The development of acute kidney injury (AKI) is a major cause of increased morbidity and mortality rates after cardiac surgery. AKI after cardiac surgery is associated with the initiation of renal replacement therapy and an increased incidence of gastrointestinal bleeding, respiratory infections, and sepsis.43,44 In this setting, postoperative AKI leads to increased intensive care and hospital length of stay. Preventative strategies focus on preoperative optimization of renal function, judicious perioperative fluid balance, and "renoprotective" pharmacologic agents. These strategies appear to have only limited benefit because the incidence of postoperative renal failure has remained constant over the last two decades. Nevertheless, considerable research has been marshaled to protect the kidneys during the high-risk perioperative period when the kidney is placed at risk through preexisting impairment, nephrotoxins, renal ischemia, and the inflammatory process.
Several patient-specific risk factors are associated with the development of renal dysfunction after cardiac surgery: female gender, age, hypertension, diabetes mellitus, ventricular dysfunction, left main coronary artery disease, chronic obstructive pulmonary disease, sepsis, hepatic failure, and chronic kidney disease (CKD).45 Because CKD also has various definitions, the association between preoperative CKD and postoperative renal injury is difficult to quantify accurately. Nevertheless, there is no doubt that the correlation is strong.46-48 Recently, pulse pressure hypertension has been shown to precipitate worsening renal function in the setting of cardiac surgery.49 Interestingly, there appears to be a complex relationship between apolipoprotein E (ApoE) and postoperative AKI. ApoE polymorphisms, although associated with atherosclerotic disease, may confer a degree of renal protection.50,51
Controversial procedure-related risk factors associated with kidney injury in the setting of cardiac surgery include length of CPB, cross-clamp time, off-pump versus on-pump, nonpulsatile flow, hemolysis, and hemodilution.45 The occurrence, alone or in combination, of compromised hemodynamics, surgery, nephrotoxins, or an inflammatory process from CPB may precipitate perioperative AKI, particularly in the patient predisposed by preexisting renal insufficiency or a genetic predisposition. Although the renal medulla receives the minority of renal blood flow, the medullary process of urinary concentration has a high metabolic requirement. Any compromise to renal blood flow increases the regional perfusion imbalance and renders the medulla ischemic. Compromise may result from aortic occlusion, atheromatous embolism, hypotension, low blood flow states, and hypovolemia. Ultimately the pathophysiologic lesion characterizing the AKI of the perioperative cardiac period may be acute tubular necrosis.45
CPB and the interaction between blood components and the extracorporeal circuit can diminish renal blood flow through the release of vasoconstrictive compounds. It is important to note, however, that the development of AKI after cardiac surgery appears to vary with the type of surgery. Patients undergoing coronary artery bypass grafting (CABG) have the lowest incidence of injury followed by those undergoing valvular surgery. The highest incidence of renal dysfunction occurs in patients undergoing combined CABG and valvular surgery.45,52