DOCSLIB.ORG

2012 CKD Guideline

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
2012 CKD Guideline OFFICIAL JOURNAL OF THE INTERNATIONAL SOCIETY OF NEPHROLOGY KDIGO 2012 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease VOLUME 3 | ISSUE 1 | JANUARY 2013 http://www.kidney-international.org KDIGO 2012 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease KDIGO gratefully acknowledges the following consortium of sponsors that make our initiatives possible: Abbott, Amgen, Bayer Schering Pharma, Belo Foundation, Bristol-Myers Squibb, Chugai Pharmaceutical, Coca-Cola Company, Dole Food Company, Fresenius Medical Care, Genzyme, Hoffmann-LaRoche, JC Penney, Kyowa Hakko Kirin, NATCO—The Organization for Transplant Professionals, NKF-Board of Directors, Novartis, Pharmacosmos, PUMC Pharmaceutical, Robert and Jane Cizik Foundation, Shire, Takeda Pharmaceutical, Transwestern Commercial Services, Vifor Pharma, and Wyeth. Sponsorship Statement: KDIGO is supported by a consortium of sponsors and no funding is accepted for the development of specific guidelines. http://www.kidney-international.org contents & 2013 KDIGO VOL 3 | ISSUE 1 | JANUARY (1) 2013 KDIGO 2012 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease v Tables and Figures vii KDIGO Board Members viii Reference Keys x CKD Nomenclature xi Conversion Factors & HbA1c Conversion xii Abbreviations and Acronyms 1 Notice 2 Foreword 3 Work Group Membership 4 Abstract 5 Summary of Recommendation Statements 15 Introduction: The case for updating and context 19 Chapter 1: Definition, and classification of CKD 63 Chapter 2: Definition, identification, and prediction of CKD progression 73 Chapter 3: Management of progression and complications of CKD 91 Chapter 4: Other complications of CKD: CVD, medication dosage, patient safety, infections, hospitalizations, and caveats for investigating complications of CKD 112 Chapter 5: Referral to specialists and models of care 120 Methods for Guideline Development 128 Biographic and Disclosure Information 134 Acknowledgments 136 References This journal is a member of, and subscribes to the principles of, the Committee on Publication Ethics (COPE) www.publicationethics.org http://www.kidney-international.org contents & 2013 KDIGO TABLES 18 Table 1. KDIGO nomenclature and description for grading recommendations 20 Table 2. Criteria for CKD 20 Table 3. Criteria for definition of CKD 27 Table 4. Classification of CKD based on presence or absence of systemic disease and location within the kidney of pathologic-anatomic findings 27 Table 5. GFR categories in CKD 28 Table 6. Albuminuria categories in CKD 31 Table 7. Relationship among categories for albuminuria and proteinuria 32 Table 8. CGA staging of CKD: examples of nomenclature and comments 33 Table 9. Prognosis of CKD: Relationship of outcomes and strength of relationship to Cause (C), GFR (G), Albuminuria (A) and other measures 35 Table 10. Annual percentage change in GFR across diagnosis categories 39 Table 11. Sources of error in GFR estimating using creatinine 41 Table 12. Equations based on serum creatinine assays in adults that are traceable to the standard reference material 44 Table 13. Performance comparison of creatinine-based GFR estimating equations in North America, Europe, and Australia 48 Table 14. Performance comparison of creatinine-based GFR estimating equations outside of North America, Europe, and Australia 50 Table 15. Sources of error in GFR estimating using cystatin C 52 Table 16. Equations based on IDMS traceable creatinine and IFCC traceable cystatin C assays 54 Table 17. Performance comparison of cystatin C-based estimating equations in North American and European populations 55 Table 18. Strengths and limitations of GFR measurement methods and markers 59 Table 19. Factors affecting urinary ACR 64 Table 20. Decline in kidney function in various populations (longitudinal studies only) 65 Table 21. Decline in kidney function in CKD populations 67 Table 22. Studies evaluating rapid progression (general population studies only) 68 Table 23. CKD progression and risk of all-cause mortality and ESRD using baseline (first) eGFR 68 Table 24. Association between absolute and percentage change in kidney function and risk of ESRD, based on adjustment for eGFR at the first and last measurement 77 Table 25. Intensive versus normal glycemic control and albuminuria outcome 78 Table 26. Recommended Daily Intake of sodium for healthy children 81 Table 27. Prevalence of CKD complications by GFR category derived from CKD cohorts 81 Table 28. Hemoglobin cutoffs for people living at sea level 87 Table 29. Phosphate binding agents in routine clinical practice and their ranked cost 89 Table 30. Summary data for bisphosphonates and CKD 100 Table 31. Peripheral arterial disease and CKD 103 Table 32. Cautionary notes for prescribing in people with CKD 107 Table 33. Risk factors for infection in people with CKD 110 Table 34. Components of community CKD management programs 114 Table 35. Early versus late referral: consequences and benefits 114 Table 36. Outcomes of early versus late referral 122 Table 37. Topics of interest for the management of CKD guideline 123 Table 38. Literature yield of primary articles for all topics 123 Table 39. Classification of study quality 124 Table 40. GRADE system for grading quality of evidence 124 Table 41. Final grade for overall quality of evidence 124 Table 42. Balance of benefits and harm 125 Table 43. KDIGO nomenclature and description for grading recommendations 125 Table 44. Determinants of strength of recommendation 125 Table 45. The Conference on Guideline Standardization checklist for reporting clinical practice guidelines Kidney International Supplements (2013) 3,v v contents http://www.kidney-international.org & 2013 KDIGO FIGURES 16 Figure 1. Conceptual model of CKD 22 Figure 2. Normal values for GFR by age 23 Figure 3. Relationship of eGFR with mortality 23 Figure 4. Relationship of albuminuria with mortality 28 Figure 5. Age-standardized rates of death from any cause, cardiovascular events, and hospitalization, according to the eGFR among 1,120,295 ambulatory adults 29 Figure 6. Summary of continuous meta-analysis for general population cohorts with ACR 30 Figure 7. Summary of categorical meta-analysis for general population cohorts with ACR 31 Figure 8. Prevalence of CKD in the USA by GFR and albuminuria 34 Figure 9. Prognosis of CKD by GFR and albuminuria category 39 Figure 10. Determinants of the serum level of endogenous filtration markers 43 Figure 11. Performance of the CKD-EPI and MDRD Study equations in estimating measured GFR in the external validation data set 46 Figure 12. Comparison of distribution of GFR and CKD prevalence by age (NHANES 1999-2004) 47 Figure 13. Meta-analysis of NRI for all-cause mortality, CVD mortality, and ESRD 50 Figure 14. Association of CKD definitions with all-cause mortality and ESRD 53 Figure 15. Performance of three equations for estimating GFR 57 Figure 16. Suggested protocol for the further investigation of an individual demonstrating a positive reagent strip test for albuminuria/proteinuria or quantitative albuminuria/proteinuria test 63 Figure 17. GFR and albuminuria grid to reflect the risk of progression 69 Figure 18. Distribution of the probability of nonlinearity with three example trajectories demonstrating different probabilities of nonlinearity 86 Figure 19. Summary estimates for risks of all-cause mortality and cardiovascular mortality associated with levels of serum phosphorus, PTH, and calcium 88 Figure 20. Prevalence of deficiency of 1,25(OH)2D3, 25(OH)D3, and secondary hyperparathyroidism by GFR intervals 113 Figure 21. Referral decision making by GFR and albuminuria 116 Figure 22. The CKD chronic care model Additional information in the form of supplementary materials can be found online at http://www.kdigo.org/clinical_practice_guidelines/ckd.php vi Kidney International Supplements (2013) 3,vi http://www.kidney-international.org & 2013 KDIGO KDIGO Board Members Garabed Eknoyan, MD Norbert Lameire, MD, PhD Founding KDIGO Co-Chairs Kai-Uwe Eckardt, MD Immediate Past Co-Chair Bertram L Kasiske, MD David C Wheeler, MD, FRCP KDIGO Co-Chair KDIGO Co-Chair Omar I Abboud, MD, FRCP Michel Jadoul, MD Sharon Adler, MD, FASN Simon Jenkins, MBE, FRCGP Rajiv Agarwal, MD Suhnggwon Kim, MD, PhD Sharon P Andreoli, MD Martin K Kuhlmann, MD Gavin J Becker, MD, FRACP Nathan W Levin, MD, FACP Fred Brown, MBA, FACHE Philip K-T Li, MD, FRCP, FACP Daniel C Cattran, MD, FRCPC Zhi-Hong Liu, MD Allan J Collins, MD, FACP Pablo Massari, MD Rosanna Coppo, MD Peter A McCullough, MD, MPH, FACC, FACP Josef Coresh, MD, PhD Rafique Moosa, MD Ricardo Correa-Rotter, MD Miguel C Riella, MD Adrian Covic, MD, PhD Adibul Hasan Rizvi, MBBS, FRCP Jonathan C Craig, MBChB, MM (Clin Epi), DCH, FRACP, PhD Bernardo Rodriquez-Iturbe, MD Angel LM de Francisco, MD Robert Schrier, MD Paul E de Jong, MD, PhD Justin Silver, MD, PhD Ana Figueiredo, RN, MSc, PhD Marcello Tonelli, MD, SM, FRCPC Mohammed Benghanem Gharbi, MD Yusuke Tsukamoto, MD Gordon Guyatt, MD, MSc, BSc, FRCPC Theodor Vogels, MSW David Harris, MD Angela Yee-Moon Wang, MD, PhD, FRCP Lai Seong Hooi, MD Christoph Wanner, MD Enyu Imai, MD, PhD Elena Zakharova, MD, PhD Lesley A Inker, MD, MS, FRCP NKF-KDIGO GUIDELINE DEVELOPMENT STAFF Kerry Willis, PhD, Senior Vice-President for Scientific Activities Michael Cheung, MA, Guideline Development Director Sean Slifer, BA, Guideline Development Manager Kidney International Supplements (2013) 3, vii vii http://www.kidney-international.org
Load more

Recommended publications
  • Hydronephrosis
    Hydronephrosis Natasha Brownrigg RN(EC), MN, NP-Pediatrics Assistant Clinical Professor, McMaster School of Nursing Nurse Practitioner, Pediatric Urology, McMaster Children’s Hospital, Hamilton, ON, Canada Dr. Jorge DeMaria Pediatric Urologist, McMaster Children’s Hospital Professor Department of Surgery/Urology, McMaster University, Hamilton, ON, Canada Dr. Luis H.P. Braga Pediatric Urologist, McMaster Children’s Hospital. Associate professor Department of Surgery/Urology, McMaster University, Hamilton, ON, Canada What is hydronephrosis? Hydro Nephrosis Hydronephrosis += Refers to water Refers to the kidney A build up of fluid or fluid (urine) in the kidney Hydronephrosis is the medical term for a build-up of urine in the kidney. As the urine builds up, it stretches or dilates the inside of the kidney, known as the collecting system. If an unborn baby has hydronephrosis, an ultrasound scan will show a build-up of urine in the kidney. This is called “antenatal hydronephrosis.” Hydronephrosis is found in as many as five out of 100 pregnancies. Hydronephrosis may also be found after birth. For example, if a baby has a urinary tract infection, an ultrasound of the baby’s kidneys and bladder may detect hydronephrosis. Key points to remember if your baby has hydronephrosis • Your baby can grow and develop normally with hydronephrosis. • Hydronephrosis may affect one kidney or both. • Hydronephrosis is a finding, not a disease. • Further tests are needed to find the cause of hydronephrosis. • If the cause is known, a pediatric urologist will discuss the possible treatment. Surgery is sometimes required to correct the cause of the hydronephrosis. Hydronephrosis is often transient and improves without any intervention.
    [Show full text]
  • Case Study: Testing for Genetic Disorders
    Case study: Testing for genetic disorders Purpose: A genetic disorder is a disorder that is caused by an abnormality (or several abnormalities) in a person’s genome. Genetic disorders are often hereditary, which means they are passed down to a child from its parents. The most common genetic disorder is familial hypercholesterolaemia (a genetic predisposition to high cholesterol levels), which is thought to affect 1 in 250 people in the UK. Other disorders, such as cystic fibrosis, are rarer although they can be relatively common in particular ethnic groups; for instance, the incidence of cystic fibrosis in Scotland is almost double the global average. Collectively genetic disorders affect lots of people because there are more than 10,000 different types worldwide. Genetic testing is used to inform people whether they have a disorder, or if there is a chance they might pass a disorder on to their children. Photo credit: jxfzsy/ iStockphoto Photo credit: monkeybusiness/ iStockphoto Approaches to identifying genetic disorders In the UK, if a person is concerned they might have, or might develop, a genetic disorder based on their family history, they can: Go to their GP, who might refer them for genetic testing. Patients usually provide a DNA sample, which is then analysed for a specific abnormality. Usually a single gene will be tested, but whole-genome sequencing approaches are being developed. The 100,000 Genomes Project, for example, aims to study whole-genome sequences from patients with cancer and rare disease Use a commercial genetic testing service. In this case, customers collect samples of their own DNA and send them away for analysis and interpretation Take no action.
    [Show full text]
  • Harry Keen Pioneering Diabetes Researcher, Staunch NHS Supporter, and Champion of People with Chronic Disease
    OBITUARIES Harry Keen Pioneering diabetes researcher, staunch NHS supporter, and champion of people with chronic disease Harry Keen, professor emeritus of human Study, which helped to establish the concept of metabolism (b 1925; q St Mary’s Hospital Medical separate glucose thresholds for microvascular School 1948; CBE, MD, FRCP), d 5 April 2013. and arterial disease. He was the natural choice to chair the 1980 WHO expert committee on Harry Keen was acting as a GP locum in Eltham diabetes mellitus, which introduced the concept when he was called to see a boy whose measles of impaired glucose tolerance and laid the basis had been complicated by bronchitis. He for our current definition of diabetes. examined the boy, left a prescription, collected His experience of an early diabetes clinic— his two shilling fee, and said he would be back where five doctors or more sat at desks in the in a couple of days. same large room and exchanged muttered On his return, the mother told him that Billy comments with their patients—led him to was a lot better. “As we spoke,’’ said Harry, ‘‘a conclude that 10 minutes twice a year was loud hacking cough came from upstairs, and I not enough for the adequate management of commented that he didn’t sound better. ‘Oh no,’ diabetes. He went on to pioneer the diabetes day said the mother, ‘that’s not Billy, it’s Johnny, his centre. brother.’ When I offered to take a look at him, Another idea whose time had come was the she said, ‘I’d rather you didn’t—we really can’t I development of the diabetes nurse specialist, afford it.
    [Show full text]
  • DOI: 10.4274/Jcrpe.Galenos.2021.2020.0175
    DOI: 10.4274/jcrpe.galenos.2021.2020.0175 Case report A novel SCNN1A variation in a patient with autosomal-recessive pseudohypoaldosteronism type 1 Mohammed Ayed Huneif1*, Ziyad Hamad AlHazmy2, Anas M. Shoomi 3, Mohammed A. AlGhofely 3, Dr Humariya Heena 5, Aziza M. Mushiba 4, Abdulhamid AlSaheel3 1Pediatric Endocrinologist at Najran university hospital, Najran Saudi Arabia. 2 Pediatric Endocrinologist at Al yamammah hospital, , Riyadh, Saudi Arabia. 3 Pediatric Endocrinologist at Pediatric endocrine department,. Obesity, Endocrine, and Metabolism Center, , King Fahad Medical City, Riyadh, Saudi Arabia. 4Clinical Geneticist, Pediatric Subspecialties Department, Children's Specialized Hospital, King Fahad Medical City, Riyadh, Saudi Arabia. 5 Research Center, King Fahad Medical City, Riyadh , Saudi Arabia What is already known on this topic ? Autosomal-recessive pseudohypoaldosteronism type 1 (PHA1) is a rare genetic disorder caused by different variations in the ENaC subunit genes. Most of these variations appear in SCNN1A mainly in exon eight, which encodes for the alpha subunit of the epithelial sodium channel ENaC. Variations are nonsense, single-base deletions or insertions, or splice site variations, leading to mRNA and proteins of abnormal length. In addition, a few new missense variations have been reported. What this study adds ? We report a novel mutation [ c.729_730delAG (p.Val245Glyfs*65) ] in the exon 4 of the SCNN1A gene In case of autosomal recessive pseudohypoaldosteronism type 1. Patient with PHA1 requires early recognition, proper treatment, and close follow-up. Parents are advised to seek genetic counseling and plan future pregnancies. proof Abstract Pseudohypoaldosteronism type 1 (PHA1) is an autosomal-recessive disorder characterized by defective regulation of body sodium levels.
    [Show full text]
  • Hemolytic Disease of the Newborn
    Intensive Care Nursery House Staff Manual Hemolytic Disease of the Newborn INTRODUCTION and DEFINITION: Hemolytic Disease of the Newborn (HDN), also known as erythroblastosis fetalis, isoimmunization, or blood group incompatibility, occurs when fetal red blood cells (RBCs), which possess an antigen that the mother lacks, cross the placenta into the maternal circulation, where they stimulate antibody production. The antibodies return to the fetal circulation and result in RBC destruction. DIFFERENTIAL DIAGNOSIS of hemolytic anemia in a newborn infant: -Isoimmunization -RBC enzyme disorders (e.g., G6PD, pyruvate kinase deficiency) -Hemoglobin synthesis disorders (e.g., alpha-thalassemias) -RBC membrane abnormalities (e.g., hereditary spherocytosis, elliptocytosis) -Hemangiomas (Kasabach Merritt syndrome) -Acquired conditions, such as sepsis, infections with TORCH or Parvovirus B19 (anemia due to RBC aplasia) and hemolysis secondary to drugs. ISOIMMUNIZATION A. Rh disease (Rh = Rhesus factor) (1) Genetics: Rh positive (+) denotes presence of D antigen. The number of antigenic sites on RBCs varies with genotype. Prevalence of genotype varies with the population. Rh negative (d/d) individuals comprise 15% of Caucasians, 5.5% of African Americans, and <1% of Asians. A sensitized Rh negative mother produces anti-Rh IgG antibodies that cross the placenta. Risk factors for antibody production include 2nd (or later) pregnancies*, maternal toxemia, paternal zygosity (D/D rather than D/d), feto-maternal compatibility in ABO system and antigen load. (2) Clinical presentation of HDN varies from mild jaundice and anemia to hydrops fetalis (with ascites, pleural and pericardial effusions). Because the placenta clears bilirubin, the chief risk to the fetus is anemia. Extramedullary hematopoiesis (due to anemia) results in hepatosplenomegaly.
    [Show full text]
  • Acute Phosphate Nephropathy Alexander K
    View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector http://www.kidney-international.org the renal consult & 2009 International Society of Nephrology Acute phosphate nephropathy Alexander K. Rocuts1, Sushrut S. Waikar1, Mariam P. Alexander1,2, Helmut G. Rennke2 and Ajay K. Singh1 1Renal Division, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA and 2Department of Pathology, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA minute. The rest of the examination was unremarkable. CASE PRESENTATION HerlaboratorydataissummarizedinTable1. A 60-year-old white Latino female with a clinical diagnosis A postoperative kidney ultrasound showed no of diabetes mellitus (diagnosed in 1993) and hypertension hydronephrosis. was referred to the chronic kidney disease clinic at The etiology of the acute kidney injury was unclear. Brigham and Women’s Hospital for the evaluation of acute Progressive diabetic nephropathy exacerbated by other kidney injury; serum creatinine had increased from a contributory factors, such as exposure to lisinopril, baseline of 0.9 to 1.5 mg/dl in a 11-week period. She was acetylsalicylic acid, or naproxen, was regarded as the most asymptomatic at the time of presentation. Her past plausible explanation. Despite discontinuation of these medical history included a total abdominal hysterectomy medications, kidney function did not improve; it worsened with bilateral salpingo oophorectomy and upper in a 4-week period after presentation. Hence, a kidney vaginectomy for high-grade squamous intraepithelial biopsy was performed. lesion of the cervix, 11 weeks prior to presentation. Three weeks prior to presentation (8 weeks after surgery) and within a week of each other, she was evaluated for two consecutive episodes of acute onset of chest pain with pulmonary edema in the setting of severe hypertension.
    [Show full text]
  • Personal Histories in Health Research ~
    Personal Histories in Health Research ~ Edited by Adam Oliver ISBN: 1 905030 11 8 Personal Histories in Health collection © The Nuffield Trust 2005 ‘Ploughing a furrow in ethics’ © Raanan Gillon and The Nuffield Trust 2005 Published by The Nuffield Trust 59 New Cavendish Street London WC1 7LP telephone 020 7631 8450 fax 020 7613 8451 email: [email protected] website: www.nuffieldtrust.org.uk charity number 209201 designed and printed by Q3 Digital Litho telephone 01509 213 456 website: www.Q3group.co.uk Contents 1 Healthy Lives: reflecting on the reflections Adam Oliver 3 2 Health inequalities: from science to policy David Blane 15 3 In sickness and in health: working in medical sociology Mike Bury 29 4 Random assignments: my route into health policy: a post-hoc rationalisation Anna Coote 47 5 Last Season’s fruit John Grimley Evans 65 6 Ploughing a furrow in ethics Raanan Gillon 85 7 The Jungle: an explorer’s experiences of health services research Walter W Holland 101 8 Confessions of a graduate nurse Alison Kitson 121 9 Confessions of an accidental policy analyst, or why I am not a health service researcher Rudolf Klein 139 10 Seeking somewhere to stop Jennie Popay 155 11 Political ideals and personal encounters Albert Weale 173 12 Discovering the QALY, or how Rachel Rosser changed my life Alan Williams 191 13 Health policy, management and gardening Robert Maxwell 207 About the authors About the authors vii David Blane is Professor of Medical Sociology at Imperial College London. He trained in medicine and sociology, and enjoys teaching medical sociology as an applied subject to large classes of trainee doctors, and as an academic discipline to smaller numbers of interested medical students.
    [Show full text]
  • Evaluation of Anemia Survey (NHANES III) Data- 9 10-28% of Patients Over 65 Years Are Anemic Mark Wurster, M.D., F.A.C.P
    Anemia - Definition • National Health and Nutrition Examination Evaluation of Anemia Survey (NHANES III) data- 9 10-28% of patients over 65 years are anemic Mark Wurster, M.D., F.A.C.P. 9 One third of these are due to iron, folate, B12 The Ohio State University deficiency alone or in combination 9 One third are due to renal disease, or other chronic inflammatory response 9 One third are due to various primary marrow disorders, malignancies or other disorders Anemia Anemia - Definition Classification Schemes • A simplified approach to anemia, • Most common hematologic disorder emphasizing information already included • Decrease from normal levels of Hgb, Hct, RBC: in the CBC: 9 FlFemales – MHb14/dlMean Hgb = 14 g/dl; -2SD = 12 g /dl • Mean Cellular Volume (MCV) 9 Males – Mean Hgb = 15.5 g/dl; -2SD = 13.5 g/dl • Red Cell Distribution Width (RDW) • Caveat – Anemia is a syndrome, not a disease. • Retic count An abnormal Hgb or Hct should ALWAYS be investigated if confirmed on repeat testing. 1 Anemia Anemia Classification Schemes Classification Schemes • Mean Cellular Volume (MCV) • Red blood cell Distribution Width (RDW) • Decreased MCV (microcytic); < 80 fL 9 A numerical expression of • Normal MCV (normocytic); 80 – 99 fL anisocytosis, or variation in RBC size • Increased MCV (macrocytic); > 100 fL Anemia Anemia Classification Schemes Classification Schemes • Red blood cell Distribution Width (RDW) 9 Normal RDW - representing a uniform population • Red blood cell Distribution Width (RDW) of RBCs with respect to size (actually the standard deviation of red blood cell volume divided by the mean volume) 9 Normal; < or = to app.
    [Show full text]
  • NO-1886 Decreases Ectopic Lipid Deposition and Protects Pancreatic  Cells in Diet-Induced Diabetic Swine
    399 NO-1886 decreases ectopic lipid deposition and protects pancreatic cells in diet-induced diabetic swine W Yin*,1,2,5, D Liao*,1,2, M Kusunoki6,SXi1, K Tsutsumi3, Z Wang1, X Lian1, T Koike4, J Fan4, Y Yang5 and C Tang5 1Department of Biochemistry and Biotechnology, Nanhua University School of Life Sciences and Technology, Hengyang, Hunan 421001, China 2Department of Pathophysiology, Central South University Xiangya Medical College, Changsha, Hunan, China 3Research and Development, Otsuka Pharmaceutical Factory Inc., Tokushima, Japan 4Laboratory of Cardiovascular Disease, Department of Pathology, Institute of Basic Medical Sciences, University of Tsukuba, Tsukuba 305-8575, Japan 5Institute of Cardiovascular Research, Nanhua University Medical School, Hengyang, Hunan 421001, China 6Department of Internal Medicine, Faculty of Medicine, Aichi Medical University, Nagakute-cho, Aichigunte, Aichi 480-11, Japan (Requests for offprints should be addressed to W Yin, Department of Biochemistry and Molecular Biology, Nanhua University School of Life Sciences and Technology, Hengyang, Hunan 421001, China; Email: [email protected]) *W Yin and D Liao contributed equally to this paper Abstract The synthetic compound NO-1886 (ibrolipim) is a lipo- skeletal muscle, liver and pancreas, and also caused pan- protein lipase activator that has been proven to be highly creatic cell damage. However, supplementing 1% NO- effective in lowering plasma triglycerides. Recently, we 1886 (200 mg/kg per day) into the high-fat/high-sucrose found that NO-1886 also reduced plasma free fatty acids diet decreased ectopic lipid deposition, improved insulin and glucose in high-fat/high-sucrose diet-induced dia- resistance, and alleviated the cell damage. These results betic rabbits.
    [Show full text]
  • Assessment Report
    17 September 2020 EMA/522604/2020 Corr.1 Committee for Medicinal Products for Human Use (CHMP) Assessment report Velphoro Common name: sucroferric oxyhydroxide Procedure No. EMEA/H/C/002705/X/0020/G Note Assessment report as adopted by the CHMP with all information of a commercially confidential nature deleted. Official address Domenico Scarlattilaan 6 ● 1083 HS Amsterdam ● The Netherlands Address for visits and deliveries Refer to www.ema.europa.eu/how-to-find-us An agency of the European Union Send us a question Go to www.ema.europa.eu/contact Telephone +31 (0)88 781 6000 © European Medicines Agency, 2021. Reproduction is authorised provided the source is acknowledged. Table of contents 1. Background information on the procedure .............................................. 6 1.1. Submission of the dossier ...................................................................................... 6 1.2. Steps taken for the assessment of the product ......................................................... 7 2. Scientific discussion ................................................................................ 8 2.1. Problem statement ............................................................................................... 8 2.1.1. Disease or condition ........................................................................................... 8 2.1.2. Epidemiology and risk factors, screening tools/prevention ...................................... 8 2.1.3. Biologic features ...............................................................................................
    [Show full text]
  • Study Guide Medical Terminology by Thea Liza Batan About the Author
    Study Guide Medical Terminology By Thea Liza Batan About the Author Thea Liza Batan earned a Master of Science in Nursing Administration in 2007 from Xavier University in Cincinnati, Ohio. She has worked as a staff nurse, nurse instructor, and level department head. She currently works as a simulation coordinator and a free- lance writer specializing in nursing and healthcare. All terms mentioned in this text that are known to be trademarks or service marks have been appropriately capitalized. Use of a term in this text shouldn’t be regarded as affecting the validity of any trademark or service mark. Copyright © 2017 by Penn Foster, Inc. All rights reserved. No part of the material protected by this copyright may be reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, or by any information storage and retrieval system, without permission in writing from the copyright owner. Requests for permission to make copies of any part of the work should be mailed to Copyright Permissions, Penn Foster, 925 Oak Street, Scranton, Pennsylvania 18515. Printed in the United States of America CONTENTS INSTRUCTIONS 1 READING ASSIGNMENTS 3 LESSON 1: THE FUNDAMENTALS OF MEDICAL TERMINOLOGY 5 LESSON 2: DIAGNOSIS, INTERVENTION, AND HUMAN BODY TERMS 28 LESSON 3: MUSCULOSKELETAL, CIRCULATORY, AND RESPIRATORY SYSTEM TERMS 44 LESSON 4: DIGESTIVE, URINARY, AND REPRODUCTIVE SYSTEM TERMS 69 LESSON 5: INTEGUMENTARY, NERVOUS, AND ENDOCRINE S YSTEM TERMS 96 SELF-CHECK ANSWERS 134 © PENN FOSTER, INC. 2017 MEDICAL TERMINOLOGY PAGE III Contents INSTRUCTIONS INTRODUCTION Welcome to your course on medical terminology. You’re taking this course because you’re most likely interested in pursuing a health and science career, which entails ­proficiency­in­communicating­with­healthcare­professionals­such­as­physicians,­nurses,­ or dentists.
    [Show full text]
  • Study Protocol C31002 Protocol a M End Ment 2
    Title: Phase 1 Study to Evaluate the Effect of MLN0128 on the QTc Interval in Patients With Advanced Solid Tumors NCT Number: NCT02197572 Protocol Approve Date: 28 November 2017 Certain information within this protocol has been redacted (ie, specific content is masked irreversibly from view with a black/blue bar) to protect either personally identifiable information (PPD) or company confidential information (CCI). This may include, but is not limited to, redaction of the following: Named persons or organizations associated with the study. Proprietary information, such as scales or coding systems, which are considered confidential information under prior agreements with license holder. Other information as needed to protect confidentiality of Takeda or partners, personal information, or to otherwise protect the integrity of the clinical study. M L N 0 1 2 8 Clinical Study Protocol C31002 Protocol A m end ment 2 CLINICAL STUDY PROTOCOL C31002 PROTOCOL A MEND MENT 2 M L N 0 1 2 8 A P h as e 1 St u d y t o E v al u at e t h e Eff e ct of M L N 0 1 2 8 o n t h e Q T c I nt er v al i n P ati e nts Wit h Advanced Solid Tu mors Protocol Nu mber: C 3 1 0 0 2 Indication: Ad vanced solid tu mors P h as e: 1 S p o ns o r: Mill e n ni u m P h ar m a c e uti c als, I n c. Eudra CT Nu mber: N ot a p pli c a bl e Therapeutic Area: O n c o l og y Protocol History Ori gi n al 29 October 2013 Protocol A mend ment 1 26 June 2014 Protocol A mend ment 2 28 Nove mber 2017 Mill e n ni u m P h ar m a c e uti c als, I n c.
    [Show full text]