min) increased MAP from 63 to 90 mm Hg, RBF (47%), and medullary PO2 from 19 to 39 mm Hg. Thus, the renal medulla is susceptible to hypoxia during CPB, but medullary oxygenation can be improved by increasing pump flow or increasing target MAP by infusion of metaraminol.Copyright © 2019 International Society of Nephrology

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

Objectives: Acute kidney injury (AKI) develops in ~30% of patients following cardiac surgery on cardiopulmonary bypass (CPB). There are no interventions to prevent post-operative AKI, because its pathophysiology remains unclear. Our aims are (1) to determine the effects of CPB on the renal macro-and micro-circulation and (2) to determine the effects of altering pump flow on global and regional-kidney perfusion and oxygenation during CPB. Method(s): We implanted a flow probe on the renal artery and laser Doppler/oxygen-sensing probes in the cortex and medulla in sheep (N = 10). After baseline recordings in conscious sheep, animals were anesthetized, then placed on CPB with inspired oxygen fraction (FiO2) maintained at 0.6. From a baseline level of 80 mL/kg/min, pump flow was altered to 60, 80 and 100 mL/kg/min in random order. Result(s): During CPB, renal blood flow (RBF; 287 +/- 21 to 109 +/- 19 mL/ min), medullary perfusion (720 +/- 127 to 222 +/- 42 BPU) and medullary oxygenation (48 +/- 5 to 22 +/- 7 mmHg) were all reduced, compared with conscious sheep. Cortical oxygenation increased during CPB (46 +/- 3 to 70 +/- 17 mmHg), despite reduced perfusion (1954 +/- 378 to 872 +/- 112 BPU). Reducing pump flow exacerbated medullary hypoxia (to 11 +/- 3 mmHg), while increasing pump flow tended to improve medullary oxygenation (to 29 +/- 7 mmHg). Conclusion(s): CPB had detrimental effects on RBF, medullary and cortical perfusion and medullary oxygenation. Cortical oxygenation was maintained by the high FiO2. Medullary hypoxia may be a crucial mediator of post-CPB AKI. Thus, avoiding medullary hypoxia, by optimizing perfusion conditions on CPB, may be a feasible strategy to mitigate post-operative AKI.

Renal medullary hypoxia may be a common pathway in the development of acute kidney injury (AKI). There are no validated methods to detect medullary hypoxia in patients. However, experimental findings indicate that changes in urinary oxygen tension (UPO2) reflect changes in medullary PO2. Therefore, we evaluated the relationship between intra-operative UPO2 and the development of AKI after cardiac surgery requiring cardiopulmonary bypass (CPB). From January 2015 to July 2016, thirty-five adult patients undergoing on-pump cardiac surgery were prospectively enrolled. UPO2 was continuously recorded intra-operatively via a fiber-optic probe deployed through the lumen of the urinary catheter, with the end of the probe at the catheter tip, where it was in contact with bladder urine. UPO2 fell during surgery, particularly during CPB. The lowest (nadir) UPO2 was most frequently observed during the rewarming phase of CPB, or shortly after weaning from CPB (n=25, 71%). Fourteen patients (40%) developed AKI as defined by an increase in serum creatinine from baseline of either > 26.5 mumol/L (0.3 mg/dL) within 48 hours or > 50% within 5 days. Nadir intra-operative UPO2 was lower in patients who later developed AKI (8.5 +/- 1.6 mmHg, mean +/- SE) than in those who did not (16.5 +/- 4.2 mmHg, P = 0.02). UPO2 below 10 mmHg at any time during surgery was associated with a 4.5-fold [95% confidence limits 1.6 - 19.1] greater risk of AKI (P = 0.03). Furthermore, urinary PO2 below 15 mmHg for longer than the median time for all patients (5.6 min per hour of surgery) was associated with a 7.3-fold [1.8 - 35.1] greater risk of AKI (P = 0.01) and an area under the receiver operator curve of 0.73 [0.56 - 0.90] (P = 0.03). We conclude that low UPO2 during cardiac surgery requiring CPB is strongly associated with later development of AKI. Continuous intra-operative monitoring of UPO2 is simple and relatively noninvasive. It may provide a real-time biomarker of risk of AKI. Early detection of

Introduction: Anomalous left coronary artery from the pulmonary artery (ALCAPA) is a rare congenital heart defect with limited data on long-term outcomes after surgery. We sought to determine outcomes of patients operated for ALCAPA at the Royal Children's Hospital. Method(s): All patients who underwent repair of ALCAPA were identified from the hospital database and retrospectively reviewed. Result(s): From November 1972 to March 2014, forty four patients were operated for ALCAPA at the Royal Children's Hospital. Median age at operation was 141 days (range 49 days to 26 years) and median weight at operation was 5.8 kilograms (range 2.3 kilograms to 64 kilograms). Four (4/44, 9%) patients had associated anomalies. Twenty nine (29/44, 66%) patients underwent reimplantation technique, 13 (13/ 44, 30%) had intrapulmonary baffle repair (Takeuchi repair) and 2 patients (2/44, 4%) had ligation of the anomalous artery. Eight (8/44, 18%) patients had associated mitral valve (MV) repair and 1 patient (1/44, 3%) had aMV replacement at time of initial surgery. Fifteen (15/44, 34%) patients required left ventricular assistdevice (LVAD) support at the completion of surgery. LVADwas removed at amean 4 days (range 2 days to 8 days) after surgery. Early mortality was 2.3% (1/44). Follow-up was 100% complete for local patients. Mean follow-upwas 12.3 years (range 4months to 31 years). Therewere no late deaths. Survival was 97% at 20 years. Ten patients underwent 13 reoperations at amean 7 years (range 2months to 25 years) after surgery. Freedomfromreoperationwas 81%, 77% and 66% at 5, 10 and 20 years after surgery, respectively. Seven patients underwent late MV repair or replacement at a mean 8 years (range 2 months to 25 years) after surgery. Freedom from late MV repair or replacement was 83%, 83% and 77% at 5, 10 and 20 years after surgery, respectively. Eleven (11/44, 25%) patients had severe mitral regurgitation (MR) preoperatively. Of those 11 patients, 5 (5/11, 45%) had MVrepai

Renal medullary hypoxia may be a common pathway in the development of acute kidney injury (AKI). There are no validated methods to detect medullary hypoxia in patients. However, experimental findings indicate that changes in urinary oxygen tension (UPO2) reflect changes in medullary PO2. Therefore, we evaluated the relationship between intra-operative UPO2 and the development of AKI after cardiac surgery requiring cardiopulmonary bypass (CPB). From January 2015 to July 2016, thirty-five adult patients undergoing on-pump cardiac surgery were prospectively enrolled. UPO2 was continuously recorded intra-operatively via a fiber-optic probe deployed through the lumen of the urinary catheter, with the end of the probe at the catheter tip, where it was in contact with bladder urine. UPO2 fell during surgery, particularly during CPB. The lowest (nadir) UPO2 was most frequently observed during the rewarming phase of CPB, or shortly after weaning from CPB (n=25, 71%). Fourteen patients (40%) developed AKI as defined by an increase in serum creatinine from baseline of either > 26.5 mumol/L (0.3 mg/dL) within 48 hours or > 50% within 5 days. Nadir intra-operative UPO2 was lower in patients who later developed AKI (8.5 +/- 1.6 mmHg, mean +/- SE) than in those who did not (16.5 +/- 4.2 mmHg, P = 0.02). UPO2 below 10 mmHg at any time during surgery was associated with a 4.5-fold [95% confidence limits 1.6 - 19.1] greater risk of AKI (P = 0.03). Furthermore, urinary PO2 below 15 mmHg for longer than the median time for all patients (5.6 min per hour of surgery) was associated with a 7.3-fold [1.8 - 35.1] greater risk of AKI (P = 0.01) and an area under the receiver operator curve of 0.73 [0.56 - 0.90] (P = 0.03). We conclude that low UPO2 during cardiac surgery requiring CPB is strongly associated with later development of AKI. Continuous intra-operative monitoring of UPO2 is simple and relatively noninvasive. It may provide a real-time biomarker of risk of AKI. Early detection of

Introduction: Anomalous left coronary artery from the pulmonary artery (ALCAPA) is a rare congenital heart defect with limited data on long-term outcomes after surgery. We sought to determine outcomes of patients operated for ALCAPA at the Royal Children's Hospital. Method(s): All patients who underwent repair of ALCAPA were identified from the hospital database and retrospectively reviewed. Result(s): From November 1972 to March 2014, forty four patients were operated for ALCAPA at the Royal Children's Hospital. Median age at operation was 141 days (range 49 days to 26 years) and median weight at operation was 5.8 kilograms (range 2.3 kilograms to 64 kilograms). Four (4/44, 9%) patients had associated anomalies. Twenty nine (29/44, 66%) patients underwent reimplantation technique, 13 (13/ 44, 30%) had intrapulmonary baffle repair (Takeuchi repair) and 2 patients (2/44, 4%) had ligation of the anomalous artery. Eight (8/44, 18%) patients had associated mitral valve (MV) repair and 1 patient (1/44, 3%) had aMV replacement at time of initial surgery. Fifteen (15/44, 34%) patients required left ventricular assistdevice (LVAD) support at the completion of surgery. LVADwas removed at amean 4 days (range 2 days to 8 days) after surgery. Early mortality was 2.3% (1/44). Follow-up was 100% complete for local patients. Mean follow-upwas 12.3 years (range 4months to 31 years). Therewere no late deaths. Survival was 97% at 20 years. Ten patients underwent 13 reoperations at amean 7 years (range 2months to 25 years) after surgery. Freedomfromreoperationwas 81%, 77% and 66% at 5, 10 and 20 years after surgery, respectively. Seven patients underwent late MV repair or replacement at a mean 8 years (range 2 months to 25 years) after surgery. Freedom from late MV repair or replacement was 83%, 83% and 77% at 5, 10 and 20 years after surgery, respectively. Eleven (11/44, 25%) patients had severe mitral regurgitation (MR) preoperatively. Of those 11 patients, 5 (5/11, 45%) had MVrepai