**5. Renal protection**

The sensibility of kidneys to ischemic insults can culminate in acute kidney injury (AKI), more common in large surgeries and where extensive bleeding is present, especially if associated with hemodynamic instability, and is an independent risk factor for hospital mortality(92). Although acute renal failure requiring renal replacement therapy after cardiac surgery is rare, it has a devastating impact on outcome(93).

The incidence of postoperative AKI involves multifactorial mechanism, including hemodynamic, inflammatory and nephrotoxic factors(94). The risk factors for post-operative renal injury include increased intra-abdominal pressure, hyperglycemia, inadequate maintenance of the intravascular volume, the use of nephrotoxic drugs (i.e. radiologic contrast), duration of the CPB, and postoperative drugs(95). Also, the inflammatory response associated with the surgery, the formation oxygen-reactive species, and immune response can promote renal injury(96).

Some strategies have been suggested to prevent AKI in perioperative setting. Hypovolemia is attributed as an important risk factor for AKI and fluid therapy is implicated in diminishing the incidence of renal dysfunction, although no controlled randomized trial has directly addressed this issue(96). Currently, restrictive fluid replacement, based on goals rather than pre-defined values appear to reduce morbidity following colorectal surgery. One strategy based therapy is associated with the use of esophageal Doppler, using corrected flow time in the descending aorta and stroke volume response to a fluid challenge(97, 98). Intraoperative intravascular volume loading to optimize stroke volume is associated with a more rapid postoperative recovery and a reduced hospital stay(98). The recommendation for fluid resuscitation is to avoid 10% hydroxyl-ethyl starch 250/0.5, strategies for patients with risk of contrast nephropathy (listed below), prophylactic volume expansion with crystalloids to prevent AKI, especially with known nephrotoxic drugs(99). Also, based on the same Joannidis et al. recommendations, loop diuretics should not be used to prevent AKI(99).

Iodinated contrast has also been associated with AKI. Currently, N-Acetylcysteine and isotonic intravenous bicarbonate have been investigated, but the data supporting these interventions are controversial mainly due to methodological limitations(100). Atrial natriuretic peptide, statins and prostaglandin analogs are under study and there are some evidence of their benefit, but no large, adequately power study is present(100). Currently no grade IA recommendation exists regarding renal protection to iodinated contrasts. Prophylactic volume expansion without hydroxy-ethyl starch and sodium bicarbonate for emergency procedures appears to be beneficial in patients at risk of contrast nephropathy(99).

Pharmacological interventions, such as the use of fenoldopam, are currently under study, but large trials with adequate power are still needed in order to recommend the routine for prevention of renal failure. Atrial natriuretic peptide (ANP) is another drug implicated in renal protection, and low doses of ANP can provide better outcomes when used in low doses in the prevention of AKI and in the postsurgery management(96, 101). Inhalational and intravenous anesthetics can also have effects on renal protection(102). When comparing propofol and sevoflurane, propofol was associated with renal protection during an episode of ischemia and reperfusion in a swine model with lower levels of plasma creatinine(103). Also, lower neutrophil infiltrates, plasmatic cytokines, free radical production, lipid peroxidation and inducible nitric oxide synthase activity were found when propofol was used, suggesting a possible renal protection(103).

In conclusion, only a few recommendations exist regarding renal protection. Most of them are common sense based, maintaining adequate blood pressure, fluid therapy and avoiding the use of nephrotoxic drugs(99, 102).
