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Sepsis and septic shock are major contributing factors to AKI7 and vasopressor requirement appears to be highly associated with AKI in this population. Despite the high prevalence of AKI during critical illness in general, and severe sepsis specifically, success has been limited in improving the outcome of this complication.104 Septic shock is the prototype of a high output–low resistance condition, although severe pancreatitis, anaphylaxis, burns, and liver failure share similar physiologic alterations. Persistent hypotension, despite ongoing aggressive fluid resuscitation or after optimization of intravascular volume in patients with shock, places patients at risk for development of AKI. In the setting of vasomotor paralysis, preservation or improvement of renal perfusion can only be achieved through use of systemic vasopressors once intravascular volume has been restored.105
It is not known which vasopressor agent is most effective for prevention or treatment of patients with AKI and septic shock. Most studies have focused on norepinephrine, dopamine, or vasopressin. Small open-label studies have shown improvement in creatinine clearance (CrCl) following a 6- to 8-hour infusion of norepinephrine106 or terlipressin,107 while vasopressin reduced the need for norepinephrine and increased urine output and CrCl.108 A large RCT109 comparing dopamine to norepinephrine as initial vasopressor in patients with shock showed no significant differences between groups with regard to renal function or mortality. However, there were more arrhythmic events among the patients treated with dopamine than among those treated with norepinephrine, and a subgroup analysis showed that dopamine was associated with an increased rate of death at 28 days among the patients with cardiogenic shock, but not among the patients with septic shock or those with hypovolemic shock. Thus, although there was no difference in primary outcome with dopamine as the first-line vasopressor agent and those who were treated with norepinephrine, the use of dopamine was associated with a greater number of adverse events.109
Vasopressin is gaining popularity in the treatment of shock refractory to norepinephrine.110 Compared to norepinephrine, it increases blood pressure and enhances dieresis, but has not as yet been proven to enhance survival nor to reduce the need for RRT.111 A recent posthoc analysis of the above mentioned RCT used the RIFLE criteria for AKI to compare the effects of vasopressin vs. norepinephrine.112 In patients in the RIFLE-R category, vasopressin as compared to norepinephrine was associated with a trend to a lower rate of progression to F or L categories respectively, and a lower rate of use of RRT. Mortality rates in the R category patients treated with vasopressin compared to norepinephrine were 30.8 vs. 54.7%, P = 0.01, but this did not reach significance in a multiple logistic regression analysis. This study suggests thus that vasopressin may reduce progression to renal failure and mortality in patients at risk of kidney injury who have septic shock. The Work Group concluded that current clinical data are insufficient to conclude that one vasoactive agent is superior to another in preventing AKI, but emphasized that vasoactive agents should not be withheld from patients with vasomotor shock over concern for kidney perfusion. Indeed, appropriate use of vasoactive agents can improve kidney perfusion in volume-resuscitated patients with vasomotor shock.
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