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NDT Advance Access published online on September 3, 2008
Nephrology Dialysis Transplantation, doi:10.1093/ndt/gfn490
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© The Author [2008]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org


Changes in blood pressure before the development of nosocomial acute kidney injury

Yan Lun Liu1, John Prowle2, Elisa Licari2, Shigehiko Uchino3 and Rinaldo Bellomo2

1 Department of Medicine, Queen Elizabeth Hospital, Hong Kong SAR, China 2 Department of Intensive Care, Austin Health, Melbourne, Australia 3 Intensive Care Unit, Department of Anesthesiology, Jikei University School of Medicine, Tokyo, Japan

Correspondence and offprint requests to: Rinaldo Bellomo, Department of Intensive Care, Austin Health, Heidelberg, Victoria 3084, Australia. Tel: +61-3-9496-5992; Fax: +61-3-9496-3932; E-mail: rinaldo.bellomo{at}austin.org.au



   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 References
 
Background. Blood pressure is an important determinant of renal perfusion and acute kidney injury (AKI) is common in hospital patients. However, there is limited knowledge concerning the incidence of relative hypotension prior to its development in general wards.

Methods. We compared blood pressure recordings in a cohort of consecutive patients with no change in renal function to a cohort of patients with acute changes in renal function according to RIFLE classes R, I and F for AKI. We assessed blood pressure over a 3-day period before the development of AKI in index patients and a similar 3-day period in controls. We excluded patients with absolute hypotension [systolic blood pressure (SBP) <90 mmHg].

Results. Patients were old (mean age 76.1 ± 15.1) and mostly female (57.1%). Those who developed AKI had a lower diastolic blood pressure (P = 0.01), a trend towards lower mean arterial pressure (P = 0.077) and a greater decrease in mean systolic (P < 0.0001), mean diastolic (P < 0.0001) and mean arterial pressure (P < 0.0001) compared to controls. On multivariate logistic regression analysis, a decrease in SBP relative to pre-morbid value was a significant independent predictor of the development of AKI and of RIFLE classes I and F (odds ratio 1.084 for every –1 mmHg change in SBP).

Conclusions. Relative hypotension is more common in ward patients who develop nosocomial AKI than in controls. In these patients, a decrease in SBP relative to pre-morbid value is a significant independent predictor of the development of severe AKI.

Keywords: acute kidney injury; acute renal failure; blood pressure; hospital; hypotension



   Introduction
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 Abstract
 Introduction
Methods
 Results
 Discussion
 References
 
Acute kidney injury (AKI) is common in hospital patients [1]. It is associated with a poor outcome [2]. According to the RIFLE criteria [3,4], >20% of patients develop AKI at some stage during hospitalization [1], with increasing mortality in proportion to the loss of renal function [1,5,6].

Blood pressure is a recognized physiological determinant of renal perfusion. Indeed, in many hospital patients, AKI is associated with absolute hypotension and organ dysfunction in the setting of critical illness [7]. In addition, absolute hypotension (defined as a systolic blood pressure, SBP, <90 mmHg [8–12]) has been shown to be associated with the development of AKI in a variety of settings from major surgery to sepsis [8,12–16]. However, in non-critically ill ward patients who develop AKI, such absolute hypotension may not be present. For this reason, such patients appear to develop a type of AKI, which has been recently called ‘normotensive ischaemic acute renal failure’ [17]. Despite the use of this term, no controlled studies exist to determine how many of these patients are truly normotensive in relation to normative data for age and sex or relative to their normal pre-morbid state. This is unfortunate, because an understanding of the possible association between changes in blood pressure and subsequent changes in renal function might assist clinicians in their diagnostic assessment and therapeutic interventions.

Accordingly, we sought to explore the relationship between blood pressure and subsequent renal functional changes in non-critically ill ward patients without absolute hypotension. We did this by performing a retrospective study in a cohort of consecutive hospital patients selected from a large database. We focused on changes in blood pressure and their possible association or lack of association with subsequent changes in kidney function.



   Methods
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 Abstract
 Introduction
 Methods
Results
 Discussion
 References
 
We conducted a retrospective, observational study in selected patients who were admitted to our hospital between January 2000 and December 2002 and who were part of a previously developed database. Data collection and analysis of this purpose were approved by the Human Research Ethics Committee of our institution with waiving of the need for informed consent.

Identification of study patients
We used a previously published and described electronic database with patient hospitalization, laboratory results and discharge records details [1,18]. We excluded patients younger than 15 years of age, on long-term chronic dialysis, admitted to the intensive care unit during hospital stay, developed AKI according to the RIFLE classification system [4,18,19] within 3 days after index admission, with a kidney transplant and with a length of hospital stay <24 h. From the remaining patients, we generated random numbers for each patient and selected 100 patients with lowest number from each of the following categories of renal dysfunction according to the RIFLE classification system [18,19]: (1) no RIFLE evidence of renal dysfunction (control), (2) RIFLE-R (risk), (3) RIFLE-I (injury) and (4) RIFLE-F (failure). We retrieved and reviewed all of these patients’ records. We did this to confirm or refute whether the initial electronic assignment to a RIFLE category from the database by means of the MDRD equation alone was correct.

We refined such patient classification according to a detailed clinical assessment of true pre-morbid creatinine (see below) prior to the index admission (Figure 1). We used the RIFLE GFR criterion alone, as information on the urine output was not available. Changes in serum creatinine were referred to the pre-morbid level, which was defined as that measured at the latest hospital discharge (when available). If there was no previous discharge information available, we used the MDRD equation to estimate the pre-morbid serum creatinine, assuming an average of 75 ml/min in this age group [20]. We recorded the highest category of RIFLE reached during hospitalization for each patient and classified such changes as: (1) preserved function (control) (<1.5-fold increase in serum creatinine), (2) RIFLE-R (1.5-fold increase in serum creatinine), (3) RIFLE-I (twofold increase in serum creatinine) and (4) RIFLE-F (threefold increase in serum creatinine or serum creatinine >400 µmol/l).


Figure 1
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  		Fig. 1 Study profile.

 
This assessment was blinded to and occurred before the collection of any information on blood pressure.

Through this process, using the electronically obtained cohort of 100 patients in each group, we first identified all patients with confirmed RIFLE-F category (see Figure 1). Through the same process, using each 100 patients cohort, we then sought to identify an equal number of patients with confirmed RIFLE-R, RIFLE-I and control patients.

Assessment of blood pressure
Baseline (pre-morbid) blood pressure was defined as that measured at the latest hospital discharge. If no previous discharge information was available, we assumed it to be equivalent to the mean blood pressure of normotensive Caucasians in those patients who were not known to be hypertensive or treated for hypertension [21]. In those patients known to receive treatment for hypertension, we used adjusted published values for such patients [21]. In those patients with a documented history of hypertension but not on treatment at the time of index admission, we used adjusted values for Caucasians as published [21] (Figure 2).


Figure 2
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  		Fig. 2 Flow chart summarizing the assessment of pre-morbid blood pressure as baseline.

 
We hypothesized that there would be a relative change in blood pressure preceding the onset of AKI compared to pre-morbid values. With relevance to clinical practice, we recorded the minimum SBP, diastolic blood pressure (DBP) and mean arterial pressure (MAP) during the first, second and third 24-h periods before the time when the worst category of RIFLE criteria was reached. Any patient found to have a SBP <90 mmHg during this period of observation was excluded from analysis.

Clinical information
We collected patient characteristics including sex, age and co-morbidities. A final diagnosis of the likely aetiology of AKI was made using previously described categories [17]. Patients who likely had low perfusion states, as previously defined [17], were also identified.

Statistical analysis
Normally and non-normally distributed data are presented as mean ± standard deviation (SD) or median with inter-quartile range (IQR), respectively. Across the categories of RIFLE criteria, comparison of nominal data was performed by means of the {chi}2 test or Fisher's exact test as indicated.

We used one-way analysis of variance (ANOVA) and the Kruskal–Wallis test to compare parametric and non-parametric numerical data across all four-study groups. When comparing the differences in blood pressure measurements between one group and each one of the other groups (continuous variables) according to RIFLE criteria (nominal, ordinary variables), we applied repeated measures two-way ANOVA for the initial analysis, and ANOVA with post hoc Bonferroni correction for multiple comparisons.

We also conducted multivariate logistic regression analysis to elucidate the independent risk factors of developing severe AKI (RIFLE-I and RIFLE-F) and to obtain the odd ratios from the b coefficients. We considered variables with a P-value of <0.15 in univariate analyses as potential independent risk factors. They were then entered in a multivariable model.

We determined the sample size of this cohort with an alpha level and a power of 0.05 and 0.8, respectively; we assumed a mean SBP difference of 10 mmHg between controls and patients who developed AKI. The presumed standard deviation of SBP was calculated from the published data [21,22]. We estimated that the minimum number of patients to be included in each category to detect the predefined SBP difference was 37. Data were analysed using SPSS software, version 13 for Windows (SPSS Inc., Chicago, USA).

A P-value < 0.05 was considered statistically significant.



   Results
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 Abstract
 Introduction
 Methods
 Results
Discussion
 References
 
We identified 140 study patients (35 in each cohort). The clinical features and diagnostic categories of these study patients are summarized in Table 1. In Table 2, we present the changes in blood pressure before maximum RIFLE criteria were reached; Table 3 shows the average value for systolic, mean and diastolic blood pressure and their changes relative to pre-morbid values for patients with or without AKI. All but two patients with no AKI (control) had full blood pressure records available 3 days before their worse RIFLE category or their highest serum creatinine. We calculated the mean blood pressure changes by averaging the available data of these two patients. Table 3 shows that patients with AKI had significantly lower DBP (P = 0.010), a trend towards a lower MAP (P = 0.077) and a greater decrease in mean systolic (P < 0.0001), mean diastolic (P < 0.0001) and mean arterial pressure (P < 0.0001) compared to controls. The changes in systolic, mean and diastolic blood pressure over time are shown in Figure 3a–c. These figures illustrate the clear and consistent changes in mean systolic, diastolic and mean blood pressure over time in patients who happen to develop AKI.


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  		Table 1 Baseline characteristics according to severity of acute kidney injurya

 

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  		Table 2 Changes in blood pressure before maximum RIFLE criteria reached

 

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  		Table 3 Mean of minimal systolic blood pressure, diastolic blood pressure and mean arterial pressure and their changes with reference to pre-morbid values over 3 days before the development of acute kidney injury

 

Figure 3
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  		Fig. 3 (a) Systolic blood pressure preceding onset of acute kidney injury with reference to baseline (mean ± standard error of mean); *two-way ANOVA SBP: systolic blood pressure. (b) Diastolic blood pressure preceding onset of acute kidney injury with reference to baseline (mean ± standard error of mean); *two-way ANOVA DBP: diastolic blood pressure. (c) Mean arterial pressure preceding onset of acute kidney injury with reference to baseline (mean ± standard error of mean); *two-way ANOVA MAP: mean arterial pressure.

 
On univariate analysis, we identified several variables as carrying a P < 0.15 when comparing severe AKI (RIFLE-I and RIFLE-F) patients with controls (Table 4). We entered these variables in a predictive model using RIFLE I and F together as the categorical dependent variable. We found that a decrease in SBP relative to pre-morbid value was a significant independent predictor of the development of AKI and of RIFLE class I and F. For every 1 mmHg decrease in SBP, there was a 1.084-fold increase in the odds ratio of developing AKI [95% confidence interval (CI) 1.011–1.163] (Table 5).


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  		Table 4 Univariate analyses of risk factors for acute kidney injury (RIFLE-I and RIFLE-F)

 

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  		Table 5 Multivariable analysis of risk factors associated with the development of acute kidney injury (control versus RIFLE-I+F)

 


   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
References
 
We conducted a controlled retrospective study of non-critically ill patients who developed nosocomial acute kidney injury to assess the relationship between relative hypotension and subsequent changes in kidney function. We categorized these patients according to RIFLE criteria and compared them to a control sample of patients who did not develop any evidence of AKI according to RIFLE criteria. We obtained information about the lowest recorded systolic, mean, diastolic blood pressure for all cohorts in each of the 3 days preceding the development of the highest RIFLE class. We excluded all patients with absolute hypotension (SBP <90 mmHg). We then tested whether such blood pressure values differed between control patients and those who developed AKI. We found that patients who developed AKI were more likely to have relative hypotension (systolic, diastolic and mean arterial pressure) than control patients. We further analysed the temporal relationship between duration of relative hypotension and onset of AKI. We found that most of the patients developed relative hypotension 48 h before the onset of nosocomial AKI (Figure 3a–c). On multivariable analysis, we further found that relative systolic hypotension was independently associated with an increased odds ratio of developing AKI, such that for each 1 mmHg relative decrease in SBP the risk odds ratio increase was 1.084.

There is limited information on blood pressure and its changes in patients who develop AKI in hospital outside of the setting of critical illness or the ICU. Using the key terms ‘hypotension’ or ‘blood pressure’ and ‘acute renal failure’ or ‘acute kidney injury’ or ‘acute kidney failure’ we were only able to identify eight potentially relevant manuscripts [8,9,11–13,16,23,24]. None of these studies, however, discussed the issue under investigation (so-called ‘normotensive’ AKI). If one considers absolute hypotension (SBP <90 mmHg), however, there is evidence that such hypotension is a risk factor for the development of AKI and that it is a commonly encountered problem in elderly patients with AKI [12,25,26], patients with pre-existing renal insufficiency [27,28] and patients with low cardiac output states such as myocardial infarction and congestive cardiac failure [28–30]. In addition, patients who undergo anaesthesia and develop absolute hypotension are also at greater risk of developing AKI [14–16,31–33]. In all of these circumstances, hypotension is defined as a SBP <90 mmHg. In our study, however, we specifically excluded such patients. We did this to explore whether there is still an association between blood pressure and AKI when absolute hypotension is absent, so-called normotensive acute renal failure [17]. We found that patients with AKI had a significant decrease in systolic, diastolic and mean arterial pressure compared to baseline, and relative systolic hypotension was a significant independent predictor of the development of severe AKI (RIFLE-I and RIFLE-F).

Our findings are clinically relevant because of several aspects. First, they suggest that ‘relative hypotension’ may be an independent contributor to the development of AKI in non-critically ill ward patients. Second, as blood pressure can be manipulated with medications, they also suggest that interventions that raise blood pressure to levels at least equal to pre-morbid values may be protective to the kidney in these patients. Third, by highlighting that there is a strong relationship between changes in blood pressure according to pre-morbid values and subsequent renal outcome, they suggest that reliance on blood pressure monitoring without emphasis on pre-morbid state and the concept of relative hypotension, may be physiologically unwise. Importantly, this association was seen at a mean decrease in SBP of 14.4 mmHg, the kind of change that is commonly seen in ward patients and often accepted as normal variation. Also, most of the difference from the control population (similarly somewhat hypotensive during their hospital admission compared to baseline) occurred in the 48 h preceding the development of AKI, thus theoretically providing ample time for therapeutic intervention. Finally, our results emphasize the independent association between the relative decrease in SBP and the development of AKI. We speculate that maintenance of SBP according to pre-morbid values may play an important role in the prevention of AKI. We further speculate that both maintenance of pre-morbid blood pressure levels and timely strategic intervention can be readily applied in clinical practice.

This study has several limitations. First, it is a retrospective, observational, single-centre study with all the inherent limitations of such studies. However, the association between relative hypotension and AKI that emerged, despite the relatively low numbers, was independent and clear. We studied a general ward population from a tertiary hospital in a developed country. Our patients were old (mean age 76.1 years), had multiple co-morbidities such as diabetes (19.3%), hypertension (47.9%) and chronic kidney disease (62.9%). From previous studies, such patients may be particularly prone to develop AKI especially following sustained hypotension [12,25,26]. Accordingly, our findings do not apply to younger and healthier patients with normal or near normal baseline renal function. However, patients such as those described in this study are now extremely common, if not typical, in hospitals from developed countries. These are the very patients who, because of their physiological fragility, may be particularly exposed to the renal consequences of relative hypotension. Our results clearly illustrate that relative hypotension may play a key role in the development of AKI, especially in elderly with multiple co-morbidities. We speculate that return of these patients blood pressure to pre-morbid levels may be beneficial. Despite such speculations, our study only demonstrates an association between relative hypotension and AKI. This association cannot be taken to indicate that relative hypotension is responsible for the development of AKI. In fact such hypotension may simply be an epiphenomenon and represent a parallel physiological change due to the underlying condition that causes both AKI and hypotension itself. Only randomized interventional studies can address the nature of this relationship. We note, however, that such studies are only justified if observational investigations such as ours or, preferably, future prospective observational studies in other centres confirm this association. We also note that this association carries significant biological plausibility.

In conclusion, we conducted a controlled retrospective study of non-critically ill patients who developed nosocomial acute kidney injury and found that patients who developed AKI were more likely to have relative decreases in systolic, diastolic and mean arterial pressure than control patients. On multivariable analysis, we further found that relative systolic hypotension was independently associated with an increased odds ratio of developing AKI. These preliminary observations justify further observational studies of this issue in other geographical and organizational settings.

Conflict of interest statement. None declared.



   References
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 

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Received for publication: 13. 5.08
Accepted in revised form: 6. 8.08


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