tbuckley/cabot-search huggingface dataset:
Clinical efficacy of fecal occult blood test and colonoscopy for dasatinib-induced hemorrhagic colitis in CML patients
Authors: Satoshi Nishiwaki, Matsuyoshi Maeda, Masahiro Yamada, Shingo Okuno, Yasuhiko Harada, Kotaro Suzuki, Shingo Kurahashi, Fumihiro Urano, Shozo Okamura, Isamu Sugiura
Journal: Blood (2016)
Etoposide Priming in Patients with Lymphoma Improves Mobilization without An Increased Risk of Secondary Hematologic Malignancies.
Authors: Anuj Mahindra, Brian J. Bolwell, Robert Dean, Matt Kalaycio, Belinda Avalos, Lisa Rybicki, Shawnda Tench, Patrick Elder, Ronald Sobecks, John Sweetenham, Brad Pohlman, Steve Andresen, Steve Devine, Edward Copelan
Journal: Blood (2009)
Haplo-Cord UCB SCT with Low Cell Dose, Well Matched UCB Units. a Prospective Multicenter Study
Authors: Koen van Besien, Hongtao Liu, Usama Gergis, Melissa M. Cushing, Stephanie Tsai, Sebastian Mayer, Amittha Wickrema, Wendy Stock, Richard A. Larson, Tsiporah B. Shore, Olatoyosi Odenike, Roger N Pearse, Lucy A Godley, Tomer M Mark, Justin Kline, John M Cunningham, James LaBelle, Michael R Bishop, Andrew S. Artz
Journal: Blood (2014)
AB0810 Macrophage Migration Inhibitory Factor in Gouty Arthritis
Authors: H.-R. Kim, K.-A. Lee, K.-W. Kim, B. Kim, S.-H. Lee
Journal: Annals of the Rheumatic Diseases (2016)

<h3>Background</h3> Macrophage migration inhibitory factor (MIF) is proinflammatory, angiogenic and tissue degrading cytokine. <h3>Objectives</h3> This study aimed to determine monosodium urate (MSU)-induced MIF production and the role of MIF in gouty arthritis. <h3>Methods</h3> Peripheral blood and clinical data were obtained from 98 patients (31 patients with acute gouty arthritis and 67 patients with intercritical gout). Synovial fluid (SF) was obtained from patients with acute gouty arthritis and SF white blood cells and neutrophils were counted. SF and serum levels of MIF, interleukin (IL)-1, IL-8 and leukotriene B4, were measure using enzyme-linked immunosorbent assay (ELISA) and their relationship was analyzed. Peripheral blood mononuclear cells (PBMC) were isolated and cultured with MSU crystal, the production of MIF was determined. <h3>Results</h3> SF MIF level was higher in acute gouty arthritis than osteoarthritis. Serum MIF was higher in patients with intercritical gout than patients with acute gouty arthritis or healthy volunteers. SF MIF level was positively correlated with SF WBC and neutrophil counts, IL-1b and IL-8 levels in acute gouty arthritis. Serum MIF level was correlated with IL-1b and IL-8 levels in patients with intercritical gout. MSU crystal induced MIF production in PBMC with maximal effect at 100mg/ml. <h3>Conclusions</h3> MIF was highly produced in gouty arthritis and MSU induced MIF production. MIF could be involved in early inflammatory process in acute gouty arthritis. <h3>Acknowledgement</h3> This research was supported by the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science, and Technology (NRF-2013R1A1A1008171). <h3>Disclosure of Interest</h3> None declared
Reduced Dose PAD Combination Therapy (PS-341/Bortezomib, Adriamycin and Dexamethasone) for Previously Untreated Patients with Multiple Myeloma.
Authors: Rakesh Popat, Heather E. Oakervee, Nicola Curry, Nicola Foot, Curly Morris, Mary Drake, Samir Agrawal, Patricia Smith, David Schenkein, Dixie-Lee Esseltine, Jamie D. Cavenagh
Journal: Blood (2005)
Ethics and hepatitis B cure research
Authors: Jeremy Sugarman, Peter Revill, Fabien Zoulim, Yazdan Yazdanpanah, Harry L A Janssen, Seng Gee Lim, Sharon R Lewin
Journal: Gut (2016)

Recent scientific advances, including the development of curative therapies for HCV and the establishment of global cure initiatives for HIV, have led to international calls seeking a cure for chronic infection with HBV.1 ,2 Over 240 million people live with chronic HBV, resulting in up to 780 000 deaths annually due to hepatic fibrosis/cirrhosis and hepatocellular carcinoma (HCC).3 ,4 Persons chronically infected with HBV who do not receive treatment have a lifelong risk of developing HCC, the third most common cause of disease globally.5–7 Along with scaled-up approaches to preventing and treating chronic HBV infection, having a safe and effective cure for HBV infection promises to minimise the global burden of HBV-related morbidity and mortality and reduce the economic and other burdens of lifelong treatment. Nevertheless, as HBV cure research proceeds, it is critical to anticipate and address the associated ethical issues to best protect the rights, interests and welfare of those who participate in the research as well as those who are or will become chronically infected with HBV. In this paper, after describing briefly the rationale for work aimed at achieving HBV cure, we delineate some of the key ethical issues that are especially salient for HBV cure research: (1) risks of interventions; (2) outcome measures, monitoring and modelling; (3) selection of study population; (4) language and consent; and (5) fairness.

HBV infects hepatocytes and can establish a long-lived persistent reservoir through unintegrated covalently closed circular (ccc)DNA (and to a lesser extent integrated HBV DNA) that can continually produce HBV DNA and viral proteins, particularly hepatitis B surface antigen (HBsAg).8 Following the administration of nucleos(t)ide reverse transcriptase inhibitors or interferon α, the main strategies for treating chronic HBV infection,9 ,10 HBV DNA declines to often undetectable levels and liver inflammation improves, …
Arsenic Trioxide (As2O3) Mediated Cell Death in Hodgkin Lymphoma (HL) and Non-Hodgkin Lymphoma (NHL): Investigation of Reactive Oxygen Species (ROS), Caspase, and MAP Kinase Signaling Pathways.
Authors: Savita Bhalla, Amareshwar T.K Singh, Sheila Prachand, Qudsia Haque, Thomas V. O’Halloran, Jane N. Winter, Paul T. Schumacker, Leonidas C. Platanias, Leo I. Gordon, Andrew M. Evens
Journal: Blood (2007)
Prognostic Value of BCL2 Determination in Follicular NHL Patients Treated with Alkylating Containing Regimen Alone or in Combination with Rituximab.
Authors: Daniele Laszlo, Cristina Rabascio, Giovanna Andreola, Chiara Corsini, Fedro Peccatori, Anna Vanazzi, Rosaria Balzano, Francesco Bertolini, Giovanni Martinelli
Journal: Blood (2004)
Indian Hedgehog Stimulates Proliferation of Short-Term NOD/SCID-ß2mnull Repopulating Cells on Coculture with Human Stromal Cells.
Authors: Masayoshi Kobune, Yutaka Kawano, Junji Kato, Yoshinori Ito, Hiroki Chiba, Kageaki Kuribayashi, Rishu Takimoto, Takuya Matsunaga, Hirofumi Hamada, Yoshiro Niitsu
Journal: Blood (2004)
Prospective Evaluation of Blood Pressure Monitoring and Baroreceptor Reflex Sensitivity (BRS) in Patients with AL Amyloidosis: Prognostic and Pathophysiologic Implications
Authors: Efstathios Kastritis, Maria Roussou, Despoina Fotiou, Dimitrios Ziogas, Maria Gavriatopoulou, Kimon Stamatelopoulos, Constantinos Pamboucas, Elektra Papadopoulou, Fotios Michas, Aikaterini Lykka, Evangelos Terpos, Meletios A. Dimopoulos, Efstathios Manios
Journal: Blood (2015)
CD73-Independent Toxicity of Fludarabine on Adult Normal Bone Marrow Mesenchymal Cells (NBMMC).
Authors: Celine Pebrel-Richard, Richard Veyrat-Masson, Nathalie Boiret-Dupré, Chantal Rapatel, Juliette Berger, Olivier Tournilhac, Stephane Boisgard, Jacques Chassagne, Marc G. Berger
Journal: Blood (2006)
Transferred Donor-Derived WT1-Specific CD8+ T-Cell Clones After Hematopoietic Cell Transplantation Mediate Antileukemic Activity and Can Establish Persistent Responses without Toxicity to Normal Tissues in High-Risk Leukemia Patients
Authors: Aude G. Chapuis, Gunnar B. Ragnarsson, Hieu Nguyen, Colette N Chaney, Jeff Pufnock, Tomas Schmitt, Natalie Duerkopp, Ilana Roberts, Galina Pogosov, William Ho, Merav Bar, Jerald P. Radich, Cassian Yee, Philip Greenberg
Journal: Blood (2012)
SAT0566 Salivary Gland Ultrasonography and Its Applications in Patients with Sjögren's Syndrome and Sicca Symptoms
Authors: Y.P. Tsao, W.S. Chen, C.Y. Tsai
Journal: Annals of the Rheumatic Diseases (2016)

<h3>Background</h3> Sjögren9s syndrome is an autoimmune disease that involves the exocrine glands. In the criteria declared in 2002 and 2012, salivary gland biopsy remains crucial in diagnosing the disease, and the aggregation of lymphocytes correlates with the disease activity. However, salivary gland biopsy is invasive and is not recommended for monitoring the disease activity. Ultrasonography provides easy access, low cost and real-time image. Recent systemic review indicated ultrasonography revealing abnormalities of salivary glands, which may be helpful for rheumatologist in diagnosing Sjögren9s syndrome, but the reliabilities need to be confirmed among different scoring systems. <h3>Objectives</h3> To investigate the usefulness of salivary gland ultrasonography in Sjögren9s syndrome and its correlations with EULAR Sjögren9s Syndrome Patient Reported Index (ESSPRI) questionnaires (Seror R, 2011). <h3>Methods</h3> 50 patients, including primary and secondary Sjögren9s syndrome, as well as some patients with sicca symptoms were enrolled. Ultrasonography by a 13MHz linear probe was performed at parotid and submandibular glands. Each gland was scored from 0 to 4 according to the criteria proposed by previous study (Takagi Y, 2010), with a total maximum score with 16. ESSPRI questionnaires and blood samplings were also performed within 1 week after ultrasonography. <h3>Results</h3> Total 31 primary Sjögren9s Syndrome, 8 secondary Sjögren9s Syndrome, and 13 patients with sicca symptoms were enrolled. The average score of salivary gland ultrasonography was 8, 8, 5 respectively in each group. A significant correlations between salivary gland ultrasonography summation score with serum anti-La (SSB) (p=0.006) and ESSPRI score (p&lt;0.001) were noted. The score also correlated with the fatigue score (p&lt;0.001) and dry score (p=0.001) in the ESSPRI questionnaire, but not with the pain score (p=0.135). The correlations with serum anti-Ro antibody was not significant (p=0.902). <h3>Conclusions</h3> Summation score of salivary gland ultrasonography correlated well with serum anti-La titers and ESSPRI score. Ultrasonography provided real-time, easily accessible information on patients9 salivary gland conditions, as well as good correlations with patients9 subjective discomfort. The relationship between the ultrasonography images and disease activity deserves further investigations. <h3>References</h3> Jousse-Joulin S, et al. Rheumatology (Oxford). 2015. [Epub ahead of print] Takagi Y, et al. Ann Rheum Dis 2010;69:1321–4. Seror R, et al. Ann Rheum Dis 2011;70:968–72. <h3>Disclosure of Interest</h3> None declared
Androgen-Dependent Repression of ERRγ Reprograms Metabolism in Prostate Cancer
Authors: Étienne Audet-Walsh, Tracey Yee, Shawn McGuirk, Mathieu Vernier, Carlo Ouellet, Julie St-Pierre, Vincent Giguère
Journal: Cancer Research (2016)

Abstract How androgen signaling contributes to the oncometabolic state of prostate cancer remains unclear. Here, we show how the estrogen-related receptor γ (ERRγ) negatively controls mitochondrial respiration in prostate cancer cells. Sustained treatment of prostate cancer cells with androgens increased the activity of several metabolic pathways, including aerobic glycolysis, mitochondrial respiration, and lipid synthesis. An analysis of the intersection of gene expression, binding events, and motif analyses after androgen exposure identified a metabolic gene expression signature associated with the action of ERRγ. This metabolic state paralleled the loss of ERRγ expression. It occurred in both androgen-dependent and castration-resistant prostate cancer and was associated with cell proliferation. Clinically, we observed an inverse relationship between ERRγ expression and disease severity. These results illuminate a mechanism in which androgen-dependent repression of ERRγ reprograms prostate cancer cell metabolism to favor mitochondrial activity and cell proliferation. Furthermore, they rationalize strategies to reactivate ERRγ signaling as a generalized therapeutic approach to manage prostate cancer. Cancer Res; 77(2); 378–89. ©2016 AACR.
NOTCH1/FBXW7 Mutation Identifies a Large Subgroup with Favorable Outcome in Adult T-ALL: A GRAALL Study.
Authors: Vahid Asnafi, Agnes Buzyn, Sandrine Lenoir, Fréderic Baleydier, Arnauld Simon, Kheira Beldjord, Oumedaly Reman, Francis Witz, Thierry de Revel, Emmanuelle Tavernier, Pascal Turlure, Thibaut Leguay, Francoise Huguet, Jean- Paul Vernant, Veronique Lhéritier, Marie-Christine Béné, Norbert Ifrah, Xavier Thomas, Hervé Dombret, Elizabeth MacIntyre
Journal: Blood (2008)
Tumor Microenvironment Regulates Survival of Mantle Cell Lymphoma Cells through Various Signaling Pathways
Authors: Lalit Sehgal, Khashab Tamer, Xin Wang, Rohit Mathur, Zuzana Berkova, Jorge E. Romaguera, Alma Rodriguez, Sattva S. Neelapu, Felipe Samaniego
Journal: Blood (2015)
NPR-B Expression In Megakaryocytes and Platelets
Authors: Sinny Delacroix, Brian J Boylan, Adriana Harbuzariu, Peter J Psaltis, Shuchong Pan, Eric Holroyd, Daniel B Spoon, Laurel Kleppe, Cheryl Mueske, Tyra Witt, Gurpreet S Sandhu, Robert D Simari
Journal: Blood (2010)
Evidence for a Pathological Ratio of CD44s/CD44v6 in Chronic Lymphoctic Leukemia (CLL) Cells.
Authors: Magdalena Hertweck, Felix Erdfelder, Alexandra Filipovich, Sabrina Uhrmacher, Rajesh Kumar Gandhirajan, Iris Gehrke, Julian Paesler, Regina Razavi, Simon Jonas Poll-Wolbeck, Michael Hallek, Karl Anton Kreuzer
Journal: Blood (2009)
NHS needs 4% a year funding rise until 2030, trust heads tell peers
Authors: Adrian O'Dowd
Journal: BMJ (2016)

The NHS needs around a 4% rise in its overall budget every year to meet growing and anticipated demand over the next 15 years, health service leaders have told peers.

Chief executives at three large acute trusts gave a blunt message about their perceived underfunding of the health service during a three hour evidence session of the House of Lords NHS sustainability committee on 15 November.

The NHS was approaching a “crossroads,” said Michael Deegan, chief executive at Central Manchester University Hospitals NHS Foundation Trust, giving evidence during the session for the committee’s inquiry into the NHS’s long term sustainability.

“Our view is that the current path that we are on is taking us rapidly towards an unsustainable position,” said Deegan, also a member …
Febrile Neutropenia, Mucositis and Duration of Hospitalization Are Reduced After Pegfilgrastim Following Autologous Peripheral Blood Stem Cell Transplantation (PBSCT) for Malignant Lymphopathies: Report of 683 PBSCTs From a Single Institution.
Authors: Sophie Auger, Philippe Quittet, Marie Cecile Bozonnat, Salahedine Bouya, Tarik Kanouni, Nathalie Fegueux, Patrice Ceballos, Jean-Côme Meniane, Guillaume Cartron, Jean-Francois Rossi
Journal: Blood (2009)
FRI0392 Ultrasonographic Scoring Revealed That The Ratio of Extra-Synovial Inflammation To Synovial Inflammation in The Shoulder Is Higher in PMR Patients than That in Elderly-Onset RA Patients with PMR-like Onset
Authors: T. Suzuki, R. Yoshida, Y. Seri
Journal: Annals of the Rheumatic Diseases (2016)

<h3>Background</h3> We previously reported that shoulder synovitis in polymyalgia rheumatica (PMR) is milder than that in elderly-onset rheumatoid arthritis (EORA) patients with PMR-like onset (polymyalgic-EORA) by using semi-quantitative ultrasound (US) scoring of the synovial components in the shoulder in spite of the higher serum CRP (1). <h3>Objectives</h3> We aimed to evaluate the contribution of the extra-synovial inflammation in PMR patients by power Doppler (PD) US. <h3>Methods</h3> We analyzed US records of 14 untreated PMR patients and 14 untreated polymyalgic-EORA patients using a semi-quantitative four-point scale (0 = absent, 1 = mild, 2 = moderate or 3 = severe). For the comprehensive evaluation of shoulder synovitis, the severity of the biceps tenosynovitis, subacromial/subdeltoid bursitis and glenohumeral joint synovitis were subjectively scored on a gray scale and by PD on a 4-point scale (0–3). The sum of six scores (0–18) for one shoulder was defined as shoulder synovitis score (SSS). For the evaluation of extra-synovial inflammation in the shoulder, the hyperemia adjacent to the anterior aspect of the subscapularis tendon (SubST) was analyzed in the horizontal long axis view. The severity of PD-signals on SubST was subjectively scored on a 4-point scale (0–3) as exemplified in the figure, and the score was defined as the extra-synovial hyperemia score (ESHS). <h3>Results</h3> The ESHS/SSS ratio was significantly higher in PMR shoulders than in polymyalgic-EORA shoulders (0.447 ±0.251 vs 0.303 ±0.277, p=0.0138). The bilateral ESHS/bilateral SSS ratio was significantly higher in PMR patients than in polymyalgic-EORA patients (0.475 ±0.269 vs 0.236 ±0.182, p=0.00776). <h3>Conclusions</h3> Semi-quantitative US scoring of the synovial and the extra-synovial components in the shoulder revealed the larger involvement of the extra-synovial soft tissue inflammation in PMR patients than in EORA patients with PMR-like onset. <h3>References</h3> Arthritis Rheumatol. 2015; 67 (suppl 10) <h3>Disclosure of Interest</h3> None declared
FGFR-TACC gene fusions in human glioma
Authors: Anna Lasorella, Marc Sanson, Antonio Iavarone
Journal: Neuro-Oncology (2016)

Chromosomal translocations joining in-frame members of the fibroblast growth factor receptor-transforming acidic coiled-coil gene families (the FGFR-TACC gene fusions) were first discovered in human glioblastoma multiforme (GBM) and later in many other cancer types. Here, we review this rapidly expanding field of research and discuss the unique biological and clinical features conferred to isocitrate dehydrogenase wild-type glioma cells by FGFR-TACC fusions. FGFR-TACC fusions generate powerful oncogenes that combine growth-promoting effects with aneuploidy through the activation of as yet unclear intracellular signaling mechanisms. FGFR-TACC fusions appear to be clonal tumor-initiating events that confer strong sensitivity to FGFR tyrosine kinase inhibitors. Screening assays have recently been reported for the accurate identification of FGFR-TACC fusion variants in human cancer, and early clinical data have shown promising effects in cancer patients harboring FGFR-TACC fusions and treated with FGFR inhibitors. Thus, FGFR-TACC gene fusions provide a "low-hanging fruit" model for the validation of precision medicine paradigms in human GBM.
A Phase II Study of ZD6474, a Vascular Endothelial Growth Factor Receptor (VEGFR) and Epidermal Growth Factor Receptor (EGFR) Tyrosine Kinase Inhibitor (TKI) in Patients with Relapsed Multiple Myeloma (MM).
Authors: Michael J. Kovacs, Donna E. Reece, Deborah Marcellus, Ralph M. Meyer, Sarah Matthews, Rui-Ping Dong, Elizabeth Eisenhauer
Journal: Blood (2004)
OP0208 Emerging Role of IL-33/ST2 Axis in Endothelial Cell Injury of Lupus Nephritis
Authors: S. Yu, C.-H. Huang, W.-H. Huang, C.-H. Huang, Y. Huo, Y. Tao
Journal: Annals of the Rheumatic Diseases (2016)

<h3>Background</h3> "Alarmins" are prototypic endogenous pro-inflammatory factors as they are released from necotic cells and provoke local damage or systemic inflammation. Evidences are accumulating to support the inclusion of "Alarmins" as targets of autoreactivity as well as inducers in the pathogenesis of Systemic Lupus Erythematosus (SLE). Interleukin (IL)-33 is a novel member of the family of "Alarmins" because of its characteristics and functions in mediating host immune responses. On this background, we sought to determine the role of IL-33/ST2 axis in lupus pathogenesis. The role of IL-33/ST2 axis has not previously been described in lupus nephritis. <h3>Objectives</h3> We sought to determine the role of IL-33/ST2 axis in lupus pathogenesis. The role of IL-33/ST2 axis has not previously been described in lupus nephritis. <h3>Methods</h3> This project will study the followings: (1) To determine whether IL-33 was present in renal glomerular endothelial cells; (2) To assess the functional and intracellular signal transuction mechanisms regulating the link between IL-33/ST2-mediated innate immunity and inflammation in CD4<sup>+</sup> T cells-endothelial cells co-culture system of lupus patients. <h3>Results</h3> Immunofluorescence (IF) for IL-33 in the kidney were performed in both MRL<sup>lpr</sup> lupus mice and C57BL/6J mice. On double staining for IL-33 and lectin, IL-33 was clearly seen in glomeruli and also in peritubular areas. To determine whether the IL-33 staining in glomeruli and peritubular areas was in endothelium, double IF staining for IL-33 and von Willebrand factor (vWF) was performed. IL-33 co-localized with vWF in glomeruli and in peritubular areas. The increased levels of IL-33 mRNA transcripts were detected in kidney of MRL<sup>lpr</sup> lupus mice compared with C57BL/6J mice. Expression of cell-surface ST2 was increased on the CD4<sup>+</sup> T cells of lupus patients when compared with healthy controls. Serum sST2 level was significantly higher in SLE patients with <i>flare</i> than those without <i>flare</i> (p&lt;0.05). <h3>Conclusions</h3> As a result of external stimuli or infection, renal glomerular endothelial cells undergo cellular death and release the "Alarmin", IL-33, to alert the lupus immune system. Released IL-33 interact with their target cells, CD4<sup>+</sup> T cells via their specific receptor ST2 to subsequently induce innate and adaptive responses, activate inflammatory pathways in the pathogenesis of lupus nephritis. <h3>References</h3> Yu SL, Wong CKTam LS. The alarmin functions of high-mobility group box-1 and IL-33 in the pathogenesis of systemic lupus erythematosus. Expert review of clinical immunology, 2013,9: 739–749. <h3>Disclosure of Interest</h3> None declared
Acute Kidney Injury as a Risk Factor for Delirium and Coma during Critical Illness
Authors: Edward D. Siew, William H. Fissell, Christina M. Tripp, Jeffrey D. Blume, Matthew D. Wilson, Amanda J. Clark, Andrew J. Vincz, E. Wesley Ely, Pratik P. Pandharipande, Timothy D. Girard
Journal: American Journal of Respiratory and Critical Care Medicine (2017)

Rationale: Acute kidney injury may contribute to distant organ dysfunction. Few studies have examined kidney injury as a risk factor for delirium and coma.Objectives: To examine whether acute kidney injury is associated with delirium and coma in critically ill adults.Methods: In a prospective cohort study of intensive care unit patients with respiratory failure and/or shock, we examined the association between acute kidney injury and daily mental status using multinomial transition models adjusting for demographics, nonrenal organ failure, sepsis, prior mental status, and sedative exposure. Acute kidney injury was characterized daily using the difference between baseline and peak serum creatinine and staged according to Kidney Disease Improving Global Outcomes criteria. Mental status (normal vs. delirium vs. coma) was assessed daily with the Confusion Assessment Method for the ICU and Richmond Agitation-Sedation Scale.Measurements and Main Results: Among 466 patients, stage 2 acute kidney injury was a risk factor for delirium (odds ratio [OR], 1.55; 95% confidence interval [CI], 1.07–2.26) and coma (OR, 2.04; 95% CI, 1.25–3.34) as was stage 3 injury (OR for delirium, 2.56; 95% CI, 1.57–4.16) (OR for coma, 3.34; 95% CI, 1.85–6.03). Daily peak serum creatinine (adjusted for baseline) values were also associated with delirium (OR, 1.35; 95% CI, 1.18–1.55) and coma (OR, 1.44; 95% CI, 1.20–1.74). Renal replacement therapy modified the association between stage 3 acute kidney injury and daily peak serum creatinine and both delirium and coma.Conclusions: Acute kidney injury is a risk factor for delirium and coma during critical illness.