AKI, CHD - Congenital Heart Disease, Surgery
Conditions
Brief summary
Acute kidney injury (AKI) following cardiac surgery for congenital heart defects (CHD) in children affects up to 60% of high risk-patients and is a major cause of both short- and long-term morbidity and mortality. Despite effort, to date, no successful therapeutic agent has gained widespread success in preventing this postoperative decline in renal function. Nitric oxide is an intricate regulator of acute inflammation and coagulation and is a potent vasodilator. The investigators hypothesize that nitric oxide, administered during cardiopulmonary bypass (CPB), may reduce the incidence of AKI.
Interventions
DRUGNitric Oxide
gNO will be entrained at 20 ppm into the oxygenator of the CPB circuit
DRUGOxygen
Oxygen alone will be entrained for placebo arm
Sponsors
Children's Hospital Medical Center, Cincinnati
Mallinckrodt
Indiana University
Study design
Allocation
RANDOMIZED
Intervention model
SEQUENTIAL
Primary purpose
PREVENTION
Masking
TRIPLE (Subject, Caregiver, Investigator)
Intervention model description
• This pilot study is a single center, double-blind, randomized controlled trial.
Eligibility
Sex/Gender
ALL
Age
1 Days to 31 Days
Healthy volunteers
No
Inclusion criteria
* All neonates (≤31 days) undergoing cardiac surgery with CPB for CHD will be deemed eligible for enrollment.
Exclusion criteria
1. Failure to obtain informed consent from parent/guardian 2. Clinical signs of preoperative persistent elevated pulmonary vascular resistance, 3. Emergency surgery, 4. Episode of cardiac arrest within 1 week before surgery, 5. Recent treatment with steroids and/or a condition that may require treatment with steroids (excluding steroid administration specifically for CPB), 6. Use of inhaled NO (iNO) immediately prior to surgery, 7. Structural renal abnormalities by ultrasound, 8. Preoperative AKI, 9. Use of other investigational drugs, 10. Weight less than \<2 kg, 11. Gestational age \<36 weeks, 12. Major extracardiac congenital anomalies, 13. Non-English speakers.
Design outcomes
Primary
| Measure | Time frame | Description |
|---|---|---|
| AKI | 72 hours | Incidence of AKI in the first 72 hours postoperative as defined by the Kidney Disease Improving Global Outcomes (KDIGO) diagnostic classification |
Secondary
| Measure | Time frame | Description |
|---|---|---|
| Biomarker evidence of AKI - NGAL | 72 hours | Incidence of structural AKI in the first 72 hours postoperative will be assessed by measurement of urine biomarker neutrophil gelatinase-associated lipocalin (NGAL) |
| Biomarker evidence of AKI - KIM-1 | 72 hours | Incidence of structural AKI in the first 72 hours postoperative will be assessed by measurement of urine biomarker kidney injury molecule-1 (KIM-1) |
| Biomarker evidence of AKI - IL-18 | 72 hours | Incidence of structural AKI in the first 72 hours postoperative will be assessed by measurement of urine biomarker interleukin-18 (IL-18) |
| Biomarker evidence of AKI - L-FABP | 72 hours | Incidence of structural AKI in the first 72 hours postoperative will be assessed by measurement of urine biomarker liver-type fatty acid-binding protein (L-FABP) |
| Biomarker evidence of AKI - urinary nitrite | 72 hours | Incidence of structural AKI in the first 72 hours postoperative will be assessed by measurement of urine biomarker urinary nitrate. |
| Impact on GFR | 72 hours | Postoperative GFR measured using serum cystatin C. |
| Low Cardiac Output | 48 hours | Incidence of low cardiac output syndrome (LCOS) during the first 48 hours postoperative |
Countries
United States
Contacts
CONTACTDavid S Cooepr, MD
Outcome results
None listed