Hemolysis and Kidney Injury in Cardiac Surgery: The Protective Role of Nitric Oxide Therapy.

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.