Urinary indices have limited effectiveness in separating transient acute kidney
injury (AKI) from persistent AKI in ICU patients. Their time-course may vary with
the mechanism of AKI. The primary objective of this study was to evaluate the
diagnostic value of changes over time of the usual urinary indices in separating
transient AKI from persistent AKI.
An observational prospective multicenter study was performed in six ICUs involving
244 consecutive patients, including 97 without AKI, 54 with transient AKI, and 93
with persistent AKI. Urinary sodium, urea and creatinine were measured at ICU
admission (H0) and on 6-hour urine samples during the first 24 ICU hours (H6, H12,
H18, and H24). Transient AKI was defined as AKI with a cause for renal
hypoperfusion and reversal within 3 days.
Significant increases from H0 to H24 were noted in fractional excretion of urea
(median, 31% (22 to 41%) and 39% (29 to 48%) at H24, P < 0.0001),
urinary urea/plasma urea ratio (15 (7 to 28) and 20 (9 to 40), P <
0.0001), and urinary creatinine/plasma creatinine ratio (50 (24 to 101) and 57 (29
to 104), P = 0.01). Fractional excretion of sodium did not change
significantly during the first 24 hours in the ICU (P = 0.13). Neither
urinary index values at ICU admission nor changes in urinary indices between H0
and H24 performed sufficiently well to recommend their use in clinical setting
(area under the receiver-operating characteristic curve ≤0.65).
Although urinary indices at H24 performed slightly better than those at H0 in
differentiating transient AKI from persistent AKI, they remain insufficiently
reliable to be clinically relevant.
Acute kidney injury (AKI) frequently occurs in the setting of critical illness and its management poses a challenge for the intensivist. Optimal management of volume status is critical in the setting of AKI in the ICU patient. The use of urine sodium, the fractional excretion of sodium (FeNa), and the fractional excretion of urea (FeUrea) are common clinical tools used to help guide fluid management especially further volume expansion but should be used in the context of the patient's overall clinical scenario as they are not completely sensitive or specific for the finding of volume depletion and can be misleading. In the case of oliguric or anuric AKI, diuretics are often utilized to increase the urine output although current evidence suggests that they are best reserved for the treatment of volume overload and hyperkalemia in patients who are likely to respond to them. Management of volume overload in ICU patients with AKI is especially important as volume overload has several negative effects on organ function and overall morbidity and mortality.
The Acute Kidney Injury Network proposed a new classification for acute kidney injury (AKI) distinguishing between three stages. We applied the criteria to a large intensive care unit (ICU) population and evaluated the impact of AKI in the context of other risk factors.
Using the Riyadh Intensive Care Program database, we applied the AKI classification to 22,303 adult patients admitted to 22 ICUs in the UK and Germany between 1989 and 1999, who stayed in the ICU for 24 hours or longer and did not have end-stage dialysis dependent renal failure.
Of the patients, 7898 (35.4%) fulfilled the criteria for AKI (19.1% had AKI I 3.8% had AKI II and 12.5% had AKI III). Mortality in the ICU was 10.7% in patients with no AKI, 20.1% in AKI I, 25.9% in AKI II and 49.6% in AKI III. Multivariate analysis confirmed that AKI III, but not AKI I and AKI II, were independently associated with ICU mortality (odds ratio (OR) = 2.27). Other independent risk factors for ICU mortality were age (OR = 1.03), sequential organ failure assessment (SOFA) score on admission to the ICU (OR = 1.11), pre-existing end-stage chronic health (OR = 1.65), emergency surgery (OR = 2.33), mechanical ventilation (OR = 2.83), maximum number of failed organ systems (OR = 2.80) and non-surgical admission (OR = 3.57). Cardiac surgery, AKI I and renal replacement therapy were associated with a reduced risk of dying in the ICU. AKI II was not an independent risk factor for ICU mortality. Without renal replacement therapy as a criterion, 21% of patients classified as AKI III would have been classified as AKI II or AKI I. Renal replacement therapy as a criterion for AKI III may inadvertently diminish the predictive power of the classification.
The proposed AKI classification correlated with ICU outcome but only AKI III was an independent risk factor for ICU mortality. The use of renal replacement therapy as a criterion for AKI III may have a confounding effect on the predictive power of the classification system as a whole.
Acute kidney injury (AKI) is an uncommon but serious complication after trauma. The objective of this study was to evaluate the prevalence, clinical characteristics and outcome of AKI after trauma.
Patients and Methods:
This was a retrospective study performed from January 2006 to January 2008 in an emergency specialized hospital in Fortaleza city, northeast of Brazil. All patients with AKI admitted in the study period were included. Prevalence of AKI, clinical characteristics and outcome were investigated.
Of the 129 patients admitted to the intensive care unit (ICU), 52 had AKI. The mean age was 30.1 ± 19.2 years, and 79.8% were males. The main causes of AKI were sepsis in 27 cases (52%) and hypotension in 18 (34%). Oliguria was observed in 33 cases (63%). Dialysis was required for 19 patients (36.5%). Independent risk factors associated with AKI were abdominal trauma [odds ratio (OR) = 3.66, P = 0.027] and use of furosemide (OR = 4.10, P = 0.026). Patients were classified according to RIFLE criteria as Risk in 12 cases (23%), Injury in 13 (25%), Failure in 24 (46%), Loss in 1 (2%) and End-stage in 2 (4%). Overall in-hospital mortality was 95.3%. The main cause of death was sepsis (24%). Mortality was 100% among patients with AKI.
AKI is a fatal complication after trauma, which presented with a high mortality in the studied population. A better comprehension of factors associated with death in trauma-associated AKI is important, and more effective measures of prevention and treatment of AKI in this population are urgently needed.
Acute kidney injury; mortality; outcome; risk factors; trauma
Background. Neutrophil gelatinase-associated lipocalin (NGAL) in serum and urine have been suggested as potential early predictive biological markers of acute kidney injury (AKI) in selected critically ill patients. Methods. We performed a secondary analysis of a multicenter prospective observational cohort study of unselected critically ill patients. Results. The analysis included 140 patients, including 57 patients who did not develop AKI, 31 patients who developed AKI, and 52 patients with AKI on admission to the ICU. Levels of sNGAL and uNGAL on non-AKI days were significantly lower compared to levels of sNGAL on RIFLERISK days, RIFLEINJURY days, and RIFLEFAILURE days. The AUC of sNGAL for predicting AKI was low: 0.45 (95% confidence interval (CI) 0.27–0.63) and 0.53 (CI 0.38–0.67), 2 days and 1 day before development of AKI, respectively. The AUC of uNGAL for predicting AKI was also low: 0.48 (CI 0.33–0.62) and 0.48 (CI 0.33–0.62), 2 days and 1 day before development of AKI, respectively. AUC of sNGAL and uNGAL for the prediction of renal replacement therapy requirement was 0.47 (CI 0.37–0.58) and 0.26 (CI 0.03–0.50). Conclusions. In unselected critically ill patients, sNGAL and uNGAL are poor predictors of AKI or RRT.
Aim: To assess and compare the roles of plasma and urine concentrations of neutrophil gelatinase associated lipocalin (NGAL) and Cystatin C for early diagnosis of septic acute kidney injury (AKI) in adult critically ill patients.
Methods: Patients were divided into three groups as sepsis-non AKI, sepsis-AKI and non sepsis-non AKI. Plasma samples for NGAL and Cystatin C were determined on admission and on alternate days and urinary samples were collected for every day until ICU discharge.
Results: One hundred fifty one patients were studied; 66 in sepsis-non AKI, 63 in sepsis-AKI, 22 in non-sepsis-non-AKI groups. Although plasma NGAL performed less well (AUC 0.44), urinary NGAL showed significant discrimination for AKI diagnosis (AUC 0.80) with a threshold value of 29.5 ng/ml (88% sensitivity, 73% specificity). Both plasma and urine Cystatin C worked well for the diagnosis of AKI (AUC 0.82 and 0.86, thresholds 1.5 and 0.106 mg/L respectively).
Conclusion: Plasma and urinary Cystatin C and urinary NGAL are useful markers in predicting AKI in septic critically ill patients. Plasma NGAL raises in patients with sepsis in the absence of AKI and should be used with caution as a marker of AKI in septic ICU patients.
NGAL protein; human; Cystatin C; Acute kidney injury; biomarkers; sepsis; Intensive Care Units; predictive value of tests
There are few studies on long-term mortality among intensive care unit (ICU) patients with acute kidney injury (AKI). We assessed the prevalence of AKI at ICU admission, its impact on mortality during one year of follow-up, and whether the influence of AKI varied in subgroups of ICU patients.
We identified all adults admitted to any ICU in Northern Denmark (approximately 1.15 million inhabitants) from 2005 through 2010 using population-based medical registries. AKI was defined at ICU admission based on the risk, injury, failure, loss of kidney function, and end-stage kidney disease (RIFLE) classification, using plasma creatinine changes. We included four severity levels: AKI-risk, AKI-injury, AKI-failure, and without AKI. We estimated cumulative mortality by the Kaplan-Meier method and hazard ratios (HRs) using a Cox model adjusted for potential confounders. We computed estimates for all ICU patients and for subgroups with different comorbidity levels, chronic kidney disease status, surgical status, primary hospital diagnosis, and treatment with mechanical ventilation or with inotropes/vasopressors.
We identified 30,762 ICU patients, of which 4,793 (15.6%) had AKI at ICU admission. Thirty-day mortality was 35.5% for the AKI-risk group, 44.2% for the AKI-injury group, and 41.0% for the AKI-failure group, compared with 12.8% for patients without AKI. The corresponding adjusted HRs were 1.96 (95% confidence interval (CI) 1.80-2.13), 2.60 (95% CI 2.38 to 2.85) and 2.41 (95% CI 2.21 to 2.64), compared to patients without AKI. Among patients surviving 30 days (n = 25,539), 31- to 365 day mortality was 20.5% for the AKI-risk group, 23.8% for the AKI-injury group, and 23.2% for the AKI-failure group, compared with 10.7% for patients without AKI, corresponding to adjusted HRs of 1.33 (95% CI 1.17 to 1.51), 1.60 (95% CI 1.37 to1.87), and 1.64 (95% CI 1.42 to 1.90), respectively. The association between AKI and 30-day mortality was evident in subgroups of the ICU population, with associations persisting in most subgroups during the 31- to 365-day follow-up period, although to a lesser extent than for the 30-day period.
AKI at ICU admission is an important prognostic factor for mortality throughout the subsequent year.
Sepsis commonly contributes to acute kidney injury (AKI); however, the frequency with which sepsis develops as a complication of AKI and the clinical consequences of this sepsis are unknown. This study examined the incidence of, and outcomes associated with, sepsis developing after AKI.
We analyzed data from 618 critically ill patients enrolled in a multicenter observational study of AKI (PICARD). Patients were stratified according to their sepsis status and timing of incident sepsis relative to AKI diagnosis.
We determined the associations among sepsis, clinical characteristics, provision of dialysis, in-hospital mortality, and length of stay (LOS), comparing outcomes among patients according to their sepsis status. Among the 611 patients with data on sepsis status, 174 (28%) had sepsis before AKI, 194 (32%) remained sepsis-free, and 243 (40%) developed sepsis a median of 5 days after AKI. Mortality rates for patients with sepsis developing after AKI were higher than in sepsis-free patients (44 vs. 21%; p < 0.0001) and similar to patients with sepsis preceding AKI (48 vs. 44%; p = 0.41). Compared with sepsis-free patients, those with sepsis developing after AKI were also more likely to be dialyzed (70 vs. 50%; p < 0.001) and had longer LOS (37 vs. 27 days; p < 0.001). Oliguria, higher fluid accumulation and severity of illness scores, non-surgical procedures after AKI, and provision of dialysis were predictors of sepsis after AKI.
Sepsis frequently develops after AKI and portends a poor prognosis, with high mortality rates and relatively long LOS. Future studies should evaluate techniques to monitor for and manage this complication to improve overall prognosis.
Acute kidney injury; Dialysis; Intensive care unit; Outcomes; Sepsis; Severity of illness
This study aimed to compare the incidence and clinical significance of transient versus persistent acute kidney injury (AKI) on acute ST elevation myocardial infarction (STEMI).
Materials and Methods
The study was a retrospective cohort of 855 patients with STEMI. AKI was defined as an increase of ≥0.3 mg/dL in creatinine level at any point during hospital stay. The study population was classified into 5 groups: 1) patients without AKI; 2) patients with mild AKI that was resolved by discharge (creatinine change less than 0.5mg/dL compared with admission creatinine during hospital stay, transient mild AKI); 3) patients with mild AKI that did not resolve by discharge (persistent mild AKI); 4) patients with moderate/severe AKI that was resolved by discharge (creatinine change more than 0.5 mg/dL compared with admission creatinine, transient moderate/severe AKI); 5) patients with moderate/severe AKI that did not resolve by discharge (persistent moderate/severe AKI). We investigated 1-year all-cause mortality after hospital discharge for the primary outcome of the study. The relation between AKI and 1-year mortality after STEMI was analyzed.
AKI occurred in 74 (8.7%) patients during hospital stay. Adjusted hazard ratio for mortality was 3.139 (95% CI 0.764 to 12.897, p=0.113) in patients with transient, mild AKI, and 8.885 (95% CI 2.710 to 29.128, p<0.001) in patients with transient, moderate/severe AKI compared to patients without AKI. Persistent moderate/severe AKI was also independent predictor of 1 year mortality (hazard ratio, 5.885; 95% CI 1.079 to 32.101, p=0.041).
Transient and persistent moderate/severe AKI during acute myocardial infarction is strongly related to 1-year all cause mortality after STEMI.
Acute kidney injury; myocardial infarction; mortality
The incidence of acute kidney injury (AKI) in the intensive care unit (ICU) has increased during the past decade due to increased acuity as well as increased recognition. Early epidemiology studies were confounded by erratic definitions of AKI until recent consensus guidelines (RIFLE and AKIN) standardized its definition. This paper discusses the incidence of AKI in the ICU with focuses on specific patient populations. The overall incidence of AKI in ICU patients ranges from 20% to 50% with lower incidence seen in elective surgical patients and higher incidence in sepsis patients. The incidence of contrast-induced AKI is less (11.5%–19% of all admissions) than seen in the ICU population at large. AKI represents a significant risk factor for mortality and can be associated with mortality greater than 50%.
The addition of relevant parameters to acute kidney injury (AKI) criteria might allow better prediction of patient mortality than AKI criteria alone. Here, we evaluated whether inclusion of AKI duration could address this issue.
AKI was defined according to the Kidney Disease: Improving Global Outcomes (KDIGO) guidelines in 2,143 critically ill patients, within 15 days of patient admission. AKI cases were categorized according to tertiles of AKI duration: 1st tertile, 1–2 days; 2nd tertile, 3–5 days; and 3rd tertile, ≥6 days. The hazard ratios (HRs) for overall survival rates in three groups were calculated after adjustment for multiple covariates compared with ICU patients without AKI as the reference group. The predictive ability for mortality was assessed by calculating the area under the curve (AUC) of the receiver operating characteristic curve.
AKI increased the HRs for overall mortality, and the mortality rate increased with AKI duration: the adjusted HRs were 1.99 (1st tertile), 2.67 (2nd tertile), and 2.85 (3rd tertile) compared with the non-AKI group (all Ps < 0.001). The AUC of the ROC curve for overall mortality based on the AKI duration groups (0.716) was higher than the AUC of AKI staging using the KDIGO guidelines (0.696) (P = 0.001). When considering KDIGO stage and AKI duration together, the AUC (0.717) was also significantly higher than that using the KDIGO stage alone (P < 0.001).
AKI duration is an additional parameter for the prediction of mortality in critically ill patients. The inclusion of AKI duration could be considered as a refinement of the AKI criteria.
Acute kidney injury; Acute renal failure; Duration; Mortality; Survival
To apply the modified pediatric RIFLE criteria for severity of acute kidney injury (AKI) to pediatric burn ICU patients and to evaluate the overall incidence of AKI, risk factors for AKI and influence of AKI on outcome.
Retrospective, descriptive cohort study.
10-bed burn PICU facility.
All consecutive patients with a burn injury of 10% or more of total body surface area percentage (TBSA, %) admitted during a 2 year period.
Measurements and results
Data of 123 patients were studied. The incidence of AKI was 45.5%. Patients with AKI tended to have higher mortality than those without AKI (p = 0.057). All nonsurvivors attained pRIFLE AKI by combination of serum creatinine and urine output criteria. Patients with a more severe form of AKI (Failure and Injury) as well as patients with late AKI had more episodes of sepsis as compared to patients with early AKI and the Risk category of AKI. Logistic regression analysis indicated that PRISM score and TBSA were the independent risk factors for acute kidney injury in pediatric burn patients; the presence of sepsis and septic shock were the independent risk factors for the Failure class of AKI.
We observed a high incidence of AKI in the burn PICU population. Sepsis seems to contribute to the development of the Failure class of AKI. Maximum Failure class of AKI is associated with high mortality.
Critically ill children; Burn; Acute kidney injury; RIFLE; Risk factors; Mortality
Sequential physicochemical alterations in blood and urine in the course of acute kidney injury (AKI) development have not been previously described. We aimed to describe these alterations in parallel to traditional renal and acid–base parameters.
One hundred and sixty eight consecutive critically ill patients with no previous kidney disease, who had an indwelling urinary catheter at ICU admission and who remained with the catheter for at least two days without dialysis were included. A sample of blood and spot urine were collected simultaneously, once daily, until catheter removal or dialysis requirement. Traditional acid–base and renal parameters were sequentially evaluated in parallel to blood and urinary physicochemical parameters. Patients were classified during this period as having or not AKI and, for patients with AKI, duration (transient or persistent) and severity (creatinine-based AKIN stage) were evaluated.
One hundred and thirteen patients (67.3%) had AKI: 92 at ICU admission and 21 during the observation period. AKI development was characterized in blood by increased values of phosphate and unmeasured anions (SIG), decreased albumin, and in urine by decreased values of sodium (NaU), chloride (ClU) as well as high urinary strong ion difference (SIDu). These alterations began to occur before AKI diagnosis, and they reverted in transient AKI but remained in persistent AKI. NaU, ClU and albumin decreased, and phosphate, SIG and SIDu increased with AKI severity progression. NaU and ClU values increased again when AKIN stage 3 was reached.
Simultaneous physicochemical analysis of blood and urine revealed standardized alterations that characterize AKI development in critically ill patients. These alterations paralleled AKI duration and severity. Future studies should consider including sequential evaluation of urine biochemistry as part of the armamentarium for AKI diagnosis and management.
Urine biochemistry; Urine electrolytes; Physicochemical analysis; Stewart approach; Acute kidney injury; Strong ion gap; Strong ion difference; Critically ill patients
Acute kidney injury (AKI) is a common source of morbidity after trauma. We sought to determine novel risk factors for AKI, by Acute Kidney Injury Network (AKIN) criteria, in critically ill trauma patients.
Materials and Methods
Prospective cohort study of 400 patients admitted to the ICU of a level one trauma center, followed for development of AKI over five days.
AKI developed in 147/400 (36.8%) patients. In multivariable regression analysis, independent risk factors for AKI included African American race (OR 1.86; 95% CI 1.08,3.18; p=0.024), body mass index ≥30 (OR 4.72 versus normal BMI, 95% CI 2.59, 8.61, p<0.001), diabetes mellitus (OR 3.26; 95% CI 1.30,8.20; p=0.012), abdominal Abbreviated Injury Scale score ≥4 (OR 3.78; 95% CI 1.79,7.96; p<0.001), and unmatched packed red blood cells administered during resuscitation (OR 1.13 per unit; 95% CI 1.04,1.23; p=0.004). AKIN stages 1, 2, and 3 were associated with hospital mortality rates of 9.8%, 13.7%, and 30.4%, respectively, compared with 3.8% for those without AKI (p<0.001).
AKI in critically ill trauma patients is associated with substantial mortality. The findings of African American race, obesity, and blood product administration as independent risk factors for AKI deserve further study to elucidate underlying mechanisms.
acute kidney injury; trauma; critical illness; race; obesity; transfusion; epidemiology; risk factors
Acute kidney injury (AKI) is common in hospitalized patients and is an important cause of mortality. This is a descriptive study of AKI in patients from Himachal Pradesh, India, located in Western Himalayan region. Over a period of 1 year, 102 patients with clinical and laboratory evidence of azotemia were included. Out of 102 patients, 84.3% had community acquired AKI and 15.7% had hospital acquired AKI. Medical causes were leading contributors (85.3%), with septicemia being the main factor (33.3%). Multiorgan failure was present in 59.8% patients. The overall mortality was 29.2%, and community acquired AKI was associated with higher mortality as compared to hospital-acquired AKI (22.5% vs 6.7%). AKI is still common in community and associated with high mortality. Septicemia, volume depletion and nephrotoxins were the leading cause of AKI in our study. Our study highlights the presence of hypotension, multiorgan failure and oliguria with mortality. Community-acquired AKI had higher mortality than hospital-acquired AKI.
Acute kidney injury; community-acquired acute kidney injury; hospital-acquired acute kidney injury; Western Himalayas
The diagnosis of acute kidney injury (AKI) is usually based on measurements of blood urea nitrogen (BUN) and serum creatinine. BUN and serum creatinine are not very sensitive or specific for the diagnosis of AKI because they are affected by many renal and nonrenal factors that are independent of kidney injury or kidney function. Biomarkers of AKI that are made predominantly by the injured kidney have been discovered in preclinical studies. In clinical studies of patients with AKI, some of these biomarkers (eg, interleukin-18, neutrophil gelatinase-associated lipocalin, and kidney injury molecule-1) have been shown to increase in the urine before the increase in serum creatinine. These early biomarkers of AKI are being tested in different types of AKI and in larger clinical studies. Biomarkers of AKI may also predict long-term kidney outcomes and mortality.
Biomarkers; Acute kidney injury; Interleukin-18; Neutrophil gelatinase-associated lipocalin; Kidney injury molecule-1; Cystatin C
To investigate the association between severity of acute kidney injury (AKI) and outcome, systemic inflammatory phenotype and HLA genotype in severe sepsis.
Prospective multicenter observational study done in 4 intensive care units in two university hospitals. Severe sepsis and septic shock patients with at least 2 organ failures based on the SOFA score were classified: 1) "no AKI", 2) "mild AKI" (grouping stage 1 and 2 of AKIN score) and 3) "severe AKI" (stage 3 of AKIN score). Sequential measurements: The vasopressor dependency index (VDI; dose and types of drugs) to evaluate the association between hemodynamic status and the development of early AKI; plasma levels of IL-10, macrophage migration inhibitory factor (MIF), IL-6 and HLA-DR monocyte expression. Genotyping of the 13 HLA-DRB1 alleles with deduction of presence of HLA-DRB3, -DRB4 and -DRB5 genes. We used multivariate analysis with competitive risk model to study associations. Overall, 176 study patients (146 with septic shock) were classified from AKIN score as "no AKI" (n = 43), "mild AKI" (n = 74) or "severe AKI" (n = 59). The VDI did not differ between groups of AKI. After adjustment, "mild and severe AKI" were an independent risk factor for mortality (HR 2.42 95%CI[1.01-5.83], p = 0.048 and HR 1.99 95%CI[1.30-3.03], p = 0.001 respectively). "Severe AKI" had higher levels of plasma IL-10, MIF and IL-6 compared to “no AKI” and mild AKI (p<0.05 for each), with no difference in mHLA-DR at day 0. HLA-DRB genotyping showed a significantly lower proportion of 4 HLA-DRB alleles among patients requiring renal replacement therapy (RRT) (58%) than in patients with severe AKI who did not receive RRT (84%) (p = 0.004).
AKI severity is independently associated with mortality and plasma IL-10, MIF or IL-6 levels. Presence of 4 alleles of HLA-DRB in severe AKI patients seems associated with a lower need of RRT.
Little information exists about the impact of acute kidney injury (AKI) in critically ill patients with the pandemic 2009 influenza A (H1N1) virus infection.
We conducted a prospective, observational, multicenter study in 148 Spanish intensive care units (ICUs). Patients with chronic renal failure were excluded. AKI was defined according to Acute Kidney Injury Network (AKIN) criteria.
A total of 661 patients were analyzed. One hundred eighteen (17.7%) patients developed AKI; of these, 37 (31.4%) of the patients with AKI were classified as AKI I, 15 (12.7%) were classified as AKI II and 66 (55.9%) were classified as AKI III, among the latter of whom 50 (75.7%) required continuous renal replacement therapy. Patients with AKI had a higher Acute Physiology and Chronic Health Evaluation II score (19.2 ± 8.3 versus 12.6 ± 5.9; P < 0.001), a higher Sequential Organ Failure Assessment score (8.7 ± 4.2 versus 4.8 ± 2.9; P < 0.001), more need for mechanical ventilation (MV) (87.3% versus 56.2%; P < 0.01, odds ratio (OR) 5.3, 95% confidence interval (CI) 3.0 to 9.4), a greater incidence of shock (75.4% versus 38.3%; P < 0.01, OR 4.9, 95% CI, 3.1 to 7.7), a greater incidence of multiorgan dysfunction syndrome (92.4% versus 54.7%; P < 0.01, OR 10.0, 95% CI, 4.9 to 20.21) and a greater incidence of coinfection (23.7% versus 14.4%; P < 0.01, OR 1.8, 95% CI, 1.1 to 3.0). In survivors, patients with AKI remained on MV longer and ICU and hospital length of stay were longer than in patients without AKI. The overall mortality was 18.8% and was significantly higher for AKI patients (44.1% versus 13.3%; P < 0.01, OR 5.1, 95% CI, 3.3 to 7.9). Logistic regression analysis was performed with AKIN criteria, and it demonstrated that among patients with AKI, only AKI III was independently associated with higher ICU mortality (P < 0.001, OR 4.81, 95% CI 2.17 to 10.62).
In our cohort of patients with H1N1 virus infection, only those cases in the AKI III category were independently associated with mortality.
Pre-renal acute kidney injury (AKI) is assumed to represent a physiological response to underperfusion. Its diagnosis is retrospective after a transient rise in plasma creatinine, usually associated with evidence of altered tubular transport, particularly that of sodium. In order to test whether pre-renal AKI is reversible because injury is less severe than that of sustained AKI, we measured urinary biomarkers of injury (cystatin C, neutrophil gelatinase-associated lipocalin (NGAL), γ-glutamyl transpeptidase, IL-18, and kidney injury molecule-1 (KIM-1)) at 0, 12, and 24 h following ICU admission. A total of 529 patients were stratified into groups having no AKI, AKI with recovery by 24 h, recovery by 48 h, or the composite of AKI greater than 48 h or dialysis. Pre-renal AKI was identified in 61 patients as acute injury with recovery within 48 h and a fractional sodium excretion <1%. Biomarker concentrations significantly and progressively increased with the duration of AKI. After restricting the AKI recovery within the 48 h cohort to pre-renal AKI, this increase remained significant. The median concentration of KIM-1, cystatin C, and IL-18 were significantly greater in pre-renal AKI compared with no-AKI, while NGAL and γ-glutamyl transpeptidase concentrations were not significant. The median concentration of at least one biomarker was increased in all but three patients with pre-renal AKI. Thus, the reason why some but not all biomarkers were increased requires further study. The results suggest that pre-renal AKI represents a milder form of injury.
acute kidney injury; acute renal failure; creatinine
This study aimed to determine the diagnostic and prognostic value of urinary biomarkers of intrinsic acute kidney injury (AKI) when patients were triaged in the emergency department.
Intrinsic AKI is associated with nephron injury and results in poor clinical outcomes. Several urinary biomarkers have been proposed to detect and measure intrinsic AKI.
In a multicenter prospective cohort study, 5 urinary biomarkers (urinary neutrophil gelatinase–associated lipocalin, kidney injury molecule-1, urinary liver-type fatty acid binding protein, urinary interleukin-18, and cystatin C) were measured in 1,635 unselected emergency department patients at the time of hospital admission. We determined whether the biomarkers diagnosed intrinsic AKI and predicted adverse outcomes during hospitalization.
All biomarkers were elevated in intrinsic AKI, but urinary neutrophil gelatinase-associated lipocalin was most useful (81% specificity, 68% sensitivity at a 104-ng/ml cutoff) and predictive of the severity and duration of AKI. Intrinsic AKI was strongly associated with adverse in-hospital outcomes. Urinary neutrophil gelatinase-associated lipocalin and urinary kidney injury molecule 1 predicted a composite outcome of dialysis initiation or death during hospitalization, and both improved the net risk classification compared with conventional assessments. These biomarkers also identified a substantial subpopulation with low serum creatinine at hospital admission, but who were at risk of adverse events.
Urinary biomarkers of nephron damage enable prospective diagnostic and prognostic stratification in the emergency department.
acute kidney injury; biomarkers; outcomes
Despite the substantial progress in the quality of critical care, the incidence and mortality of acute kidney injury (AKI) continues to rise during hospital admissions. We conducted a national, multicenter, prospective, epidemiological survey to evaluate the importance of AKI in intensive care units (ICUs) in Hungary. The objectives of this study were to determine the incidence of AKI in ICU patients; to characterize the differences in aetiology, illness severity and clinical practice; and to determine the influencing factors of the development of AKI and the patients' outcomes.
We analysed the demographic, morbidity, treatment modality and outcome data of patients (n = 459) admitted to ICUs between October 1st, 2009 and November 30th, 2009 using a prospectively filled in electronic survey form in 7 representative ICUs.
The major reason for ICU admission was surgical in 64.3% of patients and medical in the remaining 35.7%. One-hundred-twelve patients (24.4%) had AKI. By AKIN criteria 11.5% had Stage 1, 5.4% had Stage 2 and 7.4% had Stage 3. In 44.0% of patients, AKI was associated with septic shock. Vasopressor treatment, SAPS II score, serum creatinine on ICU admission and sepsis were the independent risk factors for development of any stage of AKI. Among the Stage 3 patients (34) 50% received renal replacement therapy. The overall utilization of intermittent renal replacement therapy was high (64.8%). The overall in-hospital mortality rate of AKI was 49% (55/112). The ICU mortality rate was 39.3% (44/112). The independent risk factors for ICU mortality were age, mechanical ventilation, SOFA score and AKI Stage 3.
For the first time we have established the incidence of AKI using the AKIN criteria in Hungarian ICUs. Results of the present study confirm that AKI has a high incidence and is associated with high ICU and in-hospital mortality.
To determine clinical and genomic characteristics and in-hospital mortality risk associated with acute kidney injury (AKI) in the multicenter prospective cohort of patients with blunt trauma.
Summary Background Data
Less severe stages of AKI characterized by small changes in serum creatinine (sCr) are inadequately studied among trauma patients.
We performed a secondary analysis of the “Inflammation and the Host Response to Injury” (GlueGrant) database to include adult blunt trauma patients without history of kidney disease. AKI was defined by the RIFLE (Risk, Injury, Failure, Loss, and End-stage Kidney) classification, which requires a 50% increase in sCr and stratifies patients into three severity stages: risk, injury, and failure. Association between all stages of AKI and in-hospital mortality was analyzed using a multivariable logistic regression analysis. Genome-wide expression analysis was performed on whole blood leukocytes obtained within 12 hours of trauma.
AKI occurred in 26% of 982 patients. The adjusted risk for hospital death was three times higher for patients with AKI compared to patients without AKI (odds ratio [OR] 3.05 (95% confidence interval [CI], (1.73, TO 5.40). This risk was evident in a dose-response manner and even patients with mild AKI had OR for dying of 2.57 (95% CI, 1.19 to 5.50) compared to patients without AKI. Genome-wide expression analysis failed to show a significant number of genes whose expression could discriminate among patients with and without AKI.
In a multi-center prospective cohort of blunt trauma patients, AKI characterized by small changes in sCr was associated with an independent risk of hospital death.
trauma; inflammation; genomics; leukocytes
The aim of this study was to investigate the factors associated with acute kidney injury (AKI) in patients with visceral leishmaniasis (VL). The study patients had a diagnosis of VL and were admitted to a tertiary hospital. A multivariate analysis was performed to analyze the risk factors for AKI. A total of 224 patients were included. The mean age was 36 ± 15 years. AKI was observed in 33.9% of cases. Risk factors associated with AKI were male gender (odds ratio [OR] = 2.2; P = 0.03), advanced age (OR = 1.05; P < 0.001), and jaundice (OR = 2.9; P = 0.002). There was an association between amphotericin B use and AKI (OR = 18.4; P < 0.0001), whereas glucantime use was associated with lower incidence of AKI compared with amphotericin B use (OR = 0.05; P < 0.0001). Mortality was 13.3%, and it was higher in AKI patients (30.2%). Therefore, factors associated with AKI were male gender, advanced age, and jaundice. Amphotericin B was an important cause of AKI in VL.
Renal resistive index (RI), determined by Doppler ultrasonography, directly reveals and quantifies modifications in renal vascular resistance. The aim of this study was to evaluate if mean arterial pressure (MAP) is determinant of renal RI in septic, critically ill patients suffering or not from acute kidney injury (AKI).
This prospective observational study included 96 patients. AKI was defined according to RIFLE criteria and transient or persistent AKI according to renal recovery within 3 days.
Median renal RIs were 0.72 (0.68-0.75) in patients without AKI and 0.76 (0.72-0.80) in patients with AKI (P=0.001). RIs were 0.75 (0.72-0.79) in transient AKI and 0.77 (0.70-0.80) in persistent AKI (P=0.84). RI did not differ in patients given norepinephrine infusion and was not correlated with norepinephrine dose. RI was correlated with MAP (ρ= -0.47; P=0.002), PaO2/FiO2 ratio (ρ= -0.33; P=0.04) and age (ρ=0.35; P=0.015) only in patients without AKI.
A poor correlation between renal RI and MAP, age, or PaO2/FiO2 ratio was found in septic and critically ill patients without AKI compared to patients with AKI. These findings suggest that determinants of RI are multiple. Renal circulatory response to sepsis estimated by Doppler ultrasonography cannot reliably be predicted simply from changes in systemic hemodynamics. As many factors influence its value, the interest in a single RI measurement at ICU admission to determine optimal MAP remains uncertain.
Acute kidney injury (AKI) occurs commonly in the setting of orthotopic liver transplantation (OLT). To date, the correlation between AKI post-OLT and pre-operative changes in renal function has not been rigorously examined.
To determine the impact of pre-OLT changes in renal function on AKI post-OLT, as well as to identify risk factors for AKI, we analyzed the prospectively maintained NIDDK Liver Transplantation Database, which includes patients who received their first OLT between April 15, 1990, and June 30, 1994. We used the AKI Network definition of AKI.
Surprisingly, univariate analysis revealed that worsening renal function while awaiting OLT was protective to the development of AKI post-OLT. Independent predictors of AKI were increased body mass index, increased Childs-Pugh-Turcott score, decreased urine output during cross-clamp, improved renal function while awaiting OLT, increased post-operative stroke volume, non-Caucasian race, and post-operative use of tacrolimus.
The correlation between improving renal function pre-OLT and AKI post-OLT may represent true protection (via ischemic pre-conditioning) or, alternatively, a masking of milder forms of AKI (via improved renal perfusion through correction of the cirrhotic milieu). These results highlight the complex interaction between liver and kidney disease, and suggest that not only the etiology but also the course of pre-OLT renal dysfunction may be a critical determinant of renal function post-OLT.