Relation between mean arterial pressure and renal function in the early phase of shock: a prospective, explorative cohort study

Introduction: Because of disturbed renal autoregulation, patients experiencing hypotension-induced renal insult might need higher levels of mean arterial pressure (MAP) than the 65 mmHg recommended level in order to avoid the progression of acute kidney insufficiency (AKI). Methods: In 217 patients with sustained hypotension, enrolled and followed prospectively, we compared the evolution of the mean arterial pressure (MAP) during the first 24 hours between patients who will show AKI 72 hours after inclusion (AKIh72) and patients who will not. AKIh72 was defined as the need of renal replacement therapy or “Injury” or “Failure” classes of the 5-stage RIFLE classification (Risk, Injury, Failure, Loss of kidney function, End-stage renal disease) for acute kidney insufficiency using the creatinine and urine output criteria. This comparison was performed in four different subgroups of patients according to the presence or not of AKI at the sixth hour after inclusion (AKIh6 as defined as a serum creatinine level above 1.5 times baseline value within the first six hours) and the presence or not of septic shock at inclusion.The ability of MAP averaged over H6 to H24 to predict AKIh72 was assessed by the area under the receiver operating characteristic curve (AUC) and compared between groups. Results: The MAP averaged over H6 to H24 or over H12 to H24 was significantly lower in patients who showed AKIh72 than in those who did not, only in septic shock patients with AKIh6, whereas no link was found between MAP and AKIh72 in the three others subgroups of patients. In patients with septic shock plus AKIh6, MAP averaged over H6 to H24 or over H12 to H24 had an AUC of 0.83 (0.72 to 0.92) or 0.84 (0.72 to 0.92), respectively, to predict AKIh72 . In these patients, the best level of MAP to prevent AKIh72 was between 72 and 82 mmHg. Conclusions: MAP about 72 to 82 mmHg could be necessary to avoid acute kidney insufficiency in patients with septic shock and initial renal function impairment.

We read with interest the paper by Badin and colleagues [1] in a recent issue of Critical Care. Th e paper concerns the relation between arterial pressure and renal function in the early phase of shock. Th e authors found that a threshold of mean arterial pressure (MAP) of 72 to 82 mm Hg could be necessary to avoid acute kidney injury (AKI) in septic shock. Th is result was not found when sepsis was not the cause of shock. Th e authors state that this may be related to the loss of renal autoregulation ability in the early course of sepsis, thus explaining the absence of MAP threshold in non-septic shock. However, human studies on this subject are lacking and this hypothesis remains mainly theoretical.
In this study, a diff erence exits between patients with AKI and those without AKI. Patients with AKI at 6 hours have a signifi cantly higher volume expansion in the last 6 hours before inclusion. Volume expansion (a cornerstone of sepsis treatment) can lead to an increase in abdominal pressure [2]. Th is condition is not infrequent, even among medical patients [3], particularly during early septic shock [4].
Th us, the benefi cial eff ect on renal function of a higher MAP may be linked to the preservation of abdominal perfusion pressure and fi ltration gradient (FG) rather than to the impairment of renal autoregulation. We have shown (though only with pre limi nary results) that even a very moderate elevation of intra-abdominal pressure (IAP) can lead to a signifi cant decrease of FG when the systemic hemodynamic is profoundly altered [5].
Th us, it cannot be excluded that the higher MAP threshold in the septic group is linked to a higher IAP value. Th e relevant goal may be not to aim for a minimal MAP of more than 65 mm Hg to prevent AKI at the early phase of septic shock but to target a suffi cient MAP value to preserve abdominal perfusion pressure and FG by monitoring IAP.

© 2010 BioMed Central Ltd
Relation between mean arterial pressure and renal function in the early phase of shock: a prospective, explorative cohort study

Julie Badin and Thierry Boulain
We thank Dr. Jacobs for his relevant remarks concerning our work [1]. Although we did not measure IAP, we examined the infl uence of the amount of fl uid administered on AKI: the amount of fl uid, administered either before or during the fi rst 72 hours and examined by quartiles, was not linked to the proportion of AKI at 72 hours in the whole population or in patients with sepsis or AKI at 6 hours (P >0.1 in all cases by chi-square test). Furthermore, in the population that Dr. Jacobs refers to (septic shock and initial AKI), the areas under the receiver operating characteristic curve of time-averaged MAP to predict AKI at 72 hours were very similar in patients who received less than 2,000 mL (the median amount of fl uid received) before inclusion and those who received 2,000 mL or more: 0.82 versus 0.86, respectively. Th e best MAP thresholds in the two groups were also similar: 71 versus 73 mm Hg. To explain these results that do not support the hypotheses of a major infl uence of the amount of fl uid received and of the indirect infl uence of IAP, one might argue that (a) the link between fl uids and IAP was not found in all studies [3] and (b) abdominal compartment syndrome secondary to aggressive fl uid therapy often occurs after several days [6]. Finally, we acknowledge that randomized inter ven tional studies are necessary to know whether, in order to prevent AKI, resuscitation of shock should target a fi xed level of MAP or of MAP minus IAP.