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1.
Antoine Dewitte Olivier Joannès-Boyau Carole Sidobre Catherine Fleureau Marie-Lise Bats Philippe Derache Sébastien Leuillet Jean Ripoche Christian Combe Alexandre Ouattara 《Clinical journal of the American Society of Nephrology》2015,10(11):1900-1910
Background and objectives
Prompt recognition of severe renal impairment could improve the early management of critically ill patients. We compared the value of kinetic eGFR, plasma neutrophil gelatinase–associated lipocalin (NGAL), and urine tissue inhibitor of metalloproteinase-2 and urine insulin-like growth factor–binding protein 7 ([TIMP-2]*[IGFBP7]) in predicting short-term recovery from AKI and major adverse kidney events.Design, setting, participants, & measurements
During the 6-month study period, 245 patients were admitted to our intensive care unit. This study included 57 consecutive patients presenting with AKI within the first 24 hours after admission. AKI markers were evaluated at inclusion (day 0) and 24 hours later (day 1). Kinetic eGFR was calculated on day 1 according to serum creatinine evolution. Renal recovery was defined as normalization of serum creatinine with reversal of oliguria within 48 hours. Major adverse kidney events included death, need for RRT, or persistence of renal dysfunction at hospital discharge.Results
Plasma NGAL and [TIMP-2]*[IGFBP7] predicted renal recovery, with area under the receiver-operating characteristic curve (AUC-ROC) values between 0.70 and 0.79 at inclusion. Although plasma NGAL values frequently reached the maximal measurement range, their decrease on day 1 predicted recovery. The kinetic eGFR calculation after initial resuscitation provided the best AUC-ROC value for renal recovery, at 0.87. The best predictions for major adverse kidney events were provided by [TIMP-2]*[IGFBP7] and kinetic eGFR (equal AUC-ROCs of 0.81). Combining AKI markers in addition to clinical prediction models improved the discrimination and reclassification of patients who will recover from AKI or suffer from major adverse kidney events.Conclusions
Biomarkers of kidney damage predicted short-term renal recovery and major adverse kidney events for an unselected cohort of critically ill patients. Calculating the kinetic eGFR imposed a delay after initial resuscitation but provided a good diagnostic and prognostic approach. The utility of functional and damage AKI marker combinations in addition to clinical information requires validation in larger prospective studies. 相似文献2.
Jonathan Bazeley Brian Bieber Yun Li Hal Morgenstern Patricia de Sequera Christian Combe Hiroyasu Yamamoto Martin Gallagher Friedrich K. Port Bruce M. Robinson 《Clinical journal of the American Society of Nephrology》2011,6(10):2452-2461
Summary
Background and objectives
Measurement of C-reactive protein (CRP) levels remains uncommon in North America, although it is now routine in many countries. Using Dialysis Outcomes and Practice Patterns Study data, our primary aim was to evaluate the value of CRP for predicting mortality when measured along with other common inflammatory biomarkers.Design, setting, participants, & measurements
We studied 5061 prevalent hemodialysis patients from 2005 to 2008 in 140 facilities routinely measuring CRP in 10 countries. The association of CRP with mortality was evaluated using Cox regression. Prediction of 1-year mortality was assessed in logistic regression models with differing adjustment variables.Results
Median baseline CRP was lower in Japan (1.0 mg/L) than other countries (6.0 mg/L). CRP was positively, monotonically associated with mortality. No threshold below which mortality rate leveled off was identified. In prediction models, CRP performance was comparable with albumin and exceeded ferritin and white blood cell (WBC) count based on measures of model discrimination (c-statistics, net reclassification improvement [NRI]) and global model fit (generalized R2). The primary analysis included age, gender, diabetes, catheter use, and the four inflammatory markers (omitting one at a time). Specifying NRI ≥5% as appropriate reclassification of predicted mortality risk, NRI for CRP was 12.8% compared with 10.3% for albumin, 0.8% for ferritin, and <0.1% for WBC.Conclusions
These findings demonstrate the value of measuring CRP in addition to standard inflammatory biomarkers to improve mortality prediction in hemodialysis patients. Future studies are indicated to identify interventions that lower CRP and to identify whether they improve clinical outcomes. 相似文献3.
Nattachai Srisawat Xiaoyan Wen MinJae Lee Lan Kong Michele Elder Melinda Carter Mark Unruh Kevin Finkel Anitha Vijayan Mohan Ramkumar Emil Paganini Kai Singbartl Paul M. Palevsky John A. Kellum 《Clinical journal of the American Society of Nephrology》2011,6(8):1815-1823
Summary
Background and objectives
Despite significant advances in the epidemiology of acute kidney injury (AKI), prognostication remains a major clinical challenge. Unfortunately, no reliable method to predict renal recovery exists. The discovery of biomarkers to aid in clinical risk prediction for recovery after AKI would represent a significant advance over current practice.Design, setting, participants, & measurements
We conducted the Biological Markers of Recovery for the Kidney study as an ancillary to the Acute Renal Failure Trial Network study. Urine samples were collected on days 1, 7, and 14 from 76 patients who developed AKI and received renal replacement therapy (RRT) in the intensive care unit. We explored whether levels of urinary neutrophil gelatinase-associated lipocalin (uNGAL), urinary hepatocyte growth factor (uHGF), urinary cystatin C (uCystatin C), IL-18, neutrophil gelatinase-associated lipocalin/matrix metalloproteinase-9, and urine creatinine could predict subsequent renal recovery.Results
We defined renal recovery as alive and free of dialysis at 60 days from the start of RRT. Patients who recovered had higher uCystatin C on day 1 (7.27 versus 6.60 ng/mg·creatinine) and lower uHGF on days 7 and 14 (2.97 versus 3.48 ng/mg·creatinine; 2.24 versus 3.40 ng/mg·creatinine). For predicting recovery, decreasing uNGAL and uHGF in the first 14 days was associated with greater odds of renal recovery. The most predictive model combined relative changes in biomarkers with clinical variables and resulted in an area under the receiver-operator characteristic curve of 0.94.Conclusions
We showed that a panel of urine biomarkers can augment clinical risk prediction for recovery after AKI. 相似文献4.
Hall IE Coca SG Perazella MA Eko UU Luciano RL Peter PR Han WK Parikh CR 《Clinical journal of the American Society of Nephrology》2011,6(12):2740-2749
Summary
Background and objectives
Studies have evaluated acute kidney injury (AKI) using biomarkers in various settings, but their prognostic utility within current practice is unclear. Thus, we sought to determine the prognostic utility of newer biomarkers or traditional markers (fractional excretion of sodium [FeNa] and urea [FeUrea] and microscopy) over clinical assessment alone.Design, setting, participants, & measurements
This is a prospective cohort study of adults on the first day of meeting AKI criteria. We measured urine concentrations of neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), and IL-18 and determined FeNa, FeUrea, and microscopy score for casts and tubular cells. Primary outcome was worsened AKI stage from enrollment to peak serum creatinine or in-hospital death.Results
In 249 recipients, 57% were ≥65 years old, 48% were from intensive care, and mean baseline GFR was 69 ± 30 ml/min per 1.73 m2. AKI was considered prerenal in 164 (66%), acute tubular necrosis (ATN) in 51 (20%), and “other” in 34 (14%). All mean protein biomarker concentrations, FeNa, FeUrea, and microscopy scores were statistically different between prerenal and ATN. Seventy-two patients (29%) developed the primary outcome. There was an approximate three-fold increase in adjusted risk for the outcome for upper versus lower values of NGAL, KIM-1, IL-18, and microscopy score (P values <0.05). Net reclassification improved after adding these to baseline clinical assessment. FeNa and FeUrea were not useful.Conclusions
On the first day of AKI, urine protein biomarkers and microscopy significantly improve upon clinical determination of prognosis, indicating their potential utility in current practice. 相似文献5.
Dinna N. Cruz Asunción Ferrer-Nadal Pasquale Piccinni Stuart L. Goldstein Lakhmir S. Chawla Elisa Alessandri Clara Belluomo Anello Will Bohannon Tiziana Bove Nicola Brienza Mauro Carlini Francesco Forfori Francesco Garzotto Silvia Gramaticopolo Michele Iannuzzi Luca Montini Paolo Pelaia Claudio Ronco 《Clinical journal of the American Society of Nephrology》2014,9(4):663-672
Background and objectives
Disease biomarkers require appropriate clinical context to be used effectively. Combining clinical risk factors, in addition to small changes in serum creatinine, has been proposed to improve the assessment of AKI. This notion was developed in order to identify the risk of AKI early in a patient''s clinical course. We set out to assess the performance of this combination approach.Design, setting, participants, & measurements
A secondary analysis of data from a prospective multicenter intensive care unit cohort study (September 2009 to April 2010) was performed. Patients at high risk using this combination approach were defined as an early increase in serum creatinine of 0.1–0.4 mg/dl, depending on number of clinical factors predisposing to AKI. AKI was defined and staged using the Acute Kidney Injury Network criteria. The primary outcome was evolution to severe AKI (Acute Kidney Injury Network stages 2 and 3) within 7 days in the intensive care unit.Results
Of 506 patients, 214 (42.2%) patients had early creatinine elevation and were deemed at high risk for AKI. This group was more likely to subsequently develop the primary endpoint (16.4% versus 1.0% [not at high risk], P<0.001). The sensitivity of this grouping for severe AKI was 92%, the specificity was 62%, the positive predictive value was 16%, and the negative predictive value was 99%. After adjustment for Sequential Organ Failure Assessment score, serum creatinine, and hazard tier for AKI, early creatinine elevation remained an independent predictor for severe AKI (adjusted relative risk, 12.86; 95% confidence interval, 3.52 to 46.97). Addition of early creatinine elevation to the best clinical model improved prediction of the primary outcome (area under the receiver operating characteristic curve increased from 0.75 to 0.83, P<0.001).Conclusion
Critically ill patients at high AKI risk, based on the combination of clinical factors and early creatinine elevation, are significantly more likely to develop severe AKI. As initially hypothesized, the high-risk combination group methodology can be used to identify patients at low risk for severe AKI in whom AKI biomarker testing may be expected to have low yield. The high risk combination group methodology could potentially allow clinicians to optimize biomarker use. 相似文献6.
Tomoko Fujii Shigehiko Uchino Masanori Takinami Rinaldo Bellomo 《Clinical journal of the American Society of Nephrology》2014,9(5):848-854
Background and objectives
AKI is a major clinical problem and predictor of outcome in hospitalized patients. In 2013, the Kidney Disease: Improving Global Outcomes (KDIGO) group published the third consensus AKI definition and classification system after the Risk, Injury, Failure, Loss of Kidney Function, and End-Stage Kidney Disease (RIFLE) and the Acute Kidney Injury Network (AKIN) working group systems. It is unclear which system achieves optimal prognostication in hospital patients.Design, setting, participants, & measurements
A retrospective observational study using hospital laboratory, admission, and discharge databases was performed that included adult patients admitted to a teaching hospital in Tokyo, Japan between April 1, 2008, and October 31, 2011. AKI occurring during each hospital stay was identified, and discriminative ability of each AKI classification system based on serum creatinine for the prediction of hospital mortality was assessed. The receiver operating characteristic curve, a graphical measure of test performance, and the area under the curve were used to evaluate how classifications preformed on the study population.Results
In total, 49,518 admissions were studied, of which 11.0% were diagnosed with RIFLE criteria and 11.6% were diagnosed with KDIGO criteria, but only 4.8% were diagnosed with AKIN criteria. Overall hospital mortality was 3.0%. AKI staging and hospital mortality were closely correlated in all systems. Discrimination for hospital mortality was similar for RIFLE and KDIGO criteria (area under the curve=0.77 versus 0.78; P=0.02), whereas AKIN discrimination was inferior (area under the curve=0.69 versus RIFLE [P<0.001] versus KDIGO [P<0.001]).Conclusion
Among hospital patients, KDIGO and RIFLE criteria achieved similar discrimination, but the discrimination of AKIN was inferior. 相似文献7.
David S. Cooper Donna Claes Stuart L. Goldstein Michael R. Bennett Qing Ma Prasad Devarajan Catherine D. Krawczeski 《Clinical journal of the American Society of Nephrology》2016,11(1):21-29
Background and objectives
Novel urinary kidney damage biomarkers detect AKI after cardiac surgery using cardiopulmonary bypass (CPB-AKI). Although there is growing focus on whether AKI leads to CKD, no studies have assessed whether novel urinary biomarkers remain elevated long term after CPB-AKI. We assessed whether there was clinical or biomarker evidence of long-term kidney injury in patients with CPB-AKI.Design, setting, participants, & measurements
We performed a cross-sectional evaluation for signs of chronic kidney injury using both traditional measures and novel urinary biomarkers in a population of 372 potentially eligible children (119 AKI positive and 253 AKI negative) who underwent surgery using cardiopulmonary bypass for congenital heart disease at Cincinnati Children’s Hospital Medical Center between 2004 and 2007. A total of 51 patients (33 AKI positive and 18 AKI negative) agreed to long-term assessment. We also compared the urinary biomarker levels in these 51 patients with those in healthy controls of similar age.Results
At long-term follow-up (mean duration±SD, 7±0.98 years), AKI-positive and AKI-negative patients had similarly normal assessments of kidney function by eGFR, proteinuria, and BP measurement. However, AKI-positive patients had higher urine concentrations of IL-18 (48.5 pg/ml versus 20.3 pg/ml [P=0.01] and 20.5 pg/ml [P<0.001]) and liver-type fatty acid–binding protein (L-FABP) (5.9 ng/ml versus 3.9 ng/ml [P=0.001] and 3.2 ng/ml [P<0.001]) than did AKI-negative patients and healthy controls.Conclusions
Novel urinary biomarkers remain elevated 7 years after an episode of CPB-AKI in children. However, there is no conventional evidence of CKD in these children. These biomarkers may be a more sensitive marker of chronic kidney injury after CPB-AKI. Future studies are needed to understand the clinical relevance of persistent elevations in IL-18, kidney injury molecule-1, and L-FABP in assessments for potential long-term kidney consequences of CPB-AKI. 相似文献8.
Justin M. Belcher Guadalupe Garcia-Tsao Arun J. Sanyal Heather Thiessen-Philbrook Aldo J. Peixoto Mark A. Perazella Naheed Ansari Joseph Lim Steven G. Coca Chirag R. Parikh 《Clinical journal of the American Society of Nephrology》2014,9(11):1857-1867
Background and objectives
AKI is a common and severe complication in patients with cirrhosis. AKI progression was previously shown to correlate with in-hospital mortality. Therefore, accurately predicting which patients are at highest risk for AKI progression may allow more rapid and targeted treatment. Urinary biomarkers of structural kidney injury associate with AKI progression and mortality in multiple settings of AKI but their prognostic performance in patients with liver cirrhosis is not well known.Design, setting, participants, & measurements
A multicenter, prospective cohort study was conducted at four tertiary care United States medical centers between 2009 and 2011. The study comprised patients with cirrhosis and AKI defined by the AKI Network criteria evaluating structural (neutrophil gelatinase–associated lipocalin, IL-18, kidney injury molecule-1 [KIM-1], liver-type fatty acid–binding protein [L-FABP], and albuminuria) and functional (fractional excretion of sodium [FENa]) urinary biomarkers as predictors of AKI progression and in-hospital mortality.Results
Of 188 patients in the study, 44 (23%) experienced AKI progression alone and 39 (21%) suffered both progression and death during their hospitalization. Neutrophil gelatinase–associated lipocalin, IL-18, KIM-1, L-FABP, and albuminuria were significantly higher in patients with AKI progression and death. These biomarkers were independently associated with this outcome after adjusting for key clinical variables including model of end stage liver disease score, IL-18 (relative risk [RR], 4.09; 95% confidence interval [95% CI], 1.56 to 10.70), KIM-1 (RR, 3.13; 95% CI, 1.20 to 8.17), L-FABP (RR, 3.43; 95% CI, 1.54 to 7.64), and albuminuria (RR, 2.07; 95% CI, 1.05–4.10) per log change. No biomarkers were independently associated with progression without mortality. FENa demonstrated no association with worsening of AKI. When added to a robust clinical model, only IL-18 independently improved risk stratification on a net reclassification index.Conclusions
Multiple structural biomarkers of kidney injury, but not FENa, are independently associated with progression of AKI and mortality in patients with cirrhosis. Injury marker levels were similar between those without progression and those with progression alone. 相似文献9.
Claudia S. Lennartz John William Pickering Sarah Seiler-Mu?ler Lucie Bauer Kathrin Untersteller Insa E Emrich Adam M. Zawada J?rg Radermacher Navdeep Tangri Danilo Fliser Gunnar H. Heine 《Clinical journal of the American Society of Nephrology》2016,11(4):609-615
Background and objectives
Progression of CKD toward ESRD is heterogeneous. The Kidney Failure Risk Equation (KFRE) was developed to identify CKD patients at high risk of ESRD. We aimed to externally validate KFRE and to test whether the addition of predefined Duplex ultrasound markers – renal resistive index (RRI) or difference of resistive indices in spleen and kidney (DI-RISK) – improved ESRD prediction.Design, setting, participants, & measurements
The prospective Cardiovascular and Renal Outcome in CKD 2-4 Patients—The Fourth Homburg evaluation (CARE FOR HOMe) study recruits CKD stage G2–G4 patients referred to a tertiary referral center for nephrologic care. Four hundred three CARE FOR HOMe participants enrolled between 2008 and 2012 had available RRI measurements at study inclusion; they were subsequently followed for a mean of 4.4±1.6 years. This subcohort was used to validate KFRE and to assess the added value of the ultrasound markers (new models KFRE+RRI and KFRE+DI-RISK). Model performance was assessed by log-likelihood ratio test, c-statistic, integrated discrimination improvement metrics (for study participants without subsequent ESRD [IDI No ESRD] and for patients with ESRD [IDI ESRD]), and calibration plots. If either new model improved on KFRE, we determined to validate it in an independent cohort of 162 CKD patients.Results
KFRE predicted ESRD in CARE FOR HOMe participants with a c-statistic of 0.91 (95% confidence interval, 0.83 to 0.99). Adding RRI improved the KFRE model (P<0.001), and the KFRE+RRI model was well calibrated; however, the c-statistic (0.91 [0.83–1.00]) was similar, and overall sensitivity (IDI No ESRD=0.05 [0.00–0.10]) or overall specificity (IDI ESRD=0.00 [0.00–0.01]) did not improve. Adding DI-RISK did not improve the KRFE model. In the external validation cohort, we confirmed that the KFRE+RRI model did not outperform KFRE.Conclusions
Routine Duplex examinations among CKD patients did not improve risk prediction for progression to ESRD beyond a validated equation. 相似文献10.
Scott M. Sutherland John J. Byrnes Manish Kothari Christopher A. Longhurst Sanjeev Dutta Pablo Garcia Stuart L. Goldstein 《Clinical journal of the American Society of Nephrology》2015,10(4):554-561
Background and objectives
Although several standardized definitions for AKI have been developed, no consensus exists regarding which to use in children. This study applied the Pediatric RIFLE (pRIFLE), AKI Network (AKIN), and Kidney Disease Improving Global Outcomes (KDIGO) criteria to an anonymized cohort of hospitalizations extracted from the electronic medical record to compare AKI incidence and outcomes in intensive care unit (ICU) and non-ICU pediatric populations.Design, setting, participants, & measurements
Observational, electronic medical record–enabled study of 14,795 hospitalizations at the Lucile Packard Children’s Hospital between 2006 and 2010. AKI and AKI severity stage were defined by the pRIFLE, AKIN, and KDIGO definitions according to creatinine change criteria; urine output criteria were not used. The incidences of AKI and each AKI stage were calculated for each classification system. All-cause, in-hospital mortality and total hospital length of stay (LOS) were compared at each subsequent AKI stage by Fisher exact and Kolmogorov–Smirnov tests, respectively.Results
AKI incidences across the cohort according to pRIFLE, AKIN, and KDIGO were 51.1%, 37.3%, and 40.3%. Mortality was higher among patients with AKI across all definitions (pRIFLE, 2.3%; AKIN, 2.7%; KDIGO, 2.5%; P<0.001 versus no AKI [0.8%–1.0%]). Within the ICU, pRIFLE, AKIN, and KDIGO demonstrated progressively higher mortality at each AKI severity stage; AKI was not associated with mortality outside the ICU by any definition. Both in and outside the ICU, AKI was associated with significantly higher LOS at each AKI severity stage across all three definitions (P<0.001). Definitions resulted in differences in diagnosis and staging of AKI; staging agreement ranged from 76.7% to 92.5%.Conclusions
Application of the three definitions led to differences in AKI incidence and staging. AKI was associated with greater mortality and LOS in the ICU and greater LOS outside the ICU. All three definitions demonstrated excellent interstage discrimination. While each definition offers advantages, these results underscore the need to adopt a single, universal AKI definition. 相似文献11.
Mario Raimundo Siobhan Crichton Yadullah Syed Jonathan R. Martin Richard Beale David Treacher Marlies Ostermann 《Clinical journal of the American Society of Nephrology》2015,10(8):1340-1349
Background and objectives
The optimal hemodynamic management of patients with early AKI is unknown. This study aimed to investigate the association between hemodynamic parameters in early AKI and progression to severe AKI and hospital mortality.Design, setting, participants, & measurements
This study retrospectively analyzed the data of all patients admitted to the adult intensive care unit in a tertiary care center between July 2007 and June 2009 and identified those with stage 1 AKI (AKI I) per the AKI Network classification. In patients in whom hemodynamic monitoring was performed within 12 hours of AKI I, hemodynamic parameters in the first 12 hours of AKI I and on the day of AKI III (if AKI III developed) or 72 hours after AKI I (if AKI III did not develop) were recorded. Risk factors for AKI III and mortality were identified using univariate and multivariate logistic regression analyses.Results
Among 790 patients with AKI I, 210 (median age 70 years; 138 men) had hemodynamic monitoring within 12 hours of AKI I; 85 patients (41.5%) progressed to AKI III and 91 (43%) died in the hospital. AKI progressors had a significantly higher Sequential Organ Failure Assessment score (8.0 versus 9.6; P<0.001), lower indexed systemic oxygen delivery (DO2I) (median 325 versus 405 ml/min per m2; P<0.001), higher central venous pressure (16 versus 13; P=0.02), and lower mean arterial blood pressure (MAP) (median 71 versus 74 mmHg; P=0.01) in the first 12 hours of AKI I compared with nonprogressors. Multivariate analysis confirmed that raised lactate, central venous pressure, and Sequential Organ Failure Assessment score as well as mechanical ventilation were independently associated with progression to AKI III; higher DO2I and MAP were independently associated with a lower risk of AKI III but not survival. The associations were independent of sepsis, heart disease, recent cardiac surgery, or chronic hypertension.Conclusions
Higher DO2I and MAP in early AKI were independently associated with a lower risk of progression. 相似文献12.
John P. Reilly Brian J. Anderson Nilam S. Mangalmurti Tam D. Nguyen Daniel N. Holena Qufei Wu Ethan T. Nguyen Muredach P. Reilly Paul N. Lanken Jason D. Christie Nuala J. Meyer Michael G.S. Shashaty 《Clinical journal of the American Society of Nephrology》2015,10(11):1911-1920
Background and objective
ABO blood types are determined by antigen modifications on glycoproteins and glycolipids and associated with altered plasma levels of inflammatory and endothelial injury markers implicated in AKI pathogenesis. We sought to determine the association of ABO blood types with AKI risk in critically ill patients with trauma or sepsis.Design, setting, participants, & measurements
We conducted two prospective cohort studies at an urban, academic, level I trauma center and tertiary referral center; 497 patients with trauma admitted to the surgical intensive care unit between 2005 and 2010 with an injury severity score >15 and 759 patients with severe sepsis admitted to the medical intensive care unit between 2008 and 2013 were followed for 6 days for the development of incident AKI. AKI was defined by Acute Kidney Injury Network creatinine and dialysis criteria.Results
Of 497 patients with trauma, 134 developed AKI (27%). In multivariable analysis, blood type A was associated with higher AKI risk relative to type O among patients of European descent (n=229; adjusted risk, 0.28 versus 0.14; risk difference, 0.14; 95% confidence interval, 0.03 to 0.24; P=0.02). Of 759 patients with sepsis, AKI developed in 326 (43%). Blood type A again conferred higher AKI risk relative to type O among patients of European descent (n=437; adjusted risk, 0.53 versus 0.40; risk difference, 0.14; 95% confidence interval, 0.04 to 0.23; P=0.01). Findings were similar when analysis was restricted to those patients who did not develop acute respiratory distress syndrome or were not transfused. We did not detect a significant association between blood type and AKI risk among individuals of African descent in either cohort.Conclusions
Blood type A is independently associated with AKI risk in critically ill patients with trauma or severe sepsis of European descent, suggesting a role for ABO glycans in AKI susceptibility. 相似文献13.
Sinan Demirtas Ahmet Caliskan Oguz Karahan Celal Yavuz Orkut Guclu Mustafa Cagdas Cayir Faruk Toktas Osman Tiryakioglu 《Experimental & Clinical Cardiology》2013,18(2):107-109
BACKGROUND/OBJECTIVE:
The development of acute renal injury (ARI) is an important indicator of clinical outcomes after cardiac surgery. Neutrophil gelatinase-associated lipocalin (NGAL) has been certified as a predictive biomarker of hypoxic ARI. The present study aimed to determine the predictive role of NGAL in coronary bypass graft (CABG) surgery.METHOD:
A total of 72 consecutive patients undergoing elective CABG were enrolled in the study. NGAL levels were determined preoperatively and postoperatively after 6 h, 24 h and 72 h for all participants. The participants were then divided into two groups according to their preoperative creatinine levels (group I, creatinine 111.38 μmol/L to 361.55 μmol/L; group II, creatinine <111.38 μmol/L).RESULTS:
There was no statistically significant difference between the groups according to their NGAL values (P>0.05), except at 6 h (P=0.045). Three patients required continuous hemodialysis. Comparison of the NGAL levels of these three patients with those of the other participants did not reveal any correlation with serum creatinine levels. In contrast, the NGAL levels were significantly lower in the continuous hemodialysis patients (1.9±1 ng/mL) compared with those of the other participants (22.6±12.8 ng/mL; P=0.001).CONCLUSION:
NGAL is one of the most frequently used biomarkers for ARI after cardiac operations, especially in younger patients. The participants in the present study were coronary artery disease patients and were, therefore, older than patients in previous reports. These results support the view that NGAL is not a relevant predictive factor for ARI in patients with CABG, including older patients. 相似文献14.
Morgan E. Grams Sushrut S. Waikar Blaithin MacMahon Seamus Whelton Shoshana H. Ballew Josef Coresh 《Clinical journal of the American Society of Nephrology》2014,9(4):682-689
Background and objectives
Billing codes are frequently used to identify AKI events in epidemiologic research. The goals of this study were to validate billing code–identified AKI against the current AKI consensus definition and to ascertain whether sensitivity and specificity vary by patient characteristic or over time.Design, setting, participants, & measurements
The study population included 10,056 Atherosclerosis Risk in Communities study participants hospitalized between 1996 and 2008. Billing code–identified AKI was compared with the 2012 Kidney Disease Improving Global Outcomes (KDIGO) creatinine-based criteria (AKIcr) and an approximation of the 2012 KDIGO creatinine- and urine output–based criteria (AKIcr_uop) in a subset with available outpatient data. Sensitivity and specificity of billing code–identified AKI were evaluated over time and according to patient age, race, sex, diabetes status, and CKD status in 546 charts selected for review, with estimates adjusted for sampling technique.Results
A total of 34,179 hospitalizations were identified; 1353 had a billing code for AKI. The sensitivity of billing code–identified AKI was 17.2% (95% confidence interval [95% CI], 13.2% to 21.2%) compared with AKIcr (n=1970 hospitalizations) and 11.7% (95% CI, 8.8% to 14.5%) compared with AKIcr_uop (n=1839 hospitalizations). Specificity was >98% in both cases. Sensitivity was significantly higher in the more recent time period (2002–2008) and among participants aged 65 years and older. Billing code–identified AKI captured a more severe spectrum of disease than did AKIcr and AKIcr_uop, with a larger proportion of patients with stage 3 AKI (34.9%, 19.7%, and 11.5%, respectively) and higher in-hospital mortality (41.2%, 18.7%, and 12.8%, respectively).Conclusions
The use of billing codes to identify AKI has low sensitivity compared with the current KDIGO consensus definition, especially when the urine output criterion is included, and results in the identification of a more severe phenotype. Epidemiologic studies using billing codes may benefit from a high specificity, but the variation in sensitivity may result in bias, particularly when trends over time are the outcome of interest. 相似文献15.
Ali CM Johnson Lorraine B. Ware Jonathan Himmelfarb Richard A. Zager 《Clinical journal of the American Society of Nephrology》2011,6(9):2108-2113
Summary
Background and objectives
Experimental acute kidney injury (AKI) activates the HMG–CoA reductase (HMGCR) gene, producing proximal tubule cholesterol loading. AKI also causes sloughing of proximal tubular cell debris into tubular lumina. This study tested whether these two processes culminate in increased urinary pellet cholesterol content, and whether the latter has potential AKI biomarker utility.Design, setting, participants, & measurements
Urine samples were collected from 29 critically ill patients with (n = 14) or without (n= 15) AKI, 15 patients with chronic kidney disease, and 15 healthy volunteers. Centrifuged urinary pellets underwent lipid extraction, and the extracts were assayed for cholesterol content (factored by membrane phospholipid phosphate content). In vivo HMGCR activation was sought by measuring levels of RNA polymerase II (Pol II), and of a gene activating histone mark (H3K4m3) at exon 1 of the HMGCR gene (chromatin immunoprecipitation assay of urine chromatin samples).Results
AKI+ patients had an approximate doubling of urinary pellet cholesterol content compared with control urine samples (versus normal; P < 0.001). The values significantly correlated (r, 0.5; P < 0.01) with serum, but not urine, creatinine concentrations. Conversely, neither critical illness without AKI nor chronic kidney disease raised pellet cholesterol levels. Increased HMGCR activity in the AKI+ patients was supported by three- to fourfold increased levels of Pol II, and of H3K4m3, at the HMGCR gene (versus controls or AKI− patients).Conclusions
(1) Clinical AKI, like experimental AKI, induces HMGCR gene activation; (2) increased urinary pellet cholesterol levels result; and (3) urine pellet cholesterol levels may have potential AKI biomarker utility. The latter will require future testing in a large prospective trial. 相似文献16.
Michael Darmon Christophe Clec’h Christophe Adrie Laurent Argaud Bernard Allaouchiche Elie Azoulay Lila Bouadma Ma?té Garrouste-Orgeas Hakim Haouache Carole Schwebel Dany Goldgran-Toledano Hatem Khallel Anne-Sylvie Dumenil Samir Jamali Bertrand Souweine Fabrice Zeni Yves Cohen Jean-Fran?ois Timsit 《Clinical journal of the American Society of Nephrology》2014,9(8):1347-1353
Background and objectives
Increasing experimental evidence suggests that acute respiratory distress syndrome (ARDS) may promote AKI. The primary objective of this study was to assess ARDS as a risk factor for AKI in critically ill patients.Design, setting, participants, & measurements
This was an observational study on a prospective database fed by 18 intensive care units (ICUs). Patients with ICU stays >24 hours were enrolled over a 14-year period. ARDS was defined using the Berlin criteria and AKI was defined using the Risk, Injury, Failure, Loss of kidney function, and End-stage kidney disease criteria. Patients with AKI before ARDS onset were excluded.Results
This study enrolled 8029 patients, including 1879 patients with ARDS. AKI occurred in 31.3% of patients and was more common in patients with ARDS (44.3% versus 27.4% in patients without ARDS; P<0.001). After adjustment for confounders, both mechanical ventilation without ARDS (odds ratio [OR], 4.34; 95% confidence interval [95% CI], 3.71 to 5.10) and ARDS (OR, 11.01; 95% CI, 6.83 to 17.73) were independently associated with AKI. Hospital mortality was 14.2% (n=1140) and was higher in patients with ARDS (27.9% versus 10.0% in patients without ARDS; P<0.001) and in patients with AKI (27.6% versus 8.1% in those without AKI; P<0.001). AKI was associated with higher mortality in patients with ARDS (42.3% versus 20.2%; P<0.001).Conclusions
ARDS was independently associated with AKI. This study suggests that ARDS should be considered as a risk factor for AKI in critically ill patients. 相似文献17.
Sandra M.S. Herrmann Ahmed Saad Alfonso Eirin John Woollard Hui Tang Michael A. McKusick Sanjay Misra James F. Glockner Lilach O. Lerman Stephen C. Textor 《Clinical journal of the American Society of Nephrology》2016,11(3):458-469
Background and objectives
Atherosclerotic renal artery stenosis (ARAS) can reduce renal blood flow, tissue oxygenation, and GFR. In this study, we sought to examine associations between renal hemodynamics and tissue oxygenation with single-kidney function, pressor hormones, and inflammatory biomarkers in patients with unilateral ARAS undergoing medical therapy alone or stent revascularization.Design, setting, participants, & measurements
Nonrandomized inpatient studies were performed in patients with unilateral ARAS (>60% occlusion) before and 3 months after revascularization (n=10) or medical therapy (n=20) or patients with essential hypertension (n=32) under identical conditions. The primary study outcome was change in single-kidney GFR. Individual kidney hemodynamics and volume were measured using multidetector computed tomography. Tissue oxygenation (using R2* as a measure of deoxyhemoglobin) was determined by blood oxygen level–dependent magnetic resonance imaging at 3 T. Renal vein neutrophil gelatinase–associated lipocalin (NGAL), monocyte chemoattractant protein-1 (MCP-1), and plasma renin activity were measured.Results
Total GFR did not change over 3 months in either group, but the stenotic kidney (STK) GFR rose over time in the stent compared with the medical group (+2.2[−1.8 to 10.5] versus −5.3[−7.3 to −0.3] ml/min; P=0.03). Contralateral kidney (CLK) GFR declined in the stent group (43.6±19.7 to 36.6±19.5 ml/min; P=0.03). Fractional tissue hypoxia fell in the STK (fraction R2* >30/s: 22.1%±20% versus 14.9%±18.3%; P<0.01) after stenting. Renal vein biomarkers correlated with the degree of hypoxia in the STK: NGAL(r=0.3; P=0.01) and MCP-1(r=0.3; P=0.02; more so after stenting). Renal vein NGAL was inversely related to renal blood flow in the STK (r=−0.65; P<0.001). Biomarkers were highly correlated between STK and CLK, NGAL (r=0.94; P<0.001), and MCP-1 (r=0.96; P<0.001).Conclusions
These results showed changes over time in single-kidney GFR that were not evident in parameters of total GFR. Furthermore, they delineate the relationship of measurable tissue hypoxia within the STK and markers of inflammation in human ARAS. Renal vein NGAL and MCP-1 indicated persistent interactions between the ischemic kidney and both CLK and systemic levels of inflammatory cytokines. 相似文献18.
Keiko I. Greenberg Mara A. McAdams-DeMarco Anna K?ttgen Lawrence J. Appel Josef Coresh Morgan E. Grams 《Clinical journal of the American Society of Nephrology》2015,10(5):776-783
Background and objectives
Higher urate levels are associated with higher risk of CKD, but the association between urate and AKI is less established. This study evaluated the risk of hospitalized AKI associated with urate concentrations in a large population-based cohort. To explore whether urate itself causes kidney injury, the study also evaluated the relationship between a genetic urate score and AKI.Design, setting, participants, & measurements
A total of 11,011 participants from the Atherosclerosis Risk in Communities study were followed from 1996–1998 (baseline) to 2010. The association between baseline plasma urate and risk of hospitalized AKI, adjusted for known AKI risk factors, was determined using Cox regression. Interactions of urate with gout and CKD were tested. Mendelian randomization was performed using a published genetic urate score among the participants with genetic data (n=7553).Results
During 12 years of follow-up, 823 participants were hospitalized with AKI. Overall, mean participant age was 63.3 years, mean eGFR was 86.3 ml/min per 1.73 m2, and mean plasma urate was 5.6 mg/dl. In patients with plasma urate >5.0 mg/dl, there was a 16% higher risk of hospitalized AKI for each 1-mg/dl higher urate (adjusted hazard ratio, 1.16; 95% confidence interval, 1.10 to 1.23; P<0.001). When stratified by history of gout, the association between higher urate and AKI was significant only in participants without a history of gout (P for interaction=0.02). There was no interaction of CKD and urate with AKI, nor was there an association between genetic urate score and AKI.Conclusions
Plasma urate >5.0 mg/dl was independently associated with risk of hospitalized AKI; however, Mendelian randomization did not provide evidence for a causal role of urate in AKI. Further research is needed to determine whether lowering plasma urate might reduce AKI risk. 相似文献19.
F. Perry Wilson Wei Yang Carlos A. Machado Laura H. Mariani Yuliya Borovskiy Jeffrey S. Berns Harold I. Feldman 《Clinical journal of the American Society of Nephrology》2014,9(4):673-681
Background and objectives
The benefit of the initiation of dialysis for AKI may differ depending on patient factors, but, because of a lack of robust evidence, the decision to initiate dialysis for AKI remains subjective in many cases. Prior studies examining dialysis initiation for AKI have examined outcomes of dialyzed patients compared with other dialyzed patients with different characteristics. Without an adequate nondialyzed control group, these studies cannot provide information on the benefit of dialysis initiation. To determine which patients would benefit from initiation of dialysis for AKI, a propensity-matched cohort study was performed among a large population of patients with severe AKI.Design, setting, participants, & measurements
Adults admitted to one of three acute care hospitals within the University of Pennsylvania Health System from January 1, 2004, to August 31, 2010, who subsequently developed severe AKI were included (n=6119). Of these, 602 received dialysis. Demographic, clinical, and laboratory variables were used to generate a time-varying propensity score representing the daily probability of initiation of dialysis for AKI. Not-yet-dialyzed patients were matched to each dialyzed patient according to day of AKI and propensity score. Proportional hazards analysis was used to compare time to all-cause mortality among dialyzed versus nondialyzed patients across a spectrum of prespecified variables.Results
After propensity score matching, covariates were well balanced between the groups, and the overall hazard ratio for death in dialyzed versus nondialyzed patients was 1.01 (95% confidence interval, 0.85 to 1.21; P=0.89). Serum creatinine concentration modified the association between dialysis and survival, with a 20% (95% confidence interval, 9% to 30%) greater survival benefit from dialysis for each 1-mg/dl increase in serum creatinine concentration (P=0.001). This finding persisted after adjustment for markers of disease severity. Dialysis initiation was associated with more benefit than harm at a creatinine concentration≥3.8 mg/dl.Conclusions
Dialysis was associated with increased survival when initiated in patients with AKI who have a more elevated creatinine level but was associated with increased mortality when initiated in patients with lower creatinine concentrations. 相似文献20.
Margarida Alvelos Rodrigo Pimentel Elika Pinho André Gomes Patricia Louren?o Maria José Teles Pedro Almeida Jo?o Tiago Guimar?es Paulo Bettencourt 《Clinical journal of the American Society of Nephrology》2011,6(3):476-481