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Neurocrit Care (2015) 22:184–191

DOI 10.1007/s12028-014-0067-8


Hypernatremia is a Significant Risk Factor for Acute Kidney
Injury After Subarachnoid Hemorrhage: A Retrospective
Avinash B. Kumar • Yaping Shi • Matthew S. Shotwell
Justin Richards • Jesse M. Ehrenfeld

Published online: 18 September 2014
Ó Springer Science+Business Media New York 2014

A. B. Kumar (&)
Department of Anesthesiology, Division of Critical Care
Medicine, Vanderbilt University, 1211 21st Avenue, S,
526 MAB, Nashville, TN 37212, USA

72 h and 14 days following admission. A Cox proportional
hazards survival model with multiple time varying covariates was developed to evaluate the effect of maximum
sodium exposure on the risk of AKI. Sodium exposure was
captured as the running maximum of daily maximum
serum sodium concentration (mEq/L). Sodium exposure
was used as a surrogate for hypertonic saline therapy.
Results The final cohort of patients included 736 patients
admitted to the neuro intensive care unit between 2006 and
2012. The number of patients who developed AKI was 64
(9 %). These patients had an increased length of stay
(15.6 ± 9.4 vs. 12.5 ± 8.7 days). The odds of death were
more than two fold greater among patients who developed
AKI (odds ratio 2.33 95 % CI 1.27, 4.3). Sodium exposure
was significantly associated with the hazard of developing
AKI, adjusting for age, sex, preexisting renal disease,
diabetes mellitus, radiocontrast exposure, number of days
on mechanical ventilation, and admission Glasgow Coma
Scale score. For each 1 mEq/L increase in the running
maximum daily serum sodium, the hazard of developing
AKI was increased by 5.4 % (95 % CI 1.4, 9.7).
Conclusion The maximum daily sodium is a significant
risk factor for developing AKI in patients with SAH.

Y. Shi  M. S. Shotwell
Department of Biostatistics, Vanderbilt University,
1211 21st Avenue, S, 526 MAB, Nashville, TN 37212, USA

Keywords Hypernatremia  Acute kidney injury 
Subarachnoid hemorrhage  Hyperosmolar therapy 
Hypertonic saline  Serum sodium

Background Hypertonic saline therapy is often used in
critically ill subarachnoid hemorrhage (SAH) patients for
indications ranging from control of intracranial hypertension to managing symptomatic hyponatremia. The risk
factors for developing acute kidney injury (AKI) in this
patient population are not well defined.
Specific Aim To study the role of serum sodium in developing AKI (based on the AKIN definition) in the SAH
population admitted to a large academic neurocritical care
Methods This is an IRB-approved, retrospective cohort
study of patients admitted to a tertiary neuro intensive care
unit. We included adult (age C18 years) SAH patients
admitted to the neuro intensive care unit for at least 72 h.
Development of AKI after admission to the ICU was
defined using the AKIN serum creatinine criteria between

M. S. Shotwell
J. Richards  J. M. Ehrenfeld
Department of Anesthesiology, Vanderbilt University,
1211 21st Avenue, S, 526 MAB, Nashville, TN 37212, USA
J. M. Ehrenfeld


Subarachnoid hemorrhage (SAH) accounts for only about
5 % of all strokes but remains a devastating disease with
mortality approaching 50 % and with less than 1 in 2 survivors reaching functional independence [1]. The

since there is accumulating evidence that even minor increments in serum creatinine are associated with adverse outcomes. The AKIN criteria has been utilized and validated in prospective studies in patients with AKI after cardiac surgery. The secondary outcomes were intensive care length of stay (LOS) and 28day mortality.5 % solution (1283 mmol/L). intracranial hypertension. patients with septic shock or heart failure) due to exposure to specific interventions and management strategies. current smoking status. Preoperative renal insufficiency was defined as a baseline serum Cr C1. with the most recent serum creatinine including upto day of admission being considered the baseline value. height. Data were obtained from the Vanderbilt Perioperative Data Warehouse. We excluded patients who did not survive the first 24 h of admission. and mixed ICU populations [3]. Specific Aim In this retrospective analysis. In the AKIN definitions. validated and reproducible definition of acute renal failure. admission 185 neurologic exam. hyperosmolar therapy (mannitol and hypertonic saline).Neurocrit Care (2015) 22:184–191 neurocritical care course of these patients is frequently complicated by non-neurologic complications including cardiorespiratory complications including the development of acute kidney injury or AKI [2]. irrespective of urine output or sCr.3 mg/dl over baseline. Urine output has traditionally been a bellwether of renal dysfunction in the general ICU patient population. and euvolemic fluid management strategies as well as development of hyponatremia. All variables were followed for 14 days post ICU admission. Any patient treated with RRT. The intensive care course of this patient population deviates from other ICU encounters (e. BMI.g. daily fluid balances. Stage 2 is defined as an increase of 2–3 fold over the baseline sCr. Prior studies of renal dysfunction following neurologic injury have been challenging due to the lack of a consistent. or in a 23. Stage 1 in the AKIN classification includes patients with an increase in sCr of at least 0. 7. cryoprecipitate. sex.2 mg/dl. Data Collection and Definitions Preoperative data points included age. and recombinant Factor 7). Intensive care variables included duration of mechanical ventilation. an IRB-approved data registry containing case and outcomes information on all surgical and ICU patients cared for at our institution. Traumatic brain injury patients were not in the dataset since at our institution. Currently. The AKIN classification uses a 48-hour time window for assessment of renal function based on the evidence that adverse outcomes were reported when the creatinine elevation occurred within 24–48 h of hospitalization [5]. Materials and Methods Our retrospective study was approved by the Vanderbilt University Institutional Review Board. Although hypertonic saline is used in varying strengths from 3 % solution (513 mmol/L). Laboratory values assessed included daily maximum and minimum serum sodium. and location of bleed and aneurysm (if applicable). We followed the patients for development of SAHAKI for a period of 14 days. The decision to initiate RRT was at the discretion of the attending consultant nephrologist. The SAH patient population is frequently complicated by high output renal states such as cerebral salt wasting. we seek to study the incidence. acute kidney injury has replaced the term acute renal failure and has been validated in various patient populations by the RIFLE and AKIN criteria [3].g. We chose to use the creatinine-based definition of AKI. We also excluded patients whose primary source of intracranial blood was not a SAH (e. This has largely been overcome with the changes in the definition and criteria for diagnosis of acute renal failure. weight. and outcomes following development of new onset acute kidney injury (based on the new validated definition) following SAH (SAHAKI) population admitted to a large academic neuro intensive care unit. These include potential repeated exposure to IV contrast media. and high urine output states. We set out to analyze all patients admitted to the Vanderbilt neuroscience intensive care unit with the diagnosis of SAH (aneurysmal and non-aneurysmal) between 2006 and 2012. and patients on renal replacement therapy (RRT). diabetes mellitus. However. a large intraparenchymal bleed with some subarachnoid blood was excluded). ARDS. minimum and maximum serum osmolality. and the AKIN urine output criteria have not been validated in this patient population. and transfusion support (including use of packed red blood cells. preoperative kidney function (defined as the latest available serum creatinine prior to admission). admission Glasgow coma score. fresh frozen plasma. hyperosmolar agents. their primary location of admission is a different ICU. Hunt and Hess class of SAH. little is known about the specific risk factors for AKI in the SAH patient population and its subsequent impact on outcomes [4]. or with a C3 fold rise in sCr is categorized as stage 3 in the AKIN system. The primary outcome was development of AKI based on the acute kidney injury network (AKIN) serum creatinine (sCr) criteria. risk factors. septic shock. hypertension. We focused on this time frame since this is considered the highest risk period for clinically 123 .4 % solution (4008 mmol/L). the thresholds for urine flow for the definition of AKI have been derived empirically and are less well substantiated than the thresholds for increase in SCr. in our study hypertonic saline was limited to 3 % NaCl.

sex.05 was used for statistical inference. the majority patients were female (59 %). Unadjusted AKI free survival was depicted using a Kaplan–Meier curve. We explored the temporal exposure patterns of patients to IV contrast over a period of 14 days.0. preexisting renal disease. Among those who developed AKI. The SAH centric risk factors for AKI that we explored included packed red blood cell transfusions. Patients were removed from the at-risk pool once AKI had been observed.0 % (64 out of 736).3). 0.10. diabetes mellitus.2 (R Foundation for Statistical Computing. preexisting renal disease. and BMI. 1. There were only 2 patients who needed RRT and or had an increase of sCr >300 % putting them in the AKI-Class III category.9 in the AKI cohort and 11. Among the 64 patients in the AKI cohort. (p = 0. Intravenous contrast media is a known risk factor for development of acute kidney injury. 4.5 ± 8. diabetes mellitus. median. An estimated six percent of patients developed early AKISAH by day 3. Patients who did not develop AKI during their ICU stay were censored at the time of ICU discharge or at 14 days.7 ± 4. We utilized previously published independent risk factors as predictors of AKISAH [6]. The unadjusted odds of death were more than two fold greater among patients who developed AKI during their clinical ICU course (odds ratio 2. Serum creatinine was measured daily from ICU admission (day 1) to discharge or day 14 whichever was the earlier. and DM. Results Our study included 736 consecutive adult SAH patients with an overall AKISAH incidence of 9.33 95 % CI 1. and Glasgow coma score. preexisting kidney disease. The primary outcome was indicated when serum creatinine increased by more than 0. 24 h fluid balances. 2 (contrast exposure). The first peak of AKI developed around day 3 followed by a second smaller peak by day 7.6 %) patients had a change in serum Cr <199 % of baseline hence classifying them as AKI-Class I. Mechanical ventilation was initiated on admission in 35 % (22/63) of patients in the AKI cohort compared to 29 % (194/669) in the No AKI cohort.32). 0.054) in the AKI versus no-AKI group (Table 1).002). IV contrast. Patients who developed AKI had an increased length of ICU stay (15. and the running maximum of daily maximum serum sodium concentration. All analyses were implemented using R 3. A significance level of 0. Statistical Analysis Patient demographics and clinical data were summarized using the 25th percentile.186 significant vasospasm and subsequent exposure to multiple interventions. Austria).15) in non-AKI patients. The time varying risk factors included the cumulative count of radiocontrast exposure in days. highest serum sodium every 24 h. exposure to contrast.27. There was no significant unadjusted difference between cohorts with respect to exposure to hypertonic saline. 12. However. Of the 736 patients in our final cohort. p = 0. Unadjusted comparisons between those who did and did not develop AKI on demographic and clinical data were conducted using the Wilcoxon rank sum test for continuous variables and the Pearson Chi square test for categorical variables. mannitol. mechanical ventilation. and 75th percentile for continuous variables.25 (95 % CI 0. and with percentages for categorical variables. A Cox proportional hazards model with time varying covariates was used to identify risk factors for developing AKI during the ICU stay. the cumulative count of days on mechanical ventilation.3 % of all patients) as anticipated. due to . 58 (90.4 vs.7 days. and location of bleed. GCS. The fixed risk factors included patient age at hospital admission.69)]. There was a difference in the baseline count of patients with diabetes mellitus (p = 0. there was no statistically significant difference between the cohorts regarding endotracheal intubation and mechanical ventilation on admission (p = 0. The median age at time of hospital admission was 55 ± 15 Y. there was no statistically significant difference between cohorts with regard to admission Glasgow coma score [11.016) and exposure to packed red cell transfusion (p = 0. There was insufficient evidence associating the development of AKI with age. However.3 mg/dl within a 48hour period.36) and 0. and cumulative count of radiocontrast exposure or cumulative count of days on mechanical ventilation. These independent risk factors included age.16.6 ± 9. Two patients had a sCr increase from 200 to 299 % of baseline and were 123 Neurocrit Care (2015) 22:184–191 classified as Class II AKI. non-aneurysmal). sex. rising to 12 % at 14 days.6 in nonAKI cohort. The AKI incidence and mortality rate were estimated and reported with 95 % confidence intervals using a nonparametric bootstrap method.3 ± 4. The Kaplan–Meier (K–M) curve for the unadjusted time to development of AKISAH is illustrated in Fig. Glasgow coma score on presentation. The overall mortality in the AKI cohort was 0.12 (95 % CI 0. etiology of SAH (aneurysmal vs. or baseline levels of serum sodium on admission. The exposure to IV contrast exposure is shown in Fig. whichever came earlier. The highest exposure was on day 1 (39. 19 and 14 % of the patients had diabetes mellitus and preexisting renal disease respectively. sex. The results are shown in Table 2. compared to 12 and 6 % of patients who did not develop AKI. A Cox proportional hazards regression with multiple time varying covariates was implemented to evaluate the effect of specific risk factors and development of AKISAH. Vienna.

Hypernatremia secondary to the use of hypertonic saline was the strongest risk factor for developing AKISAH in our 123 . HR for AKI was 1.53).3) (28. 137.16 Preexisting renal disease (%) Glasgow coma score 14 % (8/64) 7. 1. p = 0. The distribution of daily maximum sodium is shown in Fig. 140 0.07 0.44 Mannitol (%) 6 % (4/64) 3 % (20/672) 3 % (26/736) 0.3 ± 4.78.1) (28.0.0. 55. 15. the hazard of developing AKI was increased by 5.09 (0. There was a second peak of contrast exposure on day 8 and 9 (10. This exposure was reduced significantly by day 3 (about 3.01. based on our Cox proportional hazards regression model.09 (0.96. 317 (303 ± 25) (308 ± 18) (308 ± 19) 4.6.42. which is lower compared to reported AKI rates in post cardiac surgical and general post surgical intensive care units.7 ± 4.55.30) 0.1.0 7 % (51/736) 7.6) (11. 9.69 (11.74 (0. 31.5 % (3/64) 1 % (7/672) 1.9.5 % (95 % CI 1. 140 0. 320 298.9) Diabetes mellitus-type II (%) 19 % (12/64) 12 % (84/672) 13 % (96/736) 0.0. 314 298.94 (28.36 ventilation concentration (mEq/L). in spite of significant exposure. p value = 0. 73 45. 1. Discussion the nature of the diagnostic workup of a SAH.0. 305.0 6 % (40/672) 8. where rates as high as 47 % have been reported [8]. After adjusting for other covariates including sodium exposure. 1.3 23. 65 0.02 (0. The focus now rests on minimizing the non-neurologic complications associated with this disease that still has a high morbidity and mortality [7].6 ± 4.81) 0. 1. 15. percentage for categorical variables.Neurocrit Care (2015) 22:184–191 187 Table 1 Patient demographics and baseline characteristics Age AKI (N = 64) No AKI (N = 672) Combined (N = 736) p 49. 75th percentile (mean ± SD) for continuous variables.008 Cumulative count of radiocontrast exposure 1.3 BMI 23.53) 0. 15. 26.5 % of patients being exposed) and continued to be low at about 5 % until day 8 and 9.1.0. Identification of patient and procedural risk factors may therefore allow for improvements in longterm outcome by affecting changes in perioperative management and disease prevention.29 Diabetes mellitus 1. 30. 1. 30.10) 0. In our analysis.62.78.7. 55.17 (55 ± 15) (59 ± 16) (55 ± 15) Female 53 % (34/64) 60 % (402/672) 59 % (436/736) 0.054 Summary statistics are shown as the 25th.4 0. the overall incidence of AKI was 9 %. 304. 15.23 Sodium 0. 137. 15. 26.7) Contrast exposure(%) 44 % (28/64) 39 % (261/672) 39 % (289/736) 0.3 % (10/736) 0. However.0 0.47 Cumulative maximum sodium 1. The strongest risk factor associated with development of AKI in the SAH patient population was the daily maximum serum sodium.94 0.06 (1.1 ± 11. 56.1 ± 10. 50th.12) 0.45 Glasgow coma score 1.62 Cumulative count of days on mechanical 1.0.09) 0.96.94) 0.04 (0.16 Female 0. 15.4 and 17 % respectively). 137.04) 0.0. Sodium exposure was used as a surrogate for hypertonic saline therapy in our analysis and was captured as the running maximum of daily maximum serum sodium Significant strides have been made in the neurologic management of SAH in the past decade.99. 3.82. 140 0.45 (0. p values were calculated using the Wilcoxon rank sum test for continuous variables and the Pearson Chi-square test for categorical variables Table 2 Effect estimate (95 % CI) calculated from the time varying Cox proportional hazard model Variable HR (95 % CI) p Age 1.02 (0.2 ± 8. 2. For each 1 mEq/L increase in the running maximum of daily maximum serum sodium. 1.55 (0.18 Preexisting renal disease 1. 25.4 23. 1.4.008). there was insufficient evidence that the running count of IV contrast exposure events was a significant risk factor for AKISAH in our patient population.39 (100 ± 64) (93 ± 65) (94 ± 65) Osmolality RBC transfusion 296. 308.0. 3.9) (11. Hypernatremia (secondary to the use of hypertonic saline) and even small increments of daily serum sodium was a significant risk factor for AKISAH after adjusting for other risk factors. 65 45.

1 Kaplan–Meier curve showing the timeline to develop AKI in the ICU in the SAH patient population Fig. While relatively rare. Intracranial hypertension and cerebral edema are cardinal manifestations of severe brain injury resulting from diverse 123 insults ranging from traumatic brain injury to SAH. Patients who developed new onset AKI had an increased length of stay and were at an increased risk of in-hospital mortality. These findings can be explained by the fact that the kidney. in contrast to other organs. Interestingly. Dominguez et al. 2 Temporal trend of IV contrast exposure in all patients showing the proportion of patients (%) exposed to I. serious electrolyte . responds with vasoconstriction to a hypernatremic state.188 Neurocrit Care (2015) 22:184–191 Fig. Animal studies have shown a reduction of renal blood flow. HTS is not without potential major adverse effects. preexisting kidney disease. It is thought that hypernatremia can lead to renal dysfunction through the mechanism of intravascular dehydration and vasoconstriction either directly or through a tubuloglomerular feedback mechanism [13]. and an inhibition of renin secretion when the sodium level in the renal artery is increased rapidly [14]. advanced age were not significant risk factors for developing AKI in our SAH population. contrast between ICU day 1 and ICU day 14 patient population. interestingly the major reason for the preference for using hypertonic saline was the perceived ‘‘decreased risk of renal dysfunction’’ compared to mannitol [11]. Hyperosmolar therapy with mannitol and hypertonic saline has been the cornerstone in the management of intracranial hypertension [9]. glomerular filtration rate. we will gather a better renal risk profile of hypertonic saline. As our experience with the use of hypertonic saline in various concentrations grows. the traditional risk factors for AKI in mixed ICU populations such as diabetes mellitus. Raised intracranial pressure (ICP) is an independent predictor of poor neurologic outcome following SAH. Contrast-induced nephropathy was not a significant event in our patient population in spite of increasing frequency of contrast exposure each year of the study in the SAH patient population. Early and aggressive management of intracranial hypertension is a key to a good outcome.V. Recent studies including a metaanalysis showed HS to be more effective with controlling ICP compared to mannitol [10]. reported the increased risk of renal dysfunction in pediatric patients who were maintained in a hyperosmolar state at 160 mEq/L in severe traumatic brain injury [12]. In the same survey. The intensivist preferences of using mannitol versus hypertonic saline are evenly divided based on a recent national survey [11].

27]. sedation management. higher blood pressure goals. 17]. The precise reasons are unclear at this time. The increasing use of statins in patients with patients with SAH for their pleiotropic immune modulating effects (non-cholesterol lowering effects) may further confound the picture. and decreased left ventricular function are established risk factors for contrast-induced nephropathy. In addition. These procedures frequently require contrast angiography to define the anatomy. Thus. with a change in the management paradigm for SAH. 22]. and during the therapeutic intervention as well. although there has been conflicting data on the rates of CIN in the SAH population. and modified augmented cardiac index management of cerebral vasospasm may have contributed to maintaining effective renal perfusion and the overall increased vigilance to the risks of contrast exposures maybe a contributing factor as well. We speculate that the aggressive avoidance of hypovolemia. and the panel on the bottom shows the cohort with no AKI disturbances may be induced central pontine myelinolysis in malnourished patients with an acute hypernatremic state following rapid serum sodium correction [15. The predominant pathophysiologic model of AKI in general ICU patients is the ischemia–reperfusion model frequently triggered by perturbations in hemodynamics leading to the development and worsening of AKI in septic shock and ARDS [24. The precise reasons for this are unclear at this time. Hyperchloremic acidosis and acute hemolysis are further consequences of HTS administration. In the general patient population. preexisting kidney disease. Further worsening of cerebral swelling and increased ICP maybe indicative of a disrupted blood brain barrier and a ‘‘reverse osmosis’’ phenomenon (1). Investigations have been exploring the role of statins in the perioperative period to prevent or decrease the severity of AKI and need for RRT [28]. The therapeutic management of SAH has undergone significant changes in the past decade for SAH with the advent of neurovascular interventions such as stenting and endovascular coiling of aneurysms [18]. diabetes mellitus. 25]. post aneurysm intervention). the overall incidence is lower than the general mixed ICU patient population [21. SAH patients pose a relatively unique set of challenges to the intensivists compared to other non-neurologic ICU patients.g. In fact. cardiac ICU patient population) [20]. This reflects the finding in our study as well that exposure to IV contrast was not associated with an increased risk of AKI SAH in our patient population over a time course of 14 days. renal complications due to HTS therapy are an real concern [15. the MAP and cardiac output may be at a higher than baseline level in the post intervention period and during the active management of cerebral vasospasm [26. hypovolemia. Hyperosmolar therapy is also known to induce rapid intravascular volume expansion and subsequent cardiac overload with pulmonary edema.g. volume of contrast used. hemodynamic management (e. The panel on the top shows sodium max data for patients who developed AKI. augmented cardiac index therapy) often seem counterintuitive to other traditional ICU patients with diseases such as ARDS and septic shock. advanced age. The liberal fluid management strategies (i.Neurocrit Care (2015) 22:184–191 Fig.e. This clinical scenario tends to be less frequent in the SAH patient population especially with the institution of augmented cardiac index therapy or the comparable version of triple-H therapy in these patients. patients today have a higher potential for multiple exposures to IV contrast media secondary to both diagnostic and 189 therapeutic interventions during their ICU course [19]. 16]. Interestingly. 3 Sodium max on ICU day 1 through day 14. The overall incidence of AKI following SAH is lower compared to the incidence following other high mortality diagnoses such as septic shock or ARDS [23]. This increases the risk of contrast-induced nephropathy in this patient population. Statins have been tried as a prophylactic agent for CIN especially in the patients undergoing coronary angiography with limited success in 123 . Rate of contrast-induced nephropathy has been reported to be as high as 20–25 % in high-risk patients (e.

there is a need for more sensitive and specific biomarkers that can diagnose AKI earlier. 2007. medications. Ni Q. End-stage kidney disease) criteria is currently limited as SCr and UO can only indirectly reflect that kidney damage has occurred. Understanding the risk posed by hypernatremia in the pathogenesis of AKI after SAH may help us develop management strategies to minimize harm to the kidneys in this high mortality disease. muscle mass.. Fitzgerald R. Pediatric nephrology. Osmotherapy: use among neurointensivists. Crit Care Med. Huh JW. 4. 3. References 1. Zygun DA.37(4):1433–41. 2009. and rapidly measure the response to therapy. The current definitions and risk stratification of acute kidney injury has helped better define and study the problem of kidney dysfunction across various pathophysiologic spectra include SAH.249(5):851–8. Subbiah S. Richling B.29(1):13–21. 1998. Steigleder T.g. glomerular versus tubular etc. 30]. Doig CJ. Crit Care Med.23(5):1569–74. 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Long-term risk of mortality and acute kidney injury during hospitalization after major surgery. Nicholas C.39(3):554–9. 6. The burden. Neurocrit Care. Bagshaw SM. Li N.) but rather provides an overall index of function [33].e. Crit Care Med. 2009. A change in serum creatinine does not indicate the site of kidney injury (i. 11. Levin A. Acute kidney injury: an intensivist’s perspective. 2008. Bellomo R. blood pressure management strategies may have had an impact on the final outcomes. 7. Bihorac A. 123 Neurocrit Care (2015) 22:184–191 Conclusion Hypernatremia is independently associated with an increased risk of development of AKI in the SAH patient population. Neurology. and demographics of mortality from subarachnoid hemorrhage. Mehta RL.50(5):1413–8. Ougorets I. 32]. Stark D. Czech T. volume of distribution. Shah SV. and protein intake. We anticipate future studies to shed more light on this important nonneurologic complication following SAH. Ko NU. Bardutzky J. possibly indicate the cause. Caution should be exercised when maintaining a serum sodium level >160 meq/L. Serum creatinine remains the most frequently used parameter in the diagnosis of AKI. sCr is an insensitive and unreliable biomarker during short-term changes in kidney function because it lags behind the decline and recovery in glomerular filtration rate by days. Conflict of interest conflict of interest. Dominguez TE. The diagnosis of AKI using the AKIN (Acute Kidney Injury Network) or RIFLE (Risk. Gress DR. Nakagawa K. 2003. Zhao WG.18(4):238–44. The results of numerous trials have been conflicting and there is insufficient data at this time to support the routine use of statins in all SAH patients for the prevention of AKI [31. Prowle JR. sCr is affected by age. Conway-Smith C. 2011. Yavas S. ischemic vs. Crit Care Med. 2011. Hartl R. 8. Hypertonic saline versus mannitol for the treatment of elevated intracranial pressure: a meta-analysis of randomized clinical trials. Injury. Certain limitations of this current study deserve mention. Acute kidney injury in patients with severe traumatic brain injury: implementation of the acute kidney injury network stage system. Robust data on the use of biomarkers in AKI following SAH are anticipated in the near future. The use of the next generation of biomarkers for acute kidney injury such as NGAL (neutrophil gelatinase associate lipocalin). Gay S. Failure. Neyens R. Additional studies are warranted to study the pathophysiologic processes and interventions to prevent the development of AKI in his high mortality patient population.190 smaller studies [29. Loss. 10. Nephrol Dial Transplant. Hobson CE. Illievich UM. Johnston SC.14(2):222–8.32(6):1438–9 author reply 1439-1440. This is a single center retrospective study and the known inherent limitations of this kind of analysis apply to this study as well. We also did not have any biomarker specific data for AKI in this patient population. Moreover. J Crit Care. The variability of clinical practice including fluid management. . 2011. 2. Non-neurological organ dysfunction in neurocritical care. it does not discriminate the nature of renal insult (e. Gabrielli A. Reinprecht A. Therefore. Menon DK. Hauer EM. The large cohort of consecutive patients with SAH and the robustness of the data collected add strength to our study. There are however continuing limitations with the current AKIN system as well. Extracerebral organ dysfunction and neurologic outcome after aneurysmal subarachnoid hemorrhage. Funding All the author declared that they have no Departmental funds only. Nicholas J. Kellum JA. 1999. Whiting G. They may play a role in the future to further determine the patients at risk or allow early detection of AKI and in turn may provide a window of opportunity for early therapeutic interventions. 2004. trends. Shepherd E. 9. The strength of our analysis is that the data spans multiple years and multiple providers were involved with the care of patients.

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