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Summary: Acute kidney injury is a common complication after cardiac surgery that is associated with high postoperative morbidity and mortality. Levels of hemolysis are associated closely with the incidence and severity of kidney injury after cardiac surgery. Hemolysis is caused by prolonged surgical procedures and blood transfusions from cell-saver devices and is associated with the use of cardiopulmonary bypass. Plasma oxyhemoglobin is released into the circulation by damaged red blood cells that, via a dioxygenation reaction, depletes vascular nitric oxide (NO), a potent vasodilator molecule responsible for modulating organ perfusion and vascular homeostasis. Depleted plasma NO and increased levels of plasma oxyhemoglobin in the bloodstream lead to impairment of organ perfusion, inflammation, oxidative stress, and direct tubular injury, which, together, contribute to the development of renal injury after cardiac surgery. The administration of NO, a gas originally approved to treat pulmonary hypertension, maintains organ perfusion by preventing vascular NO depletion. In addition, this treatment improves cardiac output by reducing pulmonary vascular resistance and right heart workload. The clinical evidence of renal protection of NO gas therapy is supported by preclinical animal studies exploring the extrapulmonary protective effects of NO. Recent clinical trials showed a significant reduction of postoperative acute kidney injury when NO gas was administered during and after cardiac surgery.

Background: The most common complication associated with prolonged duration cardiopulmonary bypass (CPB) is acute kidney injury (AKI), which markedly increases the mortality rate. Rationale: Prolonged CPB causes hemolysis with high levels of circulating plasma hemoglobin (Hb). Plasma Hb scavenges Nitric Oxide (NO) via the dioxygenation reaction, depleting endogenous NO and causing vasoconstriction, proximal renal tubular injury and AKI. Hypothesis: Exposure to NO during and after CPB protects the kidney, by three possible mechanisms: 1. Selective vasodilation of the pulmonary circulation leading to increased cardiac output and renal perfusion. 2. Reduction of ischemia-reperfusion renal injury and 3. Oxidation of plasma Hb to metHb, which cannot scavenge NO. Study Design: A single center, prospective, randomized, double blind controlled trial comparing treatment with 80 part per million (ppm) NO (NO group) versus N2 (N2 group). Study gas was given via the gas exchanger during CPB and by inhalation for 24h post-operatively in adults. Study Population: 217 consenting adults with normal kidney function undergoing elective multiple valve replacement surgery with CPB. Study Objective: To determine whether NO reduces AKI (primary outcome), and other major complications immediately post-surgery, at 30 days, and 90 days (secondary outcomes). AKI was defined as either an increase of serum creatinine by 50% within 7 days after surgery, or an increase of serum creatinine by 0.3 mg/dl within 48 hrs. Preliminary results: are summarized in the tables 1, 2, 3 and 4. Conclusions: I) Administration of 80ppm NO for 24 hours was safe. Blood metHb was always below 10%. II) NO decreased the incidence of AKI from 63% to 50% (p=0.04, primary endpoint achieved).

Background: The most common complication associated with prolonged duration cardiopulmonary bypass (CPB) is acute kidney injury (AKI), which markedly increases the mortality rate. Rationale: Prolonged CPB causes hemolysis with high levels of circulating plasma hemoglobin (Hb). Plasma Hb scavenges Nitric Oxide (NO) via the dioxygenation reaction, depleting endogenous NO and causing vasoconstriction, proximal renal tubular injury and AKI. Hypothesis: Exposure to NO during and after CPB protects the kidney, by three possible mechanisms: 1. Selective vasodilation of the pulmonary circulation leading to increased cardiac output and renal perfusion. 2. Reduction of ischemia-reperfusion renal injury and 3. Oxidation of plasma Hb to metHb, which cannot scavenge NO. Study Design: A single center, prospective, randomized, double blind controlled trial comparing treatment with 80 part per million (ppm) NO (NO group) versus N2 (N2 group). Study gas was given via the gas exchanger during CPB and by inhalation for 24h post-operatively in adults. Study Population: 217 consenting adults with normal kidney function undergoing elective multiple valve replacement surgery with CPB. Study Objective: To determine whether NO reduces AKI (primary outcome), and other major complications immediately post-surgery, at 30 days, and 90 days (secondary outcomes). AKI was defined as either an increase of serum creatinine by 50% within 7 days after surgery, or an increase of serum creatinine by 0.3 mg/dl within 48 hrs. Preliminary results: are summarized in the tables 1, 2, 3 and 4. Conclusions: I) Administration of 80ppm NO for 24 hours was safe. Blood metHb was always below 10%. II) NO decreased the incidence of AKI from 63% to 50% (p=0.04, primary endpoint achieved).

We report a case of a young man with hypoplastic right ventricle, who presented with recurrent untreatable arrhythmias after a Bjork Fontan procedure in infancy. He underwent one-and-a-half ventricle repair as an alternative surgery to Fontan revision. doi: 10.1111/jocs.12410 (J Card Surg 2014;29:832-835)