In-hospital Acute Kidney Injury Research Articles

Clinical impact of disinvestment in hydroxyethyl starch for patients undergoing coronary artery bypass surgery: a retrospective observational study.

To examine the effect of discontinuing hydroxyethyl starch (HES) solutions on length of hospital stay, transfusion, risk of death, acute kidney injury (AKI), and dialysis. We conducted a historical cohort study of linked administrative and clinical databases in patients undergoing coronary artery bypass surgery (CABG) on cardiopulmonary bypass. We used propensity scores to match patients who did not receive HES (after discontinuation) with patients exposed to HES (before discontinuation) and also controlled for albumin exposure. Hospital length of stay (the primary outcome) was analyzed using Fine-Gray proportional hazard regression, with hospital discharge as the outcome and death as a competing risk. Adverse outcomes were compared between matched patients using conditional logistic regression. We compared 1,085 propensity score-matched pairs (n = 2,170) from a pool of 2,757 patients. Discontinuation of HES was associated with shorter length of hospital stay, as evidenced by an increased probability of discharge (hazard ratio, 1.24; 95% confidence interval [CI], 1.14 to 1.35) and a reduced risk of red blood cell transfusion (odds ratio [OR], 0.68; 95% CI, 0.55 to 0.84), plasma transfusion (OR, 0.48; 95% CI, 0.34 to 0.66), and platelet transfusion (OR, 0.62; 95% CI, 0.44 to 0.87). Discontinuation of HES was not associated with in-hospital mortality (OR, 0.74; 95% CI, 0.36 to 1.54), AKI (OR, 0.84; 95% CI, 0.57 to 1.25), or dialysis (OR, 0.83; 95% CI, 0.25 to 2.73). For patients undergoing CABG on cardiopulmonary bypass, discontinuation of HES was associated with reduced hospital length of stay and reduced blood product transfusion, without measurable change in renal failure, dialysis rate, or in-hospital mortality. Our results should be interpreted with caution, though we found no evidence of harms associated with discontinuing HES. www.clinicaltrials.gov (NCT02329158); registered 31 December, 2014.

Update on Perioperative Acute Kidney Injury.

Acute kidney injury (AKI) in the perioperative period is a common complication and is associated with increased morbidity and mortality. A standard definition and staging system for AKI has been developed, incorporating a reduction of the urine output and/or an increase of serum creatinine. Novel biomarkers may detect kidney damage in the absence of a change in function and can also predict the development of AKI. Several specific considerations for AKI risk are important in surgical patients. The surgery, especially major and emergency procedures in critically ill patients, may cause AKI. In addition, certain comorbidities, such as chronic kidney disease and chronic heart failure, are important risk factors for AKI. Diuretics, contrast agents, and nephrotoxic drugs are commonly used in the perioperative period and may result in a significant amount of in-hospital AKI. Before and during surgery, anesthetists are supposed to optimize the patient, including preventing and treating a hypovolemia and correcting an anemia. Intraoperative episodes of hypotension have to be avoided because even short periods of hypotension are associated with an increased risk of AKI. During the intraoperative period, urine output might be reduced in the absence of kidney injury or the presence of kidney injury with or without fluid responsiveness. Therefore, fluids should be used carefully to avoid hypovolemia and hypervolemia. The Kidney Disease: Improving Global Outcomes guidelines suggest implementing preventive strategies in high-risk patients, which include optimization of hemodynamics, restoration of the circulating volume, institution of functional hemodynamic monitoring, and avoidance of nephrotoxic agents and hyperglycemia. Two recently published studies found that implementing this bundle in high-risk patients reduced the occurrence of AKI in the perioperative period. In addition, the application of remote ischemic preconditioning has been studied to potentially reduce the incidence of perioperative AKI. This review discusses the epidemiology and pathophysiology of surgery-associated AKI, highlights the importance of intraoperative oliguria, and emphasizes potential preventive strategies.

Transient acute kidney injury after cardiac surgery does not independently affect postoperative outcomes.

The objective of this study was to assess the incidence of in-hospital acute kidney injury (AKI) after cardiac surgery by comparing preoperative baseline renal function with renal function during the postoperative period and at discharge, and to relate these indices with in-hospital postoperative outcomes. A retrospective analysis was performed over a 4-year period from a series of 426 adult patients. Kidney function was based on serum creatinine (SCr), Cockroft-Gault estimated creatinine clearance (eCrCl), and glomerular filtration rate estimated with the Modification of Diet in Renal Disease formula (eGFR). Baseline values were compared with "peak" values of altered kidney function postoperatively, and "discharge" values. In-hospital mortality and complication rates were compared between patients with transient and persistent AKI, and those without postoperative AKI. After surgery, AKI (Risk-Injury-Failure-Loss-Endstage [RIFLE] classes Injury and Failure) was diagnosed in 14.6-17.5% of patients based on peak values. AKI diagnosis was reduced to 3.6-4.5% when SCr, eCrCl, and eGFR were measured at discharge. In-hospital mortality of patients with transient AKI was 4% versus 26% in patients with AKI at discharge (odds ratio = 0.11, 95% confidence interval 0.02-0.62, P = 0.011). A diagnosis of AKI based on measurements of eGFR during the postoperative period was nearly four times more frequent than the same diagnosis at discharge. Transient AKI was the predominate presentation of postoperative kidney dysfunction in this study. Transient AKI did not affect in-hospital outcomes compared with patients without AKI. Patients with persistent AKI at discharge had the highest mortality.

Using the Kinetic Estimating Glomerular Filtration Rate Equation for Estimating Glomerular Filtration Rate and Detecting Acute Kidney Injury: A Pilot Study

Background: Estimating the glomerular filtration rate (eGFR) when the creatinine (Cr) is rapidly changing, as in acute kidney injury (AKI), has been a challenge. The Kinetic Estimated Glomerular Filtration Rate (KeGFR) formula by S. Chen estimates the GFR in the acute state by factoring the time interval between rising Cr values and the volume of distribution (V_D). It provides the clinician with an eGFR value for each non-steady state Cr value. We applied the KeGFR formula to detect AKI in an adult non-ICU inpatient setting. We then compared KeGFR with the current standard Acute Kidney Injury Network (AKIN criteria) and Risk Injury Failure Loss End-Stage Kidney Disease (RIFLE criteria) and new criteria (Waikar-Bonventre, Delta check) for AKI detection. Methods: A total of 250 consecutive adult patients admitted to the Medical wards were screened. Patient episodes with a change in Cr of > 4.3% (Biological Variation) were included in the study (n = 80). The KeGFR equation was applied to this cohort after calculating the V_D individually after estimating the initial GFR by using MDRD equation. A fall in KeGFR of 25% or more was considered as AKI. The AKIN, Waikar-Bonventre, RIFLE, and Delta Check criteria were also applied to this cohort and compared with the KeGFR criterion. Clinical adjudication was performed when there was discordance between AKI episodes detected by AKIN and KeGFR criteria. Results: There were 50 episodes of AKI by AKIN classification and 31 episodes by KeGFR criterion. All but 1 (30) episode detected by KeGFR criterion fulfilled the AKI definition by AKIN. AKIN diagnosed an additional 20 episodes. However, all of these had an elevated Cr level on admission; thus, requiring the incorporation of baseline Cr by AKIN which is not part of the KeGFR formula. Five of these 20 patients were deemed as not having AKI by clinical adjudication. All patients with in-hospital AKI and ongoing AKI were detected by both the criteria. The KeGFR criteria detected almost all (24/25) episodes of AKI identified by the Waikar-Bonventre method. The latter method detected 77% (24/31) of the AKI episodes identified by KeGFR. Conclusion: The KeGFR equation can be readily applied to estimate GFR in the non-steady state. A KeGFR-based criterion successfully detected ongoing and in-hospital AKI in this study. Community acquired AKI that did not progress after admission was not detected by the KeGFR criterion.

40EMF Outpatient Lisinopril and Losartan Blood Levels Are Associated With In-Hospital Acute Kidney Injury Among Patients With Acute Heart Failure

We report a novel tandem liquid chromatography mass spectrometry (LC/MS/MS) method for the simultaneous bioanalytical assessment of blood levels for multiple commonly prescribed medications, including angiotensin-converting enzyme inhibitors (ACEI) or angiotensin II receptor blockers (ARB). Despite morbidity and mortality benefits of ACEI/ARBs, these medications may cause a transient rise in creatinine and occasionally contribute to hypotension, which in turn may result in acute kidney injury (AKI). Previous studies of AKI in the setting of ACEI/ARBs have not assessed medication levels. We hypothesized ACEI/ARB plasma levels in/above reference range for patients with AHF treated by intravenous (IV) diuretics would be associated with increased risk of in-hospital AKI compared to undetectable/low ACEI/ARB plasma levels. From June 2016 to June 2017, adults with AHF were approached for consent. Exclusions were: 1) no outpatient ACEI/ARB, 2) systolic blood pressure <90 mm Hg, 3) IV diuretic before enrollment, 4) allergy to furosemide or bumetanide, or 5) any dialysis. Patients were given an initial IV dose of diuretic (2x their daily dose) and received standard clinical care during hospitalization. Medication plasma levels at ED presentation, before AHF therapy, were assessed using LC/MS/MS. Standardized plasma concentrations for each medication were computed using the median published reference range. AKI was defined as a rise in creatinine at 48 hours (or at hospital discharge, if unavailable) of ≥0.3 mg/dL or ≥1.5x baseline. Mean age for the 37 patients was 65.9 years (sd 14.6), 20 (54.0%) were female, 11 (29.7%) were African American, 10 (32.3%) had an ejection fraction <40%, and 11 (29.8%) did not have detectible ACEI/ARB levels. Of the 5 (13.5%) patients who developed in-hospital AKI, 4 had medications in/above reference range. ACEI/ARB levels were higher for patients with AKI (Figure), and levels in/above reference range were associated with a rise in creatinine (beta 0.22, 95% confidence interval 0.02-0.42, P=0.03, adjusted for age, sex, and race). Patients with AHF may be more likely to develop AKI in the hospital if they have normal/high ACEI/ARB blood levels at ED presentation. Bioanalytical assessment of ACEI/ARB levels may prove useful for guiding in-hospital medical therapy for AHF.

The ICE-AKI study: Impact analysis of a Clinical prediction rule and Electronic AKI alert in general medical patients.

BackgroundAcute kidney injury (AKI) is assoicated with high mortality and measures to improve risk stratification and early identification have been urgently called for. This study investigated whether an electronic clinical prediction rule (CPR) combined with an AKI e-alert could reduce hospital-acquired AKI (HA-AKI) and improve associated outcomes.Methods and findingsA controlled before-and-after study included 30,295 acute medical admissions to two adult non-specialist hospital sites in the South of England (two ten-month time periods, 2014–16); all included patients stayed at least one night and had at least two serum creatinine tests. In the second period at the intervention site a CPR flagged those at risk of AKI and an alert was generated for those with AKI; both alerts incorporated care bundles. Patients were followed-up until death or hospital discharge. Primary outcome was change in incident HA-AKI. Secondary outcomes in those developing HA-AKI included: in-hospital mortality, AKI progression and escalation of care. On difference-in-differences analysis incidence of HA-AKI reduced (odds ratio [OR] 0.990, 95% CI 0.981–1.000, P = 0.049). In-hospital mortality in HA-AKI cases reduced on difference-in-differences analysis (OR 0.924, 95% CI 0.858–0.996, P = 0.038) and unadjusted analysis (27.46% pre vs 21.67% post, OR 0.731, 95% CI 0.560–0.954, P = 0.021). Mortality in those flagged by the CPR significantly reduced (14% pre vs 11% post intervention, P = 0.008). Outcomes for community-acquired AKI (CA-AKI) cases did not change. A number of process measures significantly improved at the intervention site. Limitations include lack of randomization, and generalizability will require future investigation.ConclusionsIn acute medical admissions a multi-modal intervention, including an electronically integrated CPR alongside an e-alert for those developing HA-AKI improved in-hospital outcomes. CA-AKI outcomes were not affected. The study provides a template for investigations utilising electronically generated prediction modelling. Further studies should assess generalisability and cost effectiveness.Trial registrationClinicaltrials.org NCT03047382.

Comparison of Outcomes of Transfemoral Versus Transapical Approach for Transcatheter Aortic Valve Implantation

Post hoc analyses of clinical trials have shown superior outcomes for a transfemoral (TF) compared with a transapical (TA) approach for transcatheter aortic valve implantation (TAVI). There are few contemporary data on utilization and outcomes of TF versus TA TAVI in real-world patient populations. Using the National Inpatient Sample 2011 to 2014, we identified TF-TAVI and TA-TAVI procedures using ICD-9 procedure codes 35.05 and 35.06, respectively. A propensity-matched cohort of TF and TA TAVI procedures balanced on 23 baseline characteristics was assembled. Outcomes included in-hospital mortality, acute kidney injury (AKI), AKI requiring dialysis (AKI-D) and postoperative stroke. A total of 7,973 TAVI procedures representative of 39,745 procedures nationally were included in the study. Of these, 80.2% were performed using a TF approach while 19.8% used a TA approach. Patients in the TF-TAVI group were older (mean age 81.7 vs 80.4 years, p < 0.001), with a higher prevalence of heart failure (12.7% vs 7.6%, p < 0.001) and lower prevalence of peripheral vascular disease (28.0% vs 35.5%, p < 0.001) compared with the TA-TAVI group. In 1,576 propensity-matched pairs of TF-TAVI and TA-TAVI procedures, TF-TAVI was associated with significantly lower in-hospital mortality (odds ratio [OR] 0.61, 95% confidence interval [CI] 0.42 to 0.88, p = 0.01), lower rates of AKI (0.53, 95% CI 0.44 to 0.63, p < 0.001), similar rates of AKI-D (OR 0.77, 95% CI 0.44 to 1.38, p = 0.38) and postoperative stroke (OR 1.19, 95% CI 0.67 to 2.10, p = 0.56) compared with TA-TAVI. In conclusion, TF-TAVI is associated with lower rates of in-hospital mortality and AKI compared with TA-TAVI. A TF approach should be preferred over a TA approach for TAVI whenever possible.

Outpatient Lisinopril and Losartan Blood Levels are Associated With In-Hospital Acute Kidney Injury Among Patients with Acute Heart Failure

IntroductionWe report on a novel tandem liquid chromatography mass spectrometry (LC/MS/MS) method for the simultaneous bioanalytical assessment of blood levels for multiple commonly prescribed medications, including angiotensin-converting enzyme inhibitors (ACEI) and angiotensin II receptor blockers (ARB). Despite morbidity and mortality benefits of ACEI/ARBs, these medications may cause transient rise in creatinine and occasionally contribute to hypotension, which in turn may result in acute kidney injury (AKI). Previous studies of AKI in the setting of ACEI/ARBs have not assessed medication levels.HypothesisWe hypothesized ACEI/ARB plasma levels in/above reference range for patients with AHF treated by intravenous (IV) diuretics would be associated with increased risk of in-hospital AKI compared to undetectable/low ACEI/ARB plasma levels.MethodsFrom June 2016 to June 2017, adults with AHF were approached for consent. Patients were excluded for: 1) no outpatient ACEI/ARB, 2) systolic blood pressure <90 mm Hg, 3) IV diuretic before enrollment, 4) allergy to furosemide or bumetanide, or 5) any dialysis. Patients were given an initial IV dose of diuretic (2x their daily dose) and received standard clinical care during hospitalization. LC/MS/MS assessed medication plasma levels at ED presentation, before AHF therapy. Standardized plasma concentrations for each medication were computed using the median published reference range. AKI was defined as a rise in creatinine at 48 hours (or at hospital discharge, if unavailable) of ≥0.3 mg/dL or ≥1.5x baseline.ResultsMean age for the 37 patients was 65.9 years (sd 14.6), 20 (54.0%) were female, 11 (29.7%) were African American, 10 (32.3%) had an ejection fraction <40%, and 11 (29.8%) did not have detectible ACEI/ARB levels. Of the 5 (13.5%) patients who developed in-hospital AKI, 4 had medications in/above reference range. ACEI/ARB levels were higher for patients with AKI (Figure), and ACEI/ARB levels in/above reference range at the time of ED presentation were associated with an in-hospital rise in creatinine (beta 0.22, 95% confidence interval 0.02-0.42, P=0.03, adjusted for age, sex, and race).ConclusionsPatients with AHF may be more likely to develop AKI in the hospital if they have ACEI/ARB blood levels in/above reference range at ED presentation. Bioanalytical assessment of ACEI/ARB levels may prove useful for guiding in-hospital medical therapy for AHF. We report on a novel tandem liquid chromatography mass spectrometry (LC/MS/MS) method for the simultaneous bioanalytical assessment of blood levels for multiple commonly prescribed medications, including angiotensin-converting enzyme inhibitors (ACEI) and angiotensin II receptor blockers (ARB). Despite morbidity and mortality benefits of ACEI/ARBs, these medications may cause transient rise in creatinine and occasionally contribute to hypotension, which in turn may result in acute kidney injury (AKI). Previous studies of AKI in the setting of ACEI/ARBs have not assessed medication levels. We hypothesized ACEI/ARB plasma levels in/above reference range for patients with AHF treated by intravenous (IV) diuretics would be associated with increased risk of in-hospital AKI compared to undetectable/low ACEI/ARB plasma levels. From June 2016 to June 2017, adults with AHF were approached for consent. Patients were excluded for: 1) no outpatient ACEI/ARB, 2) systolic blood pressure <90 mm Hg, 3) IV diuretic before enrollment, 4) allergy to furosemide or bumetanide, or 5) any dialysis. Patients were given an initial IV dose of diuretic (2x their daily dose) and received standard clinical care during hospitalization. LC/MS/MS assessed medication plasma levels at ED presentation, before AHF therapy. Standardized plasma concentrations for each medication were computed using the median published reference range. AKI was defined as a rise in creatinine at 48 hours (or at hospital discharge, if unavailable) of ≥0.3 mg/dL or ≥1.5x baseline. Mean age for the 37 patients was 65.9 years (sd 14.6), 20 (54.0%) were female, 11 (29.7%) were African American, 10 (32.3%) had an ejection fraction <40%, and 11 (29.8%) did not have detectible ACEI/ARB levels. Of the 5 (13.5%) patients who developed in-hospital AKI, 4 had medications in/above reference range. ACEI/ARB levels were higher for patients with AKI (Figure), and ACEI/ARB levels in/above reference range at the time of ED presentation were associated with an in-hospital rise in creatinine (beta 0.22, 95% confidence interval 0.02-0.42, P=0.03, adjusted for age, sex, and race). Patients with AHF may be more likely to develop AKI in the hospital if they have ACEI/ARB blood levels in/above reference range at ED presentation. Bioanalytical assessment of ACEI/ARB levels may prove useful for guiding in-hospital medical therapy for AHF.

The relationship between ICU hypotension and in-hospital mortality and morbidity in septic patients

PurposeCurrent guidelines recommend maintaining a mean arterial pressure (MAP) ≥ 65 mmHg in septic patients. However, the relationship between hypotension and major complications in septic patients remains unclear. We, therefore, evaluated associations of MAPs below various thresholds and in-hospital mortality, acute kidney injury (AKI), and myocardial injury.MethodsWe conducted a retrospective analysis using electronic health records from 110 US hospitals. We evaluated septic adults with intensive care unit (ICU) stays ≥ 24 h from 2010 to 2016. Patients were excluded with inadequate blood pressure recordings, poorly documented potential confounding factors, or renal or myocardial histories documented within 6 months of ICU admission. Hypotension exposure was defined by time-weighted average mean arterial pressure (TWA-MAP) and cumulative time below 55, 65, 75, and 85 mmHg thresholds. Multivariable logistic regressions determined the associations between hypotension exposure and in-hospital mortality, AKI, and myocardial injury.ResultsIn total, 8,782 patients met study criteria. For every one unit increase in TWA-MAP < 65 mmHg, the odds of in-hospital mortality increased 11.4% (95% CI 7.8%, 15.1%, p < 0.001); the odds of AKI increased 7.0% (4.7, 9.5%, p < 0.001); and the odds of myocardial injury increased 4.5% (0.4, 8.7%, p = 0.03). For mortality and AKI, odds progressively increased as thresholds decreased from 85 to 55 mmHg.ConclusionsRisks for mortality, AKI, and myocardial injury were apparent at 85 mmHg, and for mortality and AKI risk progressively worsened at lower thresholds. Maintaining MAP well above 65 mmHg may be prudent in septic ICU patients.

IP011. Factors Associated With Postoperative Renal Dysfunction and the Subsequent Impact on Survival After Open Juxtarenal Abdominal Aortic Aneurysm Repair

Renal dysfunction is a well-described complication of open juxtarenal abdominal aortic aneurysm repair; however, the associated risk factors and corresponding impact on survival are not well described. We identified all patients not on hemodialysis (HD) undergoing open repair of nonruptured juxtarenal aneurysms in the Vascular Quality Initiative from 2003 to 2017. We used mixed effects logistic regression to determine factors associated with in-hospital acute kidney injury (AKI; defined as serum creatinine increase >0.5 mg/dL) and dialysis as well as the association between postoperative renal function and perioperative mortality. Cox regression was used to determine the association between postoperative renal complications and long-term survival. We identified 2635 open juxtarenal repairs, of which 621 (24%) were complicated by AKI. The majority of these (20% of the overall cohort) were AKI alone, but 2.2% required temporary HD and 1.7% were permanently dialysis dependent. Factors independently associated with postoperative renal dysfunction included renal-visceral ischemia time (per minute: odds ratio [OR], 1.01 [1.01-1.02]; P < .001), clamp site (above both renal arteries: OR, 1.4 [1.1-1.8; P = .02]; supraceliac: OR, 1.7 [1.1-2.5; P = .01]), statin use (OR, 1.5 [1.1-2.0]; P = .01), male sex (OR, 1.7 [1.2-2.2]; P = .002), and preoperative renal function (glomerular filtration rate [GFR] 45-60 mL/min/1.73 m2: OR, 1.8 [1.3-2.5; P < .001]; GFR 30-45 mL/min/1.73 m2: OR, 1.9 [1.2-2.8; P = .003]; GFR <30 mL/min/1.73 m2: OR, 8.0 [3.8-16.7; P < .001]). When renal-visceral ischemia time was categorized, there was no difference in risk of postoperative renal dysfunction until >25 minutes, but risk increased stepwise thereafter (25-39 minutes: OR, 1.6 [1.2-2.1; P = .004]; 40+ minutes: OR, 2.6 [1.9-3.5; P < .001]). Neither mannitol nor the use of cold renal perfusion was associated with renal complications or mortality in the overall cohort or in the subset of patients with clamp times >25 minutes. Postoperative renal dysfunction was associated with higher adjusted perioperative mortality (AKI: OR, 2.6 [1.4-5.0; P < .01]; HD: OR, 10.5 [4.0-27.6; P < .001]) and significantly higher risk of long-term mortality (AKI: hazard ratio, 1.5 [1.0-2.1; P = .049]; HD: hazard ratio, 5.8 [3.2-10.3; P < .001]; Fig). Although multiple patient and intraoperative factors are associated with postoperative renal dysfunction after open juxtarenal repair, the use of mannitol and cold renal perfusion were not. Postoperative renal dysfunction, even a mild elevation in creatinine concentration, is associated with higher perioperative and long-term mortality.

Impact of Pre-procedural Cerebrovascular Events on Clinical Outcomes After Transcatheter Aortic Valve Implantation in Patients with Severe Aortic Stenosis.

Transcatheter aortic valve implantation (TAVI) is an increasingly common treatment of symptomatic severe aortic valve stenosis (AS). Thus, it is reasonable to carefully investigate the impact of individual clinical factors on outcomes after TAVI. We aimed to investigate the impact of the previous cerebro-vascular events (CVEs) on outcomes of patients with severe AS undergoing TAVI. A total of 148 consecutive patients scheduled for TAVI were included and stratified as with and without a history of CVEs (stroke or transient ischemic attack). Frailty features were also assessed. The primary endpoint was a 12-month all-cause mortality. Seventeen (11.5%) patients had a history of CVEs (the CVE group). At 30 days and 12 months, all-cause mortality was higher in the CVE group [30-day: 5 (29.4%) vs. 7 (5.3%); p=0.005; 12-month: 9 (52.9%) vs. 13 (9.9%); p=0.001]. Similarly, at the longest available follow-up, mortality was higher in the CVE group [10 (58.8%) vs. 23 (17.6%); p=0.001]. Similar rates of other complications after TAVI were noted, apart from inhospital acute kidney injury (AKI) grade 3 [3 (17.6%) vs. 5 (3.8%); p=0.049] and blood transfusions [9 (52.9%) vs. 35 (26.7%); p=0.026]. Results of 5MWT and Katz index assessment indicated a greater level of frailty in the CVE group. There were no differences in subsequent events including CVEs, bleeding, myocardial infarction, and new-onset of atrial fibrillation (AF) at 12 months between the groups. We showed that a history of CVEs in patients with severe AS undergoing TAVI is associated with a higher long-term mortality.

In-Hospital Acute Kidney Injury After TKA Revision With Placement of an Antibiotic Cement Spacer

BackgroundThere is mounting evidence that treatment of periprosthetic joint infection of the knee with an antibiotic cement spacer (ACS) may increase risk for acute kidney injury (AKI). We sought to determine the incidence, as well as potential risk factors, of in-hospital AKI in this cohort. MethodsWe retrospectively identified 75 patients that received either a static or articulating ACS at a single institution. In-hospital AKI was defined by a more than 50% rise in serum creatinine from preoperative baseline to at least 1.4 mg/dL. Our secondary outcome was percent change in creatinine from preoperative to peak postoperative value. Variables were analyzed for the outcome of AKI with univariate logistic regression. A final multivariate model for percent change in creatinine was formed while controlling for age, gender, body mass index, and baseline creatinine. ResultsThe incidence of AKI was 14.6%, occurring at a mean of 6.3 days (2-8 days). A lower preoperative hemoglobin (odds ratio = 1.82, P = .015) significantly increased risk for AKI on univariate analysis. Diagnosis of either hypertension or diabetes also showed a strong statistical trend (P = .056). On multivariate regression, lower preoperative hemoglobin significantly correlated with a greater percent rise in creatinine postoperatively (β = 0.30, P = .015). ConclusionThe incidence of AKI in patients who receive ACS is relatively high, raising clinical concern in the care of periprosthetic joint infection patients. Our results suggest that a lower baseline hemoglobin may be involved in the etiology of AKI in this population. Therefore, it may be clinically appropriate to monitor anemic patients for AKI when implanting an ACS.

The Concomitant Use of Diuretics, Non-Steroidal Anti-Inflammatory Drugs, and Angiotensin-Converting Enzyme Inhibitors or Angiotensin Receptor Blockers (Triple Whammy), Extreme Heat, and In-Hospital Acute Kidney Injury in Older Medical Patients.

We investigated whether the concomitant use of diuretics, non-steroidal anti-inflammatory drugs, and angiotensin-converting enzyme inhibitors/angiotensin receptor blockers (triple whammy, TW) predicts in-hospital acute kidney injury (AKI) and whether admission during recorded periods of extreme heat influences this association. We retrospectively collected data on patient characteristics and use of TW/non-TW drugs on admission, AKI (increase in serum creatinine≥27µmol/l either within the first 48h of admission or throughout hospitalization, primary outcome), length of stay (LOS), and mortality (secondary outcomes) in medical patients ≥65years admitted (1) during five consecutive heat waves (HWs) between 2007 and 2009 (n=382) or (2) either before or after each HW, matched for HW period, age, and admission day of the week (non-HW, controls, n=1339). Number of TW and non-TW drugs, co-morbidities, number of daily admissions, incidence of in-hospital AKI, LOS, and mortality were similar in the HW and non-HW groups. After adjusting for clinical and demographic confounders, logistic regression showed that TW use did not predict AKI within 48h of admission either during non-HW periods (OR 0.79, 95% CI 0.34-1.83, P=0.58) or during HWs (OR 1.02, 95% CI 0.21-2.97, P=0.97). Similar results were observed when AKI was captured throughout hospitalization. TW use did not predict LOS or mortality irrespective of environmental temperature on admission. TW use on admission did not predict in-hospital AKI, LOS, or mortality in older medical patients admitted either during periods of normal environmental temperature or during HWs.

Admission hyperphosphatemia increases the risk of acute kidney injury in hospitalized patients.

Evidence on the association between elevated admission serum phosphate and risk of in-hospital acute kidney injury (AKI) is limited. The aim of this study was to assess the risk of AKI in hospitalized patients stratified by admission serum phosphate level. This is a single-center retrospective study conducted at a tertiary referral hospital. All hospitalized adult patients who had admission phosphate measurement available between January and December 2013 were enrolled. Admission phosphate was categorized into 6 groups (< 2.4, 2.4-2.9, 2.9-3.4, 3.4-3.9, 3.9-4.4, and ≥ 4.4mg/dl). The primary outcome was in-hospital AKI occurring after hospital admission. Logistic regression analysis was performed to obtain the odds ratio of AKI for various admission phosphate strata using the phosphate 2.4-2.9mg/dl level (lowest incidence of AKI) as the reference group. After excluding patients with end-stage renal disease (ESRD), without serum phosphate measurement, and those with AKI at time of admission, a total of 5036 patients were studied. Phosphate levels of < 2.4 and ≥ 4.4mg/dl were found in 458 (9.1%) and 585 (11.6%) patients, respectively. In-hospital AKI occurred in 595 (11.8%) patients. The incidence of AKI among patients with admission phosphate < 2.4, 2.4-2.9, 2.9-3.4, 3.4-3.9, 3.9-4.4, and ≥ 4.4mg/dl was 10.5, 9.5, 11.8, 10.0, 12.8, and 17.9%, respectively. After adjusting for potential confounders, admission serum phosphate > 4.4mg/dl was associated with an increased risk of developing AKI with an odds ratio of 1.72 (95% confidence interval 1.20-2.47), whereas admission serum phosphate levels < 4.4mg/dl were not associated with development of AKI during hospitalization. Elevated admission phosphate is associated with an increased risk for in-hospital AKI.

Hospital-Acquired Infection Is the Strongest Predictor of In-hospital Mortality in Patients With Alcoholic Hepatitis

Introduction: Alcoholic hepatitis (AH) is a clinical syndrome associated with high mortality and utilization of resources. We performed this study to evaluate predictors of in-hospital mortality (IHM) among AH patients. Methods: A retrospective chart review was done on patients discharged from our hospital with a diagnosis of AH. Patients who met a well characterized definition of AH (serum bilirubin > 3 mg/dL, AST to ALT ratio of > 1.5, recent heavy alcohol use, and absence of other causes of liver disease) were included in the study. Chi-square and t-tests were used to compare categorical and continuous variables. Multivariate logistic regression was used to evaluate the impact of several variables on IHM. Results: 105 patients with AH (median age 46yrs, 56% male, 74% white, 57% with cirrhosis, MELD score 23) were included in the study. Complications present on admission included acute kidney injury (AKI) (44%), encephalopathy (29%), infection (24%), and gastrointestinal bleeding (17%). Complications that developed during the hospitalization included AKI (48%) with 8% requiring dialysis, infection (15%), encephalopathy (12%), and gastrointestinal bleeding (5%). 67 patients (64%) received treatment for AH including steroids (n=33), pentoxifylline (21), or both (n=13).15 patients (14%) died during hospitalization. Compared to those that survived hospitalization, patients with IHM had a higher incidence of AKI on admission (73 vs. 39%, P=0.013), in-hospital AKI (73 vs. 20%, P < 0.0001), in-hospital encephalopathy(40 vs. 8%, P=0.0005), in-hospital infection (47 vs. 10% P=0.0003), pentoxifylline use (60 vs. 28%, P=0.014), and in-hospital renal replacement therapy (33 vs. 3%, P < 0.0001). They were also more likely to meet SIRS criteria (73 vs. 46%, P=0.046) and have a higher admission MELD score (32 vs. 23, P=0.0003). The use of prophylactic antibiotics was similar among patients with IHM and those who survived hospitalization (33 vs. 29%, P=0.73). On multivariate logistic regression, hospital-acquired infection was the single most important predictor for IHM (OR 15, 2.3-99, P=0.005). Prophylactic antibiotic use (OR 1.04, 0.14-8.1, P=0.96) and admission MELD score (OR 1.07, 0.98-1.17, P=0.13) were not predictive of IHM. Conclusion: Patients with AH have high in-hospital mortality and hospital acquired infection appears to be the strongest predictor of IHM. Prophylactic antibiotic use does not affect IHM and so clinicians should be vigilant to reduce the risk of infection and treat appropriately if there is evidence of an infection.

Norepinephrine Dosing in Obese Patients: Impact of Weight-Based Dosing on Short- and Long-Term Mortality

SESSION TITLE: Sepsis & Septic Shock SESSION TYPE: Original Investigation Slide PRESENTED ON: Sunday, October 29, 2017 at 01:30 PM - 03:00 PM PURPOSE: Obesity is thought to be protective in septic shock. Norepinephrine (NE) is frequently dosed by a weight-based regimen, and potentially higher doses of NE are used in the obese population. The interaction of body mass index (BMI) with NE dosing and their influence on clinical outcomes has been only limitedly explored. METHODS: Historical cohort study of all adult septic shock patients requiring NE admitted between 2010 through 2015 to all intensive care units (ICU) at Mayo Clinic Rochester. Patients with BMI 25-39.9 kg/m2 were classified into overweight (25-29.9 kg/m2), obesity class I (30-34.9 kg/m2) and obesity class II (35-39.9 kg/m2). Patients with normal BMI (18.5-24.9 kg/m2) formed the control group. Patients with chronic respiratory failure, repeat ICU admissions, ICU stay <1day, lactate <2 mmol/L and BMI <18.5 and ≥ 40 kg/m2 were excluded. The primary outcome was in-hospital mortality and secondary outcomes included new cardiac arrhythmias, acute kidney injury (AKI) and one-year mortality. Odds ratios (OR) [95% confidence intervals (CI)] were used to represent univariate and multivariate outcomes respectively. A two-tailed p<0.05 was considered significant. RESULTS: During this 6-year period, 4774 patients met our study criteria - BMI 18.5-24.9, 25-29.9, 30-34.9 and 35-39.9 kg/m2 had 1406 (29%), 1608 (34%), 1151 (24%) and 609 (13%) patients respectively. The baseline characteristics revealed significant inter-group differences in age, race, gender and baseline creatinine, but no differences in comorbidity burden, severity of illness or use of corticosteroids in the ICU. Median NE dose increased linearly with increase in BMI cohorts - 5 gm (interquartile range [IQR] 1-13) (BMI 18.5-24.9 kg/m2), 5.3 gm (IQR 2-14) (BMI 25-29.9 kg/m2), 6 gm (IQR 2-16) (BMI 30-34.9 kg/m2) and 7 gm (IQR 2-18) (BMI 35-39.9 kg/m2), p<0.001. There was no difference in number, type or total doses of additional vasoactive medications. In-hospital (29%, 24%, 22%, 22%; p<0.001) and one-year mortality (46%, 53%, 53%, 51%; p=0.001) were significantly different between patients with BMI 18.5-24.9, 25-29.9, 30-34.9 and 35-39.9 kg/m2 respectively. Unadjusted log10NE levels were associated with higher in-hospital mortality (OR 2.9 [95%CI 2.6-3.3]; p<0.001), AKI (OR 1.8 [95% CI 1.6-1.9]; p<0.001), cardiac arrhythmias (OR 1.4 [95% CI 1.3-1.5]; p<0.001) and one-year mortality (OR 1.8 [95% CI 1.6-2]; p<0.001). After adjusting for age, gender, BMI, comorbidity burden, severity of illness, cardiac injury, AKI, cardiac arrhythmia and use of mechanical ventilation, log10NE was an independent predictor of in-hospital (OR 2.2 [95% CI 1.9-2.7]; p<0.001) and one-year mortality (OR 1.4 [95% CI 1.2-1.7]; p<0.001). CONCLUSIONS: Total NE use was independently associated with worse short and long-term mortality, AKI and cardiac arrhythmias in patients independent of BMI. CLINICAL IMPLICATIONS: Alternative strategies to weight-based NE dosing are recommended in obese patients. DISCLOSURE: The following authors have nothing to disclose: Aditya Kotecha, Saraschandra Vallabhajosyula, Dinesh Apala, Erin Frazee, Vivek Iyer No Product/Research Disclosure Information

Elevated baseline potassium level within reference range is associated with worse clinical outcomes in hospitalised patients

The clinical significance of elevated baseline serum potassium (K+) levels in hospitalised patients is rarely described. Hence, we performed a retrospective study assessing the significance of elevated K+ levels in a one-year admission cohort. Adult patients without hypokalaemia or end-stage renal disease were included. Adverse outcomes were all-cause mortality, hospital-acquired acute kidney injury, and events of arrhythmia. In total, 17,777 patients were included in the study cohort, and a significant difference (P < 0.001) was observed in mortality according to baseline serum K+ levels. The adjusted hazard ratios (HRs) and associated 95% confidence intervals (CIs) of all-cause mortality for K+ levels above the reference range of 3.6–4.0 mmol/L were as follows: 4.1–4.5 mmol/L, adjusted HR 1.075 (95% CI 0.981–1.180); 4.6–5.0 mmol/L, adjusted HR 1.261 (1.105–1.439); 5.1–5.5 mmol/L, adjusted HR 1.310 (1.009–1.700); >5.5 mmol/L, adjusted HR 2.119 (1.532–2.930). Moreover, the risks of in-hospital acute kidney injury and arrhythmia were higher in patients with serum K+ levels above 4.0 mmol/L and 5.5 mmol/L, respectively. In conclusion, increased serum K+ levels, including mild elevations may be related to worse prognosis. Close monitoring and prompt correction of underlying causes or hyperkalaemia itself is warranted for admitted patients.

Echocardiographic and Electrocardiographic Predictors of Adverse Outcomes in Spontaneous Bacterial Peritonitis

Patients with cirrhosis who develop Spontaneous Bacterial Peritonitis (SBP) suffer from cirrhotic cardiomyopathy which is characterized by impaired contractility in response to stress despite a relatively normal resting cardiac output. We hypothesized that electrocardiographic and echocardiographic information would help prognosticate patients developing SBP in addition to existing scoring systems. Cirrhotic patients admitted to Einstein Medical Center from 01/01/2005 to 6/30/2012 for SBP, and did not receive a transplant within one year, were included. Patients were classified as QTc low vs. high, and E/E' low vs. high at cut points ≥480ms for QTc and ≥10 for E/E' ratio. We estimated 1-year survival using Kaplan Meier curves. Regression analysis and Cox proportional hazards model were used for QTc and E/E' ratio, respectively, for assessing 1-year survival. Among 112 patients with electrocardiogam, 78 were classified as QTc low. Among 64 patients with echocardiograms, 23 were classified as E/E' low. Higher QTc was associated with increased in-hospital acute kidney injury. QTc and E/E' ratio predicted worse 1-year survival (HR=2.16, 95% CI 1.29-3.49; HR 2.65, 95% CI 1.31-5.35, respectively) on univariate and multivariate analysis (OR=1.02, 95% CI 1.01-1.03; HR=3.26, 95% CI 1.22-9.82 respectively) after adjusting for both Child Pugh stage, MELD score among other risk factors. In conclusion, cirrhotic patients with SBP who present with a prolonged QTc interval are at a greater risk for acute renal failure during hospitalization. High QTc duration and an E/E' ratio of ≥10 independently predict increased mortality at 1-year follow-up.

Acute Kidney Injury in Cirrhosis: Baseline Serum Creatinine Predicts Patient Outcomes.

The International Ascites Club (IAC) recently defined Stage 1 acute kidney injury (AKI) for cirrhosis as an acute increase in serum creatinine (SCr) by ≥0.3 mg/dl or by ≥50% in <48 h from a stable value within 3 months. The baseline SCr may influence AKI risk and patient outcomes. The objective of this study is to determine in cirrhosis whether the baseline SCr has any effect on the in-hospital AKI course and patient survival. North American Consortium for the Study of End-Stage Liver Disease is a consortium of tertiary-care hepatology centers prospectively enroling non-elective cirrhotic inpatients. Patients with different baseline SCr levels (≤0.5, 0.51-1.0, 1.01-1.5, >1.5 mg/dl) were evaluated for the development of AKI, and compared for AKI outcomes and 30-day survival. 653 hospitalized cirrhotics (56.7±10years, 64% men, 30% with infection) were included. The incidence of AKI was 47% of enrolled patients. Patients with higher baseline SCr were more likely to develop AKI, with significantly higher delta and peak SCr (P<0.001) than the other groups, more likely to have a progressive AKI course (P<0.0001), associated with a significantly reduced 30-day survival (P<0.0001). Multivariate logistic regression showed that the delta SCr during an AKI episode to be the strongest factor impacting AKI outcomes and survival (P<0.001), with a delta SCr of 0.70 mg/dl having a 68% sensitivity and 80% specificity for predicting 30-day mortality. Admitted cirrhotic patients with higher baseline SCr are at higher risk for in-hospital development of AKI, and more likely to have AKI progression with reduced survival. Therefore, such patients should be closely monitored and treated promptly for their AKI.

The spleen as a bidirectional signal transducer in acute kidney injury

In acute kidney injury models, the lung is damaged through an interleukin-6-dependent inflammatory response. Clinically, development of lung injury requiring mechanical ventilation markedly increases in-hospital acute kidney injury mortality. Andres-Hernando etal. demonstrate that the spleen coordinates interleukin-6-dependent interleukin-10 production, which lessens lung injury during experimental acute kidney injury. This study highlights the beneficial influence of the spleen on the lung, and dovetails with other recent publications, to demonstrate the integral role of the spleen in acute kidney injury.