Kidney Disease in the Cardiac Catheterization Laboratory : A Practical Approach [1st ed.] 9783030454135, 9783030454142

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Kidney Disease in the Cardiac Catheterization Laboratory A Practical Approach Janani Rangaswami Edgar V. Lerma Peter A. McCullough Editors

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Kidney Disease in the Cardiac Catheterization Laboratory

Janani Rangaswami  •  Edgar V. Lerma Peter A. McCullough Editors

Kidney Disease in the Cardiac Catheterization Laboratory A Practical Approach

Editors Janani Rangaswami Einstein Medical Center/Thomas Jefferson University Department of Medicine/Nephrology Philadelphia, PA USA

Edgar V. Lerma UIC/Advocate Christ Medical Center Department of Medicine Chicago, Il USA

Peter A. McCullough Baylor University Medical Center, Baylor Heart and Vascular Hospital Department of Internal Medicine, Texas A & M College of Medicine, Division of Cardiology Dallas, TX USA

ISBN 978-3-030-45413-5    ISBN 978-3-030-45414-2 (eBook) https://doi.org/10.1007/978-3-030-45414-2 © Springer Nature Switzerland AG 2020 This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed. The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. The publisher, the authors, and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the editors give a warranty, expressed or implied, with respect to the material contained herein or for any errors or omissions that may have been made. The publisher remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. This Springer imprint is published by the registered company Springer Nature Switzerland AG The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland

To my family, mentors and patients – thanks for your support and guidance each step of the way. ­—Janani Rangaswami. To all my mentors, and friends, at the University of Santo Tomas Faculty of Medicine and Surgery in Manila, Philippines, and Northwestern University Feinberg School of Medicine in Chicago, IL, who have, in one way or another, influenced and guided me to become the physician that I am... To all the medical students, interns, and residents at Advocate Christ Medical Center and Macneal Hospital, whom I have taught or learned from, especially those who eventually decided to pursue Nephrology as a career... To my parents and my brothers, without whose unwavering love and support through the good and bad times, I would not have persevered and reached my goals in life… Most especially, to my two lovely and precious daughters Anastasia Zofia and Isabella Ann, whose smiles and laughter constantly provide me unparalleled joy and happiness; and my very loving and understanding wife Michelle, who has always been supportive of my endeavors both personally and professionally, and who sacrificed a lot of time and exhibited unwavering patience as I devoted a significant amount of time and effort to this project. Truly, they provide me with motivation and inspiration. —Edgar V. Lerma. This work is dedicated to the steadfastness and providence of my wife Maha, and to the energy and excitement of our young professional children Haley and Sean. —Peter A. McCullough.

Foreword

The pathophysiological interactions between the heart and kidneys represent today an interesting and cutting-edge topic of discussion among physicians and students. Since the first description of the new definition/classification of the cardio-renal syndrome, an increasing number of publications and dedicated meetings have been noted worldwide. This textbook, edited by Janani Rangaswami, Edgar V. Lerma, and Peter A. McCullough, is further demonstration of the growing interest in this discipline. The book represents an answer to a medical need and to an educational demand that has become evident in recent years. The table of content well describes the pathway from basic research and physiology, to the pathophysiological foundation of combined cardiovascular and kidney disease, to finally reach the basis, modality, and the nuances of complex cardiac catheterization laboratory procedures in patients with kidney disease. The innovative aspect of the book is the multidisciplinary approach to a patient that may or will encounter mixed cardiorenal disease. The increased use of complex cardiovascular procedures in patients with kidney disease has led to new types of complications that must be dealt with by a combined task force made of specialists of different disciplines. The last part of the book well describes the utility of the cardio-nephrology collaborative effort in the cardiac catheterization laboratory. Years ago, I advocated the advent of a critical care nephrology multidisciplinary team. Recently we applied the concept of the nephrology rapid-response team in case of early prevention/detection of acute kidney injury. Other experiences use Artificial Intelligence as a basis for a multidisciplinary approach to the critically ill patient. This book fills a gap in the area of catheterization laboratory where cardiologists and nephrologists should be working together to avoid major complications and mitigate possible detrimental effects of the numerous procedures, often performed in an elderly as well as comorbid population where the susceptibility to kidney insults are at the highest levels.

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Foreword

I must, therefore, congratulate the authors and editors for their valuable contributions to this textbook. I expect this book to become a reference for practicing physicians and specialists as well as for students and fellows interested in expanding their knowledge in this complex, yet exciting area of medicine. Claudio Ronco Padua, Italy Vicenza, Italy

Preface

The link between heart and kidney disease is of historical importance in medicine, probably first reported in the literature in 1836 by Sir Richard Bright, widely regarded as the father of modern nephrology. From that initial notation to the current times, we are faced with an epidemic of cardiovascular and kidney disease stemming from the common soil of vascular risk factors such as hypertension, diabetes, and obesity in an aging population. In parallel to this increasing burden of cardiorenal disease, there have been major advances in the field of interventional cardiology with the advent of cutting-edge technologies, minimally invasive operator techniques, and the ability to modify the course of formerly inoperable and highly complex coronary, peripheral vascular, and valvular procedures. In this context, it is imperative for the interventional cardiologist as well as the nephrologist to understand the nuances of the interface between cardiovascular and kidney disease in detail, and to deliver optimal interventional cardiac and vascular therapies in patients with dual organ disease. Patients with chronic kidney disease have traditionally been excluded from high-quality randomized trials in cardiovascular medicine and routinely get sub-optimally treated or excluded from potentially beneficial interventions, despite the well-known disproportionately high burden of cardiovascular disease in this population. Fortunately for these vulnerable patients, the recent advances in interventional cardiology have opened new avenues of therapy for patients with advanced chronic kidney disease in the cardiac catheterization laboratory, working to reduce the therapeutic nihilism that is ingrained in clinical practice. This textbook assembles the collective expertise, experience, and viewpoints of international leaders in the field of interventional cardiology and nephrology to summarize the complex interface between these two specialties in the setting of the cardiac catheterization laboratory. Authors have contributed to this field with new pioneering interventional strategies and techniques, trial leadership, and patient advocacy that allow the reader to benefit from a comprehensive and balanced view of this field and apply those principles in their clinical practice. This textbook will be immensely useful to practicing interventional cardiologists, nephrologists, trainee physicians, as well as advanced care practitioners in the fields of cardiology and nephrology as a single authoritative source for understanding the interplay ix

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Preface

between cardiovascular and kidney disease in the cardiac catheterization laboratory. We hope that the interdisciplinary cross-talk in this textbook will serve as a catalyst for future multidisciplinary cardiorenal care models and research collaborations, which would be the best use of the collective expertise of the authors that is summarized in this volume. We wish to thank each author and writing group for their valuable input and time as contribution to this project. We also thank Greg Sutorius and Andy Kwan of Springer International for their leadership in making this textbook a reality. This textbook would not have been possible without the diligence and hard work of the developmental editor Michele Aiello, whom we would like to thank on behalf of all the authors and the editorial team. We hope to see this assemblage be part of the growth in this dual specialty field and help with the delivery of the very best clinical practice to patients with the need for cardiovascular interventions in the setting of chronic kidney disease, to reduce complications, morbidity, and mortality in this fragile population. Philadelphia, PA, USA  Janani Rangaswami, Chicago, IL, USA  Edgar V. Lerma, Dallas, TX, USA Peter A. McCullough,

Contents

Part I Atherosclerotic Cardiovascular Disease Burden in Chronic Kidney Disease 1 The Burden of Coronary Artery Disease in Chronic Kidney Disease������������������������������������������������������������������������   3 Sylvia Biso and Amer K. Ardati 2 Non-invasive Testing in the Diagnosis of Ischemic Heart Disease in CKD: Scope, Pitfalls, and Future Directions��������������  19 Michelle D. Carlson and Gautam R. Shroff 3 Peripheral Arterial Disease in Chronic Kidney Disease: Disease Burden, Outcomes, and Interventional Strategies��������������������  37 Harsha S. Nagarajarao, Chandra Ojha, Archana Kedar, and Debabrata Mukherjee 4 Cardiovascular Impact of Atherosclerotic Renovascular Disease��������������������������������������������������������������������������������  69 Gates B. Colbert and Harold M. Szerlip Part II Therapeutic Considerations with Revascularization in Chronic Kidney Disease 5 Therapeutic Considerations with Revascularization in Chronic Kidney Disease: Radial Versus Femoral Arterial Access����������������������������������������������������������������������������  85 Giuseppe Andò, Felice Gragnano, Paolo Calabrò, and Marco Valgimigli 6 Antiplatelet Agent Choice and Platelet Function Testing in CKD�������������������������������������������������������������������������� 103 Udaya S. Tantry, Amit Rout, Rahul Chaudhary, and Paul A. Gurbel

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7 Choice of Stents and Clinical Outcomes in Patients with Chronic Kidney Disease�������������������������������������������������������������������� 119 Shawn X. Li and Usman Baber 8 Revascularization Strategies in Chronic Kidney Disease: Percutaneous Coronary Interventions Versus Coronary Artery Bypass Graft���������������������������������������������������������������������������������� 133 Stephani C. Wang, Elizabeth L. Nichols, Michael E. Farkouh, and Mandeep S. Sidhu 9 Approach to Revascularization in the Potential Kidney Transplant Recipient�������������������������������������������������������������������� 145 Gustavo Soares Guandalini and Sripal Bangalore 10 Nephrology Consultative Approach and Risk Stratification Prior to Revascularization in Chronic Kidney Disease�������������������������� 165 Roy O. Mathew, Valerian Fernandes, and Sripal Bangalore Part III Acute Kidney Injury in the Catheterization Laboratory: Part I 11 Contrast-Induced Acute Kidney Injury: Epidemiology, Risk Stratification, and Prognosis������������������������������������������������������������ 183 Jehan Zahid Bahrainwala, Amanda K. Leonberg-Yoo, and Michael R. Rudnick 12 Pathophysiology of Contrast Induced Acute Kidney Injury������������������ 209 Hector M. Madariaga, Tapati Stalam, Ami M. Patel, and Beje Thomas 13 Prevention of Contrast-Induced AKI: Summary of Volume Optimization Strategies �������������������������������������������������������������� 225 Jaspreet S. Arora, Brandon Kai, and Somjot S. Brar 14 Operator and Intraprocedural Strategies to Reduce Contrast-Induced Acute Kidney Injury�������������������������������������������������� 235 Sanjog Kalra, Ziad Anwar Ali, Dimitri Karmpaliotis, Ajay J. Kirtane, and Jeffrey W. Moses Part IV Acute Kidney Injury in the Catheterization Laboratory: Part II 15 Effect of Acute Mechanical Circulatory Support on Kidney Function����������������������������������������������������������������������������������� 259 Shiva K. Annamalai, Lena E. Jorde, Carlos D. Davila, and Navin K. Kapur

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16 Renal Athero-embolic Disease: An Underdiagnosed Entity in Cardiac Catheterization������������������������������������������������������������ 275 Shweta Punj and Jennifer Tuazon 17 Acute Kidney Injury After Transcatheter Aortic Valve Replacement ������������������������������������������������������������������������������������ 285 Ricardo J. Cigarroa and Sammy Elmariah 18 Impact of Kidney Disease on Catheter-­Based Mitral Valve Interventions���������������������������������������������������������������������������������������������� 299 Nikoloz Koshkelashvili, Jose F. Condado, and Vasilis Babaliaros 19 Contrast-Induced Nephropathy After Peripheral Vascular Intervention������������������������������������������������������������������������������������������������ 313 Michael James Ewing, Angela L. Gucwa, and John F. Eidt Part V Catheter Based Reno-Vascular Interventions 20 Renal Artery Stenosis: State of the Art in the Diagnosis and Management���������������������������������������������������������������������������������������� 337 Sanjum S. Sethi and Sahil A. Parikh 21 Renal Denervation: Physiology, Scope, and Current Evidence ������������ 349 Márcio Galindo Kiuchi and Markus P. Schlaich 22 Forced Matched Diuresis: Role in Renal Protection in the Cardiac Catheterization Laboratory�������������������������������������������� 367 Richard Solomon and Nina Narasimhadevara Part VI Role of Hemodynamic Evaluation in the Catheterization Laboratory 23 Traditional and Novel Invasive Hemodynamic Indices in the Evaluation of Congestive Heart Failure in Cardiorenal Syndrome�������������������������������������������������������������������������� 379 Mahek Shah, Brijesh Patel, Sahil Agrawal, and Ulrich P. Jorde 24 Pulmonary Hypertension in Chronic Kidney Disease���������������������������� 397 Salvatore P. Costa Part VII Utility of the Cardio-Nephrology Collaborative in the Cardiac Catheterization Laboratory 25 The Economic Impact of Kidney Disease in the Cardiac Catheterization Laboratory���������������������������������������������������������������������� 409 Justin M. Cloutier, David W. Allen, and Paul Komenda

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26 Biomarkers of Acute Kidney Injury and Scope of Utilization in the Cardiac Catheterization Laboratory�������������������������������������������� 429 Ladan Golestaneh and Abby Miriam Basalely 27 A Call to Action to Develop Integrated Curricula in Cardiorenal Medicine���������������������������������������������������������������������������� 449 Claudio Ronco, Federico Ronco, and Peter A. McCullough Index������������������������������������������������������������������������������������������������������������������  463

Contributors

Sahil  Agrawal, MD  Department of Cardiology, Saint Francis Hospital, Tulsa, OK, USA Ziad  Anwar  Ali, MD, DPhil  Cardio-Renal Services, New York Presbyterian Hospital/Columbia University Medical Center, Center for Interventional Vascular Therapy, New York, NY, USA David W. Allen, MD, FRCPC  Department of Medicine, Section of Cardiology, Max Rady College of Medicine, Y3543 Bergen Cardiac Care Centre, University of Manitoba, St. Boniface Hospital, Winnipeg, MB, Canada Giuseppe  Andò, MD, PhD  Azienda Ospedaliera Universitaria Policlinico “Gaetano Martino”, Department of Clinical and Experimental Medicine, University of Messina, Messina, Italy Shiva K. Annamalai, MD  Department of Cardiovascular Disease, Tufts Medical Center, Boston, MA, USA Amer  K.  Ardati, MD MSc  University of Illinois at Chicago, Department of Internal Medicine, Chicago, IL, USA Jaspreet  S.  Arora, MD  Department of Interventional Cardiology, Kaiser Permanente Los Angeles Medical Center, Cardiac Catheterization & Electrophysiology Labs, Los Angeles, CA, USA Vasilis  Babaliaros, MD  Emory University School of Medicine, Department of Cardiology, Atlanta, GA, USA Usman Baber, MD, MS  Icahn School of Medicine at Mount Sinai, Cardiovascular Institute, New York, NY, USA Jehan  Zahid  Bahrainwala, Philadelphia, PA, USA

MD  Penn

Presbyterian

Medical

Center,

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Contributors

Sripal Bangalore, MD, MHA  Department of Medicine, Division of Cardiology New York University Grossman School of Medicine, New York, NY, USA Complex Coronary Interventions, Bellevue, Leon H.  Charney Division of Cardiology, New York University School of Medicine, New York, NY, USA Abby Miriam Basalely, MD  The Children’s Hospital at Montefiore, Nephrology Division, Department of Pediatric Nephrology, Bronx, NY, USA Sylvia  Biso, MD  University of Illinois at Chicago, Department of Internal Medicine, Chicago, IL, USA Somjot  S.  Brar, MD, MPH  Kaiser Permanente Los Angeles Medical Center, Cardiac Catheterization & Electrophysiology Labs, Regional Department of Cardiac Catheterization, Los Angeles, CA, USA Paolo Calabrò, MD, PhD  Division of Clinical Cardiology, A.O.R.N. Sant’Anna e San Sebastiano, Caserta, Italy Department of Cardiothoracic and Respiratory Sciences, University of Campania “Luigi Vanvitelli”, Naples, Italy Michelle  D.  Carlson, Minneapolis, MN, USA

MD  Hennepin

Healthcare,

Cardiology

Division,

Rahul  Chaudhary, MD, FACP  Division of Hospital Internal Medicine, Department of Internal Medicine, Mayo Clinic, Rochester, MN, USA Ricardo  J.  Cigarroa, MD  Cardiology Division, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA Justin M. Cloutier, MD, FRCPC  University of Manitoba – St. Boniface Hospital, Department of Cardiology, Y3039 Bergen Cardiac Care Centre, Winnipeg, MB, Canada Gates  B.  Colbert, MD  Baylor University Medical Center, Internal Medicine, Dallas, Department of Nephrology, Dallas, TX, USA Jose F. Condado, MD, MS  Emory University School of Medicine, Department of Cardiology, Atlanta, GA, USA Salvatore  P.  Costa  Echocardiography Lab, Department of Cardiovascular Medicine, Dartmouth Hitchcock Medical Center, Lebanon, NH, USA Carlos  D.  Davila, MD  Tufts Medical Center, Department of Cardiovascular Disease, Boston, MA, USA John F. Eidt, MD  Baylor Scott & White Heart and Vascular Hospital, and Texas A&M College of Medicine, Dallas, TX, USA Sammy  Elmariah, MD, MPH  Cardiology Division, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA

Contributors

xvii

Michael James Ewing, MD, MS  Baylor University Medical Center, Department of Surgery, Dallas, TX, USA Michael  E.  Farkouh, MD, MSc, FRCPC, FACC, FAHA  Department of Medicine, University of Toronto, Toronto General Hospital, Toronto, ON, Canada Valerian Fernandes, MD, MRCP, FACC  Department of Medicine, Division of Cardiology, Medical University of South Carolina (MUSC) and Ralph H. Johnson VA Medical Center, Charleston, SC, USA Ladan Golestaneh, MD, MS  Albert Einstein College of Medicine, Bronx, NY, USA Felice  Gragnano, MD  Division of Clinical Cardiology, A.O.R.N.  Sant’Anna e San Sebastiano, Caserta, Italy Department of Cardiothoracic and Respiratory Sciences, University of Campania “Luigi Vanvitelli”, Naples, Italy Gustavo  Soares  Guandalini, MD  Cardiovascular Diseases Fellow, New  York University School of Medicine, Leon H.  Charney Division of Cardiology, New York, NY, USA Angela  L.  Gucwa, MD  Doctors Community Medical Center, Luminis Health, Department of Surgery, Lanham, MD, USA Paul A. Gurbel, MD  Sinai Center for Thrombosis Research and Drug Development, Sinai Hospital of Baltimore, Baltimore, MD, USA Lena E. Jorde, BA  Tufts Medical Center, Department of Cardiovascular Disease, Boston, MA, USA Ulrich P. Jorde, MD  Department of Cardiology, Montefiore Medical Center, The Bronx, NY, United States of America Brandon  Kai, MD  Kaiser Permanente Los Angeles Medical Center, Cardiac Catheterization & Electrophysiology Labs, Los Angeles, CA, USA Sanjog  Kalra, MD, Philadelphia, PA, USA

MSc  Einstein

Medical

Center

Philadelphia,

Navin  K.  Kapur, MD  Tufts Medical Center, Department of Cardiovascular Disease, Boston, MA, USA Dimitri  Karmpaliotis, MD, FACC, PhD  Cardiovascular Research Foundation, New York, NY, USA NYPH/Columbia University Irving Medical Center, Center For Interventional Vascular Therapy, New York, NY, USA Archana Kedar, MBBS  Cardiovascular Research Foundation, New York, NY, USA NYPH/Columbia University Irving Medical Center, Center For Interventional Vascular Therapy, New York, NY, USA

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Contributors

Ajay J. Kirtane, MD, SM, FACC, FSCAI  Cardiovascular Research Foundation, New York, NY, USA NYPH/Columbia University Irving Medical Center, Center For Interventional Vascular Therapy, New York, NY, USA Márcio Galindo Kiuchi, MD, MSc, PhD  Dobney Hypertension Centre, School of Medicine - Royal Perth Hospital Unit, University of Western Australia, Perth, WA, Australia Paul  Komenda, MD, FRCPC, MHA  University of Manitoba, Research and Home Hemodialysis, Seven Oaks Hospital, Chronic Disease Innovation Centre, Winnipeg, MB, Canada Nikoloz Koshkelashvili, MD  Emory University School of Medicine, Department of Cardiology, Atlanta, GA, USA Amanda  K.  Leonberg-Yoo, MD, MS  Renal Electrolyte and Hypertension Division, Penn Presbyterian Medical Center, Philadelphia, PA, USA Shawn X. Li  Massachusetts General Hospital, New York Mount Sinai School of Medicine, Boston, MA, USA Hector  M.  Madariaga, MD  Good Samaritan Medical Center, Department of Medicine, Brockton, MA, USA Roy O. Mathew, MD  Department of Medicine, Division of Nephrology, University of South Carolina School of Medicine, Columbia VA Health Care System, Columbia, SC, USA Peter  A.  McCullough, MD, MPH  Baylor University Medical Center, Baylor Heart and Vascular Hospital, Department of Internal Medicine, Texas A & M College of Medicine, Division of Cardiology, Dallas, TX, USA Jeffrey W. Moses, MD  Cardiovascular Research Foundation, New York, NY, USA NYPH/Columbia University Irving Medical Center, Center For Interventional Vascular Therapy, New York, NY, USA Debabrata Mukherjee, MD, MS  Division of Cardiology, Department of Internal Medicine, Texas Tech University Health Sciences Center, El Paso, TX, USA Harsha  S.  Nagarajarao, MD, FSCAI  Division of Cardiology, Department of Internal Medicine, Texas Tech University Health Sciences Center, El Paso, TX, USA Nina  Narasimhadevara, MD  Division of Nephrology, University of Vermont Medical Center, Department of Nephrology, Burlington, VT, USA Elizabeth  L.  Nichols, PhD, MS  The Dartmouth Institute of Health Policy and Clinical Practice, Lebanon, NH, USA

Contributors

xix

Chandra Ojha, MD, MRCP, FACC, FSCAI  Division of Cardiology, Department of Internal Medicine, Texas Tech University Health Sciences Center, El Paso, TX, USA Sahil A. Parikh, MD  Division of Cardiology, Center for Interventional Vascular Therapy, Columbia University Irving Medical Center, New  York Presbyterian Hospital, New York, NY, USA Ami M. Patel, MD  University of Maryland School of Medicine, Department of Medicine, Division of Nephrology, Baltimore, MD, USA Brijesh Patel, DO  Department of Cardiology, West Virginia University Heart and Vascular Institute, Morgantown, WV, United States of America Shweta  Punj, MD  Northwestern University Feinberg School of Medicine, Division of Nephrology and Hypertension, Chicago, IL, USA Claudio Ronco, MD  Nephrology, University of Padova, Padua, Italy International Renal Research Institute of Vicenza, San Bortolo Hospital, Vicenza, Italy Department of Medicine, University of Padova, Padua, Italy Federico Ronco, MD  Ospedale Dell’Angelo – AULSS3 Serenissima, Interventional Cardiology, Department of Cardiac Thoracic and Vascular Sciences, Mestre  Venezia, Italy Amit Rout, MD  Sinai Center for Thrombosis Research and Drug Development, Sinai Hospital of Baltimore, Baltimore, MD, USA Michael  R.  Rudnick, MD, FASN, FACP  Perelman School of Medicine of the University of Pennsylvania, Department of Nephrology, Penn Presbyterian Medical Center, Philadelphia, PA, USA Markus P. Schlaich, MD, PhD  Dobney Hypertension Centre, School of Medicine Royal Perth Hospital Unit, University of Western Australia, Perth, WA, Australia Departments of Cardiology and Nephrology, Royal Perth Hospital, Perth, WA, Australia Neurovascular Hypertension & Kidney Disease Laboratory and Human Neurotransmitter Laboratory, Baker IDI Heart and Diabetes Institute, Melbourne, VIC, Australia Sanjum  S.  Sethi, MD, MPH  Division of Cardiology, Center for Interventional Vascular Therapy, Columbia University Irving Medical Center, New York Presbyterian Hospital, New York, NY, USA Mahek  Shah, MD  Department of Cardiology, Thomas Jefferson University Hospital, Philadelphia, PA, USA

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Contributors

Gautam R. Shroff, MBBS, FACC  Heart and Vascular Service Line, Division of Cardiology, University of Minnesota Medical School, Hennepin Healthcare and University of Minnesota, Department of Internal Medicine, Minneapolis, MN, USA Mandeep S. Sidhu, MD  Department of Medicine, Division of Cardiology, Albany Medical College and Albany Medical Center, Albany, NY, USA Richard  Solomon, MD  University of Vermont Medical Center, Department of Nephrology, Larner College of Medicine, University of Vermont, Division of Nephrology, Burlington, VT, USA Tapati  Stalam, MD  University of Maryland Medical Center, Department of Medicine, Baltimore, MD, USA Harold  M.  Szerlip, MD  Baylor University Medical Center, Dallas, Internal Medicine, Division of Nephrology, Dallas, TX, USA Udaya  S.  Tantry, PhD  Sinai Center for Thrombosis Research and Drug Development, Sinai Hospital of Baltimore, Baltimore, MD, USA Beje Thomas, MD  MedStar Georgetown University Hospital, Washington, DC, USA Jennifer  Tuazon, MD  Northwestern University Feinberg School of Medicine, Division of Nephrology and Hypertension, Chicago, IL, USA Marco Valgimigli, MD, PhD  Department of Cardiology, Bern University Hospital, University of Bern, Bern, Switzerland Stephani  C.  Wang, MD  Department of Medicine, Albany Medical Center, Albany, NY, USA

Part I

Atherosclerotic Cardiovascular Disease Burden in Chronic Kidney Disease

Chapter 1

The Burden of Coronary Artery Disease in Chronic Kidney Disease Sylvia Biso and Amer K. Ardati

Introduction Cardiovascular disease (CVD) is the leading cause of death in the general US population and in those with chronic kidney disease (CKD) [1, 2]. In patients with CKD, cardiovascular death is more common than progression to end-stage renal disease [3]. Cardiovascular death accounts for 40% of total mortality and among patients on dialysis with acute myocardial infarction accounts for a quarter of all CVD deaths [4]. CKD is an established independent risk factor for CVD and is widely considered a coronary artery disease (CAD) equivalent [5, 6]. Traditional risk factors are more prevalent in CKD patients and are more challenging to control [7]. Nontraditional risk factors like inflammation, oxidative stress, and coronary artery calcification also have profound adverse associations in patients with CKD [8]. Cardiovascular outcomes improve after kidney transplantation; however, posttransplant risk for adverse cardiac events remains higher compared to the general population [9]. This chapter reviews trends in the prevalence of CVD in CKD, contributing risk factors, and pathophysiology. We highlight studies and guidelines for prevention of CVD in the CKD population.

S. Biso · A. K. Ardati (*) University of Illinois at Chicago, Department of Internal Medicine, Chicago, IL, USA e-mail: [email protected] © Springer Nature Switzerland AG 2020 J. Rangaswami et al. (eds.), Kidney Disease in the Cardiac Catheterization Laboratory, https://doi.org/10.1007/978-3-030-45414-2_1

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4

S. Biso and A. K. Ardati

Epidemiology Chronic Kidney Disease: A Major Health Burden Chronic kidney disease (CKD) continues to be a major global health problem, with the prevalence of CKD in the USA in 2011–2014 being around 14% [1]. Roughly 7.1% adults aged 20 and older are afflicted with CKD stages 1–2 and 6.4% with CKD stages 3–5. These translate to 16 million and 14 million US adults who have CKD stages 1–2 and 3–5, respectively [10]. According to the United States Renal Data System in 2015, there were 703,243 cases of end-stage kidney disease (ESKD) and 124,114 of these were newly-reported [11]. Between 1990 and 2014, the Centers of Disease Control and Prevention – CKD surveillance program recorded that ESKD cases had more than doubled [12]. There is also a high cost burden to the healthcare system. In 2015, total Medicare expenditure for CKD and ESKD patients was almost $100 billion dollars with one out of every five Medicare dollars being spent on patients with CKD [11].

 revalence of Cardiovascular Disease in Patients with Chronic P Kidney Disease Cardiovascular disease (CVD) is the most common cause of mortality in patients with CKD (see Fig. 1.1) [2]. Compared to the 31.9% prevalence of CVD in patients

Rate (number per 1000 patient-years)

Cardiovascular deaths by CKD stage and albuminuria 45

41

40 35 30 24

25 20 15 10 5

24 19

13

11

10

6 5

0 Normal eGFR 15–59

Microalbuminuria eGFR 60–89

Macroalbuminuria eGFR 90+

Fig. 1.1  The incidence of cardiovascular mortality from 1988 to 2000 among participants with normal renal function, microalbuminuria, and macroalbuminuria. Albuminuria and kidney function correlate with cardiovascular mortality, although albuminuria appears to be more strongly associated. (Adapted from Centers for Disease Control and Prevention. Chronic Kidney Disease Surveillance System—United States website: http://www.cdc.gov/ckd)

1  The Burden of Coronary Artery Disease in Chronic Kidney Disease

5

without CKD, CVD occurs in 65.8% of patients with CKD aged 66 and older [1]. Younger patients with ESKD also exhibit a disproportionate burden of CVD [11]. A study by Foster et al. determined that 13% of patients with CKD stages 1–2 and 29.6% of patients with CKD stages 3–5 experience CVD [10]. The most common CVD conditions in patients with ESKD are coronary artery disease (CAD) and heart failure (HF) both of which independently impact survival [11].

 hronic Kidney Disease as a Risk Factor and Predictor C of Coronary Artery Disease Chronic kidney disease is an established risk factor for the occurrence of CAD [6]. Even mildly reduced estimated glomerular filtration rate (eGFR) (mean eGFR 78.5 ± 12.2 ml/min/1.73 m2) is associated with increased risk for CAD [13]. Cho et al. assessed 4297 subjects with coronary CT angiography and determined that early and asymptomatic CKD is already an independent risk factor for coronary atherosclerosis [14]. Navaneethan, Schold, and Arrigain further observed that each 5 ml/min/1.73 m2 decline in eGFR is associated with higher risk of mortality secondary to CVD [2]. In addition to patients with CKD having high prevalence for significant CAD [15], Gradaus et al. reported rapid progression for coronary atherosclerosis in dialysis patients. Comparing coronary angiography at baseline and after a mean interval of 30 months, 50% of dialysis patients developed hemodynamically significant new stenoses of >50% of the luminal diameter [16]. CKD has also been shown to be an independent predictor of cardiovascular events [17]. The 1-year risk of hospitalizations due to acute coronary syndrome (ACS) significantly increases as eGFR levels decline. The 1-year ACS risk is 0.3%, 0.7%, 1.2%, 2.2%, and 1.6% for advancing CKD stages with eGFR 60–89, 45–59, 30–44, 15–29, and 60% in patients with CKD in epidemiological surveys [30]. In a study by Foster et al., hypertension is present in only 31.7% without CKD, compared to 57.8% and 85.6% in patients with CKD stages 1–2 and 3–5, respectively [10]. The presence of HTN in patients with CKD amplifies the risk of patients

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for cardiovascular morbidity and mortality, particularly when patients also have proteinuria [31]. In the Hypertension Detection and Follow-up Program, patients with serum creatinine of 1.7 mg/dl or higher had a three-fold increased risk in 8-year mortality compared to normal participants [32].

Smoking Smoking has been significantly associated with elevated risk for end-stage kidney disease in the Multiple Risk Factor Intervention (MRFIT) trial [33]. The Prevention of Renal and Vascular Endstage Disease (PREVEND) trial found that smoking correlated to albuminuria and abnormal kidney function in non-diabetic patients (Piento-Siesma) [34]. Even after adjusting for confounding factors, Cardiovascular Health Study Cohort revealed that an increase in cigarette consumption was associated with worsening kidney function [35]. In a community-based study in Japan, smoking was found to be a predictor of developing CKD [36]. Renal graft survival in post-transplant patients has also been shown to be significantly worse in smokers compared to non-smokers [37].

Inflammatory Milieu and Oxidative Stress Inflammation and oxidative stress affect the cardiovascular system in several ways. Elevated pro-inflammatory mediators (e.g., advanced glycation products) in CKD result in vascular injury [38]. In this inflammatory environment, there are stimuli for endothelial dysfunction resulting inproliferation of vascular smooth muscle cells, [39] increased macrophage accumulation, vessel wall infiltration and adhesion with subsequent foam-cell formation, [40] and platelet activation [41]. These processes promote atherosclerotic plaque formation and rupture. Intrinsic characteristics of CKD patients (i.e., diabetes, hypertension, and advanced age) predispose them to higher oxidative stress [42], they have increased pro-inflammatory mediators with declining renal function [43], and they have defects in their anti-oxidant systems [44]. The dialysis procedure itself can activate complement pathways and circulating neutrophils when blood comes in contact with dialysis membranes. In addition, transfer of endotoxins from dialysate to the blood is a potent trigger for production of reactive oxygen species and activation of leukocytes [45]. Impaired nitric oxide synthesis in CKD patients is also a possible mechanism for endothelial dysfunction [46]. Various uremia metabolites (e.g., asymmetric dimethylarginine and p-cresylsulfate) have been associated with accelerated atherogenesis and cardiovascular events [47, 48].

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Coronary Artery Calcification Coronary artery calcification (CAC) is more common in patients with declining renal function. CAC is prevalent in young adults with ESKD. Goodman et al. found that among patients 20–30  years of age with ESKD, 87.5% had coronary artery calcification (CAC) (CAC scores 1157 ± 1996) compared to their normal counterparts where only 5% had coronary calcification (peak CAC score of 77) [49]. The occurrence of CAC varies with CKD stage. It is present in 13.9% of patients with CKD stages I and II and up to 83% in patients with CKD stages III–V [50]. Worsening renal function also correlates with higher calcium scores. The Dallas Heart Study showed that CAC scores of 400 were twice the rate in patients with CKD stages 1–2 (3.5%) and nine times higher in patients with CKD stages 3–5 (16%) when compared to normal participants (1.7%). This association was found to be significantly stronger in diabetic patients [51]. Vascular calcification is important because of its close relationship with cardiovascular morbidity and mortality in this subset of patients [52]. Vascular smooth muscle cells in CKD patients, likely induced by uremia, differentiate into osteoblast-­ like cells initiating tissue mineralization process [53]. This vascular calcification has deleterious hemodynamic consequences such as reduced coronary microcirculation, increased arterial stiffness, and increase in left ventricular hypertrophy [54]. A study by Shimoyama, Tsuruta, and Niwa showed that dialysis patients with CAC scores of 0–105, 110–1067, and >1094 have all-cause mortality of 7.6%, 43.3%, and 52.2%, respectively. The cardiovascular mortality in these groups were 3%, 22.4%, and 26.9%, respectively. CAC was, thus, found to be an independent predictor of cardiovascular events in CKD patients [55].

Risk Factor Control Lifestyle Interventions Obesity is an independent risk factor for the advancement of CKD [56]. Weight loss has been shown to remarkably reduce proteinuria and blood pressure [57]. The impact of weight loss was particularly seen in diabetic patients, in those with metabolic syndrome, and after bariatric surgery [58]. A multidisciplinary program including diet, exercise, and pharmacotherapy with orlistat showed significant body weight reduction and improved functional ability in obese CKD patients (see Fig. 1.3) [59]. In patients with BMI of 40 kg/m2 or greater in the general population, however, bariatric surgery is considered more effective than nonsurgical treatment in achieving long-lasting weight loss and improvement in comorbid conditions [60]. A concern in CKD patients is use of weight loss medications as these are generally unsafe in patients with eGFR or = 50% symptomatic vertebral or basilar artery stenosis: prospective population-based study. Brain. 2009;132(Pt 4):982–8. 84. Long A, Lepoutre A, Corbillon E, Branchereau A. Critical review of non- or minimally invasive methods (duplex ultrasonography, MR- and CT-angiography) for evaluating stenosis of the proximal internal carotid artery. Eur J Vasc Endovasc Surg. 2002;24(1):43–52. 85. Kaneko Y, Yanagawa T, Taru Y, Hayashi S, Zhang H, Tsukahara T, et al. Subclavian steal syndrome in a hemodialysis patient after percutaneous transluminal angioplasty of arteriovenous access. J Vasc Access. 2018;19:404. https://doi.org/10.1177/1129729818761279. 86. Cua B, Mamdani N, Halpin D, Jhamnani S, Jayasuriya S, Mena-Hurtado C. Review of coronary subclavian steal syndrome. J Cardiol. 2017;70(5):432–7. 87. McDermott MM, Mehta S, Greenland P. Exertional leg symptoms other than intermittent claudication are common in peripheral arterial disease. Arch Intern Med. 1999;159(4):387–92. 88. McDermott MM, Greenland P, Liu K, Guralnik JM, Criqui MH, Dolan NC, et al. Leg symptoms in peripheral arterial disease: associated clinical characteristics and functional impairment. JAMA. 2001;286(13):1599–606. 89. Khan NA, Rahim SA, Anand SS, Simel DL, Panju A. Does the clinical examination predict lower extremity peripheral arterial disease? JAMA. 2006;295(5):536–46. 90. Armstrong DW, Tobin C, Matangi MF.  The accuracy of the physical examination for the detection of lower extremity peripheral arterial disease. Can J Cardiol. 2010;26(10):e346–50. 91. Schroder F, Diehm N, Kareem S, Ames M, Pira A, Zwettler U, et al. A modified calculation of ankle-brachial pressure index is far more sensitive in the detection of peripheral arterial disease. J Vasc Surg. 2006;44(3):531–6. 92. Premalatha G, Ravikumar R, Sanjay R, Deepa R, Mohan V. Comparison of colour duplex ultrasound and ankle-brachial pressure index measurements in peripheral vascular disease in type 2 diabetic patients with foot infections. J Assoc Physicians India. 2002;50: 1240–4. 93. Allen J, Oates CP, Henderson J, Jago J, Whittingham TA, Chamberlain J, et al. Comparison of lower limb arterial assessments using color-duplex ultrasound and ankle/brachial pressure index measurements. Angiology. 1996;47(3):225–32. 94. Lijmer JG, Hunink MG, van den Dungen JJ, Loonstra J, Smit AJ. ROC analysis of noninvasive tests for peripheral arterial disease. Ultrasound Med Biol. 1996;22(4):391–8. 95. Guo X, Li J, Pang W, Zhao M, Luo Y, Sun Y, et al. Sensitivity and specificity of ankle-brachial index for detecting angiographic stenosis of peripheral arteries. Circ J. 2008;72(4):605–10.

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115. Shareghi S, Gopal A, Gul K, Matchinson JC, Wong CB, Weinberg N, et al. Diagnostic accuracy of 64 multidetector computed tomographic angiography in peripheral vascular disease. Catheter Cardiovasc Interv. 2010;75(1):23–31. 116. Ota H, Takase K, Igarashi K, Chiba Y, Haga K, Saito H, et al. MDCT compared with digital subtraction angiography for assessment of lower extremity arterial occlusive disease: importance of reviewing cross-sectional images. AJR Am J Roentgenol. 2004;182(1):201–9. 117. de Vries SO, Hunink MG, Polak JF.  Summary receiver operating characteristic curves as a technique for meta-analysis of the diagnostic performance of duplex ultrasonography in peripheral arterial disease. Acad Radiol. 1996;3(4):361–9. 118. Baril DT, Patel VI, Judelson DR, Goodney PP, McPhee JT, Hevelone ND, et al. Outcomes of lower extremity bypass performed for acute limb ischemia. J Vasc Surg. 2013;58(4):949–56. 119. Londero LS, Norgaard B, Houlind K. Patient delay is the main cause of treatment delay in acute limb ischemia: an investigation of pre- and in-hospital time delay. World J Emerg Surg. 2014;9(1):56. 120. Manojlovic V, Popovic V, Nikolic D, Milosevic D, Pasternak J, Kacanski M.  Analysis of associated diseases in patients with acute critical lower limb ischemia. Med Pregl. 2013;66(1–2):41–5. 121. Duval S, Keo HH, Oldenburg NC, Baumgartner I, Jaff MR, Peacock JM, et al. The impact of prolonged lower limb ischemia on amputation, mortality, and functional status: the FRIENDS registry. Am Heart J. 2014;168(4):577–87. 122. Morris-Stiff G, D’Souza J, Raman S, Paulvannan S, Lewis MH. Update experience of surgery for acute limb ischaemia in a district general hospital - are we getting any better? Ann R Coll Surg Engl. 2009;91(8):637–40. 123. Nigwekar SU, Thadhani R, Brandenburg VM.  Calciphylaxis. N Engl J Med. 2018;379(4):399–400. 124. Shankar AKR, Klein BE. The association among smoking, heavy drinking, and chronic kidney disease. Am J Epidemiol. 2006;164(3):263–71. 125. Hennrikus D, Joseph AM, Lando HA, Duval S, Ukestad L, Kodl M, et al. Effectiveness of a smoking cessation program for peripheral artery disease patients: a randomized controlled trial. J Am Coll Cardiol. 2010;56(25):2105–12. 126. Mukherjee D, Yadav JS. Update on peripheral vascular diseases: from smoking cessation to stenting. Cleve Clin J Med. 2001;68(8):723–33. 127. Feringa HH, Bax JJ, Hoeks S, van Waning VH, Elhendy A, Karagiannis S, et al. A prognostic risk index for long-term mortality in patients with peripheral arterial disease. Arch Intern Med. 2007;167(22):2482–9. 128. Sung JH, Lee JE, Samdarshi TE, Nagarajarao HS, Taylor JK, Agrawal KK, et al. C-reactive protein and subclinical cardiovascular disease among African-Americans: (the Jackson Heart Study). J Cardiovasc Med (Hagerstown). 2014;15(5):371–6. 129. Feringa HH, van Waning VH, Bax JJ, Elhendy A, Boersma E, Schouten O, et  al. Cardioprotective medication is associated with improved survival in patients with peripheral arterial disease. J Am Coll Cardiol. 2006;47(6):1182–7. 130. Bavry AA, Anderson RD, Gong Y, Denardo SJ, Cooper-Dehoff RM, Handberg EM, et al. Outcomes Among hypertensive patients with concomitant peripheral and coronary artery disease: findings from the INternational VErapamil-SR/Trandolapril STudy. Hypertension. 2010;55(1):48–53. 131. Paravastu SC, Mendonca DA, Da Silva A.  Beta blockers for peripheral arterial disease. Cochrane Database Syst Rev. 2013;(9):CD005508. 132. Beebe HG, Dawson DL, Cutler BS, Herd JA, Strandness DE Jr, Bortey EB, et  al. A new pharmacological treatment for intermittent claudication: results of a randomized, multicenter trial. Arch Intern Med. 1999;159(17):2041–50. 133. Benjo AM, Garcia DC, Jenkins JS, Cardoso RM, Molina TP, El-Hayek GE, et al. Cilostazol increases patency and reduces adverse outcomes in percutaneous femoropopliteal revascularisation: a meta-analysis of randomised controlled trials. Open Heart. 2014;1(1):e000154.

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Chapter 4

Cardiovascular Impact of Atherosclerotic Renovascular Disease Gates B. Colbert and Harold M. Szerlip

Introduction Renal artery stenosis (RAS), narrowing of renal arteries, can be unilateral or bilateral. This narrowing, if severe, can cause a reduction in renal blood flow with resultant ischemia of the affected kidney. The consequences of this are a decline in renal function and activation of the renin-angiotensin-aldosterone system (RAAS), with the development of renovascular hypertension. It needs to be emphasized however that the finding of RAS does not imply that hypertension or chronic kidney disease (CKD) is caused by the arterial narrowing.

Atherosclerotic Renal Artery Disease By far the most common cause of renal artery stenosis is atherosclerotic renal artery stenosis (ARAS), which is responsible for up to 90% of the cases of renovascular disease [1]. Stenosis in atherosclerotic disease occurs most commonly in the proximal renal artery. As with all atherosclerotic diseases, the prevalence increases with aging [2]. In addition, the prevalence reported varies depending on the population studied, the percent luminal narrowing considered significant, the reliability of the diagnostic tools used to identify the stenosis, and the prevailing community standard regarding the importance of making the diagnosis as far as treatment is concerned.

G. B. Colbert · H. M. Szerlip (*) Baylor University Medical Center, Dallas, Internal Medicine, Division of Nephrology, Dallas, TX, USA e-mail: [email protected]; [email protected]

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In 4429 patients referred for evaluation of secondary hypertension, the finding of ARAS increased from 1.3% in patients 30–39 years old to 6.5% in patients older than 70 years [2]. In 295 patients studied postmortem with an average age of 61 years, the overall prevalence of greater than 50% narrowing of the renal artery was 22%, whereas in those patients over 70 years, 32% had greater than 50% stenosis [3]. In patients with underlying coronary artery disease or peripheral vascular disease, the incidence of ARAS is between 30 and 50% [4–6]. In patients undergoing coronary angiography, 38.8% were noted to have greater than 50% stenosis of one or both renal arteries, with 40% of these patients having greater than 70% narrowing [7]. Similarly, 16.6% of patients undergoing angiography following an acute myocardial infarction and thus with established atherosclerotic disease had significant renal artery stenosis as defined by greater than 50% narrowing [8]. In another high-risk population, patients initiating chronic hemodialysis, 41% of the patients had greater than 50% stenosis [9]. Renal artery stenosis appears to be less common in African-Americans [10, 11], although when factored for other comorbidity race no longer appears to be significant [12]. Review of Medicare data showed that the hazard ratio for the diagnosis of ARAS increased 4.71-fold between 1992 and 2004 [13]. Between 1996 and 2000, the number of renal artery interventions increased to 62% [14]. The reason for this increase is unclear but may have been related to improvements in imaging or the increase in the ease of performing percutaneous interventions. Thus the prevalence of RAS varies significantly depending on the population studied.

Cardiovascular Consequences of Renal Artery Stenosis The most common side effects of RAS are hypertension and progressive CKD.  Although the pathophysiologic mechanism that results in hypertension is somewhat different between the Goldblatt one-clip and two-clip models, for all practical purposes a decrease in renal blood flow by activating the RAAS system increases both renal sodium retntion and systemic vascular resistance [15, 16]. The presence of significant RAS (>70%) does not necessarily cause hypertension, and similarly the finding of RAS in a hypertensive individual does not always indicate causality. In fact, both autopsy and angiographic studies demonstrate the existence of significant stenosis in the absence of hypertension [3, 7]. Unfortunately, the only definitive way to establish a diagnosis of renovascular hypertension is to show a decrease in blood pressure after relief of the blockage. In addition to activation of the RAAS, a critical decrease in renal perfusion results in activation of numerous cytokines and inflammatory mediators associated with renal injury [17, 18]. These inflammatory and pro-fibrotic cytokines as well as reactive oxygen species lead to rarefication of the renal microvascular structures, glomerular sclerosis, and interstitial fibrosis with tubular atrophy. Ongoing renal ischemia results in progressive kidney disease. Interestingly, even when renal

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perfusion is restored, these inflammatory mediators and markers of renal injury may remain elevated [19]. The presence of critical RAS is associated with increased cardiovascular morbidity and mortality even when factored for other comorbid conditions [8, 20–22]. However, it is unclear if these data are confounded by the extent of overall atherosclerosis, the presence of chronic kidney disease, or poorly controlled hypertension. Because atherosclerosis in one vascular bed is likely to be in multiple other locations [23, 24], it is no surprise that ARAS is linked to coronary disease and cardiovascular events. The fact that randomized trials evaluating the use of stents in ARAS do not show improvement in cardiovascular outcomes, whereas individuals treated for fibromuscular dysplasia (FMD) appear to have an excellent prognosis supports the role of confounders. The systemic consequences of RAS are multifactorial and can lead to dysfunction in many vital organ systems (Fig. 4.1). The majority of patients with hypertension and RAS clearly have evidence of myocardial remodeling on echocardiography [25–27]. Although both concentric and eccentric left ventricular hypertrophies are noted, concentric hypertrophy occurs more commonly. Interestingly left ventricular

Brain • Ischemic Stroke

Resistant Hypertension • Increased SVR Hypertensive Emergency

Pulmonary • Flash Pulmonary Edema

Increased RAAS

Kidney • Decreased eGFR • Ischemic Nephropathy • Increased NGAL

Cardiac • Concentric and Eccentric LV Hypertrophy • HFrEF, HFpEF

Inflammatory Markes • Increased TNF-alpha, IF-gamma, IL-6, MCP-1

Fig. 4.1  Clinical consequences and organ damage resulting from ARAS. RAAS renin angiotensin aldosterone system, SVR systemic vascular resistance, NGAL neutrophilic gelatinase-associated lipocalin, HFrEF heart failure with reduced ejection fraction, HFpEF heart failure with preserved ejection fraction, LV left ventricular, TNF tumor necrosis factor, IF interferon, MCP monocyte chemoattractant protein

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mass was greater in subjects with RAS than in subjects with similar degrees of blood pressure elevation but without RAS suggesting that other confounders must exist. In a small study of conservatively managed patients, Wright JR et al. showed an increase in left ventricular end-diastolic volume over a period of 1 year [27]. Another entity that appears to occur more frequently in patients with RAS is recurrent episodes of flash pulmonary edema [28–30]. This was initially described by Pickering in 11 patients in 1988 [29]. Patients typically present with acute-onset pulmonary edema that can be recurrent. Blood pressure is invariably markedly elevated and cardiac function is preserved. Pickering syndrome occurs more frequently with bilateral renal artery stenosis than with unilateral involvement [28–31]. The increased incidence that occurs when both kidneys are involved is likely related to the sodium and water retention that occurs more frequently with bilateral disease as opposed to the pressure natriuresis that ensues in unilateral disease. Relief of the obstruction frequently prevents reoccurrence [29–31].

Clinical Trials The diagnostic challenge for the clinician is to understand who needs to be evaluated for renal artery disease and what diagnostic tools provide the most useful information. Several randomized studies have evaluated the potential to decrease cardiovascular outcomes with revascularization intervention in patients with ARAS. Prior to 2009, there was a dearth of randomized clinical trials looking at renal artery stenosis. Finally in that year, the STAR trial was published which included a randomized cohort based in the Netherlands and France examining 140 patients with eGFR 45 or known h/o atherosclerosis

Medical therapy (BP medications / statins)

Resistant hypertension

Flash pulmonary edema

Rapid decline in renal function

Image renal arteries (modality based on local expertise) > 70% stenosis Revascularize

Fig. 4.2  Proposed algorithm for treating resistant hypertension and using objective evidence to determine which patients may benefit from revascularization

[55]. Because of their function as filtering units, the kidneys receive far more blood than is necessary for metabolic demands. In addition delivery of oxygenated blood beyond an obstruction is dependent on cardiac output and blood pressure [56]. Measurement of tissue oxygenation using blood-oxygen-level-dependent (BOLD) MRI demonstrates that despite significant decreases in renal perfusion, post-­stenosis renal cortical and medullary oxygenation is maintained [57]. The Holy Grail in the evaluation of patients with RAS is to be able to predict which the patient will respond to revascularization (Fig.  4.2). Several different methodologies have been developed to better assess renal ischemia. One method to determine if the stenosis is significant enough to limit renal perfusion is to measure the trans-stenotic pressure gradient. In 15 patients with renal artery stenosis after successful stenting, graded degrees of obstruction were obtained using a balloon catheter, and renal vein renin was measured [58]. Increases in renin occurred when the pressure distal to the graded obstruction was less than 90% of aortic pressure and became maximal at 50%. Thus measurement of pressure gradient may provide useful information. However, as already noted the translesional gradient may vary depending on cardiac output, blood pressure, and renal vascular resistance. Furthermore, post hoc analysis of the CORAL trial did not show a benefit of

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stenting over medical therapy based on peak systolic pressure gradient [59]. In a small prospective study, the translesional gradient was unable to predict a beneficial response to stenting in either blood pressure or renal function [60, 61]. In order to avoid the pitfalls associated with the use of a pressure gradient, it has been suggested that renal fractional flow reserve (FFR) might be a better parameter [55]. FFR measures the pressure gradient after post-stenotic infusion of an endothelium-­ independent dilating agent, which thus maximizes blood flow. Unfortunately, this technique has not been shown to be able to predict who will benefit from revascularization [60, 61]. Another recently reported methodology that may provide better information regarding the hemodynamic significance of a stenotic lesion is the renal frame count (RFC). This is the number cineangiographic frames obtained at 30 frames/second for radiocontrast to flow from the proximal renal artery to the smallest cortical branches. Naghi et al. found that a RFC > 30 frames/second was associated with improved blood pressure control after renal artery stenting [62]. This interesting observation needs to be verified in future studies. Newer technologies that have future potential are dynamic contrast-enhanced MRI and BOLD MRI. Dynamic contrast-enhanced MRI has the ability to measure numerous parameters including renal blood flow, single kidney glomerular filtration rate, and extraction fraction [63]. Whether such measurements will be useful for choosing those patients who will benefit from renal artery stenting has yet to be determined. BOLD MRI can show areas of renal ischemia [64]. Future studies need to examine whether this technology can be useful in identifying patients who will benefit from revascularization.

Conclusions The incidence of ARAS increases with age and affects approximately 7% of the population over the age of 65 years and is found far more frequently in individuals with other evidence of atherosclerotic disease. Because of the failure of several large randomized trials to show a benefit of renal revascularization compared to medical therapy, the initial enthusiasm associated with percutaneous interventions has waned. These studies have conclusively demonstrated that the majority of patients with ARAS can be managed medically with control of blood pressure and cholesterol-lowering agents. It is clear from the randomized studies that routine stenting of atherosclerotic renal artery stenosis is not warranted. As previously mentioned the most recent 2017 ACC/AHA Hypertension Guidelines have recommended medical therapy as the initial treatment in all patients with ARAS [42]. Yet there are clearly patients who will benefit from revascularization. The challenge is to identify those patients who will benefit from revascularization (Fig. 4.2). Although new imaging technologies are being studied, none have yet to be validated as useful to predict successful outcomes from renal stenting. Until we have better

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diagnostic tools, only those patients who are considered high-risk defined as those presenting with flash pulmonary edema, refractory hypertension, or rapidly declining renal function should be evaluated. Initially these patients should be screened noninvasively. If noninvasive techniques confirm the presence of stenosis, the next step is renal angiography. Lesions >70–80% should be corrected. This protocol will obviously miss patients who might benefit as well as intervene on patients who will not benefit but overall should provide the best evaluation and management for all.

References 1. Lao D, Parasher PS, Cho KC, Yeghiazarians Y. Atherosclerotic renal artery stenosis--diagnosis and treatment. Mayo Clin Proc. 2011;86:649–57. 2. Anderson GH, Blakeman N, Streeten DH. The effect of age on prevalence of secondary forms of hypertension in 4429 consecutively referred patients. J Hypertens. 1994;12:609–15. 3. Holley KE, Hunt JC, Brown AL Jr, Kincaid OW, Sheps SG. Renal artery stenosis. A clinical-­ pathologic study in normotensive and hypertensive patients. Am J Med. 1964;37:14–22. 4. Buller CE, Nogareda JG, Ramanathan K, et al. The profile of cardiac patients with renal artery stenosis. J Am Coll Cardiol. 2004;43:1606–13. 5. Harding MB, Smith LR, Himmelstein SI, et al. Renal artery stenosis: prevalence and associated risk factors in patients undergoing routine cardiac catheterization. J Am Soc Nephrol. 1992;2:1608–16. 6. Olin JW, Melia M, Young JR, Graor RA, Risius B. Prevalence of atherosclerotic renal artery stenosis in patients with atherosclerosis elsewhere. Am J Med. 1990;88:46N–51N. 7. Zandparsa A, Habashizadeh M, Moradi Farsani E, Jabbari M, Rezaei R. Relationship between renal artery stenosis and severity of coronary artery disease in patients with coronary atherosclerotic disease. Int Cardiovasc Res J. 2012;6:84–7. 8. Burlacu A, Siriopol D, Voroneanu L, et al. Atherosclerotic renal artery stenosis prevalence and correlations in acute myocardial infarction patients undergoing primary percutaneous coronary interventions: data from nonrandomized single-center study (REN-ACS)-a single center, prospective, observational study. J Am Heart Assoc. 2015;4:e002379. 9. van Ampting JM, Penne EL, Beek FJ, Koomans HA, Boer WH, Beutler JJ.  Prevalence of atherosclerotic renal artery stenosis in patients starting dialysis. Nephrol Dial Transplant. 2003;18:1147–51. 10. Detection, evaluation, and treatment of renovascular hypertension. Final report. Working Group on Renovascular Hypertension. Arch Intern Med. 1987;147:820–9. 11. Alhaddad IA, Blum S, Heller EN, et al. Renal artery stenosis in minority patients undergoing diagnostic cardiac catheterization: prevalence and risk factors. J Cardiovasc Pharmacol Ther. 2001;6:147–53. 12. Jazrawi A, Darda S, Burke P, et al. Is race a risk factor for the development of renal artery stenosis? Cardiol Res Pract. 2009;2009:817987. 13. Kalra PA, Guo H, Gilbertson DT, et  al. Atherosclerotic renovascular disease in the United States. Kidney Int. 2010;77:37–43. 14. Murphy TP, Soares G, Kim M. Increase in utilization of percutaneous renal artery interventions by medicare beneficiaries, 1996-2000. AJR Am J Roentgenol. 2004;183:561–8. 15. Goldblatt H, Lynch J, Hanzal RF, Summerville WW. Studies on experimental hypertension: I. The production of persistent elevation of systolic blood pressure by means of renal ischemia. J Exp Med. 1934;59:347–79. 16. Martinez-Maldonado M.  Pathophysiology of renovascular hypertension. Hypertension. 1991;17:707–19.

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17. Eirin A, Gloviczki ML, Tang H, et al. Inflammatory and injury signals released from the post-­ stenotic human kidney. Eur Heart J. 2013;34:540-8a. 18. Eirin A, Gloviczki ML, Tang H, et  al. Chronic renovascular hypertension is associated with elevated levels of neutrophil gelatinase-associated lipocalin. Nephrol Dial Transplant. 2012;27:4153–61. 19. Saad A, Herrmann SM, Crane J, et al. Stent revascularization restores cortical blood flow and reverses tissue hypoxia in atherosclerotic renal artery stenosis but fails to reverse inflammatory pathways or glomerular filtration rate. Circ Cardiovasc Interv. 2013;6:428–35. 20. Mui KW, Sleeswijk M, van den Hout H, van Baal J, Navis G, Woittiez AJ. Incidental renal artery stenosis is an independent predictor of mortality in patients with peripheral vascular disease. J Am Soc Nephrol. 2006;17:2069–74. 21. Shafique S, Peixoto AJ.  Renal artery stenosis and cardiovascular risk. J Clin Hypertens (Greenwich). 2007;9:201–8. 22. Conlon PJ, Little MA, Pieper K, Mark DB. Severity of renal vascular disease predicts mortality in patients undergoing coronary angiography. Kidney Int. 2001;60:1490–7. 23. Duvall WL, Vorchheimer DA. Multi-bed vascular disease and atherothrombosis: scope of the problem. J Thromb Thrombolysis. 2004;17:51–61. 24. Lahoz C, Mostaza JM.  Atherosclerosis as a systemic disease. Rev Esp Cardiol. 2007;60: 184–95. 25. Khan AR, Sheikh M, Kaw D, Cooper CJ, Khouri SJ. Prevalence and factors associated with left ventricular remodeling in renal artery stenosis. J Am Soc Hypertens. 2014;8:254–61. 26. Wright JR, Shurrab AE, Cooper A, Kalra PR, Foley RN, Kalra PA. Left ventricular morphology and function in patients with atherosclerotic renovascular disease. J Am Soc Nephrol. 2005;16:2746–53. 27. Wright JR, Shurrab AE, Cooper A, Kalra PR, Foley RN, Kalra PA.  Progression of cardiac dysfunction in patients with atherosclerotic renovascular disease. QJM. 2009;102:695–704. 28. Messerli FH, Bangalore S, Makani H, et al. Flash pulmonary oedema and bilateral renal artery stenosis: the Pickering syndrome. Eur Heart J. 2011;32:2231–5. 29. Pickering TG, Herman L, Devereux RB, et al. Recurrent pulmonary oedema in hypertension due to bilateral renal artery stenosis: treatment by angioplasty or surgical revascularisation. Lancet. 1988;2:551–2. 30. Pelta A, Andersen UB, Just S, Baekgaard N. Flash pulmonary edema in patients with renal artery stenosis--the Pickering Syndrome. Blood Press. 2011;20:15–9. 31. Messina LM, Zelenock GB, Yao KA, Stanley JC. Renal revascularization for recurrent pulmonary edema in patients with poorly controlled hypertension and renal insufficiency: a distinct subgroup of patients with arteriosclerotic renal artery occlusive disease. J Vasc Surg. 1992;15:73–80; discussion -2 32. Bax L, Woittiez AJ, Kouwenberg HJ, et  al. Stent placement in patients with atherosclerotic renal artery stenosis and impaired renal function: a randomized trial. Ann Intern Med. 2009;150:840–8, W150-1 33. Investigators A, Wheatley K, Ives N, et al. Revascularization versus medical therapy for renal-­ artery stenosis. N Engl J Med. 2009;361:1953–62. 34. Ritchie J, Green D, Chrysochou C, Chalmers N, Foley RN, Kalra PA.  High-risk clinical presentations in atherosclerotic renovascular disease: prognosis and response to renal artery revascularization. Am J Kidney Dis. 2014;63:186–97. 35. Cooper CJ, Murphy TP, Cutlip DE, et  al. Stenting and medical therapy for atherosclerotic renal-artery stenosis. N Engl J Med. 2014;370:13–22. 36. White CJ.  The “chicken little” of renal stent trials: the CORAL trial in perspective. JACC Cardiovasc Interv. 2014;7:111–3. 37. Riaz IB, Husnain M, Riaz H, et al. Meta-analysis of revascularization versus medical therapy for atherosclerotic renal artery stenosis. Am J Cardiol. 2014;114:1116–23. 38. Zhu Y, Ren J, Ma X, et al. Percutaneous revascularization for atherosclerotic renal artery stenosis: a meta-analysis of randomized controlled trials. Ann Vasc Surg. 2015;29:1457–67.

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39. Hollenberg NK. The treatment of renovascular hypertension: surgery, angioplasty, and medical therapy with converting-enzyme inhibitors. Am J Kidney Dis. 1987;10:52–60. 40. Chrysochou C, Foley RN, Young JF, Khavandi K, Cheung CM, Kalra PA. Dispelling the myth: the use of renin-angiotensin blockade in atheromatous renovascular disease. Nephrol Dial Transplant. 2012;27:1403–9. 41. Hricik DE, Dunn MJ. Angiotensin-converting enzyme inhibitor-induced renal failure: causes, consequences, and diagnostic uses. J Am Soc Nephrol. 1990;1:845–58. 42. Whelton PK, Carey RM, Aronow WS, et  al. ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ ASH/ASPC/NMA/PCNA guideline for the prevention, detection, evaluation, and management of high blood pressure in adults: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Hypertension. 2018;71:1269–1324 43. Murphy TP, Cooper CJ, Pencina KM, et al. Relationship of albuminuria and renal artery stent outcomes: results from the CORAL randomized clinical trial (cardiovascular outcomes with renal artery lesions). Hypertension. 2016;68:1145–52. 44. Corriere MA, Hoyle JR, Craven TE, et al. Changes in left ventricular structure and function following renal artery revascularization. Ann Vasc Surg. 2010;24:80–4. 45. Rzeznik D, Przewlocki T, Kablak-Ziembicka A, et al. Effect of renal artery revascularization on left ventricular hypertrophy, diastolic function, blood pressure, and the one-year outcome. J Vasc Surg. 2011;53:692–7. 46. Zeller T, Rastan A, Schwarzwalder U, et al. Regression of left ventricular hypertrophy following stenting of renal artery stenosis. J Endovasc Ther. 2007;14:189–97. 47. Ritchie J, Green D, Chrysochou T, et al. Effect of renal artery revascularization upon cardiac structure and function in atherosclerotic renal artery stenosis: cardiac magnetic resonance sub-­ study of the ASTRAL trial. Nephrol Dial Transplant. 2017;32:1006–13. 48. Williams GJ, Macaskill P, Chan SF, et al. Comparative accuracy of renal duplex sonographic parameters in the diagnosis of renal artery stenosis: paired and unpaired analysis. AJR Am J Roentgenol. 2007;188:798–811. 49. Olin JW, Piedmonte MR, Young JR, DeAnna S, Grubb M, Childs MB. The utility of duplex ultrasound scanning of the renal arteries for diagnosing significant renal artery stenosis. Ann Intern Med. 1995;122:833–8. 50. Rountas C, Vlychou M, Vassiou K, et al. Imaging modalities for renal artery stenosis in suspected renovascular hypertension: prospective intraindividual comparison of color Doppler US, CT angiography, GD-enhanced MR angiography, and digital subtraction angiography. Ren Fail. 2007;29:295–302. 51. Eklof H, Ahlstrom H, Magnusson A, et al. A prospective comparison of duplex ultrasonography, captopril renography, MRA, and CTA in assessing renal artery stenosis. Acta Radiol. 2006;47:764–74. 52. Eriksson P, Mohammed AA, De Geer J, et al. Non-invasive investigations of potential renal artery stenosis in renal insufficiency. Nephrol Dial Transplant. 2010;25:3607–14. 53. Albert TS, Akahane M, Parienty I, et  al. An international multicenter comparison of time-­ SLIP unenhanced MR angiography and contrast-enhanced CT angiography for assessing renal artery stenosis: the renal artery contrast-free trial. AJR Am J Roentgenol. 2015;204:182–8. 54. Angeretti MG, Lumia D, Cani A, et al. Non-enhanced MR angiography of renal arteries: comparison with contrast-enhanced MR angiography. Acta Radiol. 2013;54:749–56. 55. Subramanian R, White CJ, Rosenfield K, et al. Renal fractional flow reserve: a hemodynamic evaluation of moderate renal artery stenoses. Catheter Cardiovasc Interv. 2005;64:480–6. 56. Textor SC, Lerman LO. Paradigm shifts in atherosclerotic Renovascular disease: where are we now? J Am Soc Nephrol. 2015;26:2074–80. 57. Gloviczki ML, Glockner JF, Lerman LO, et al. Preserved oxygenation despite reduced blood flow in poststenotic kidneys in human atherosclerotic renal artery stenosis. Hypertension. 2010;55:961–6.

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58. De Bruyne B, Manoharan G, Pijls NH, et al. Assessment of renal artery stenosis severity by pressure gradient measurements. J Am Coll Cardiol. 2006;48:1851–5. 59. Murphy TP, Cooper CJ, Matsumoto AH, et  al. Renal artery stent outcomes: effect of baseline blood pressure, stenosis severity, and translesion pressure gradient. J Am Coll Cardiol. 2015;66:2487–94. 60. Kadziela J, Januszewicz A, Prejbisz A, et al. Prognostic value of renal fractional flow reserve in blood pressure response after renal artery stenting (PREFER study). Cardiol J. 2013;20:418–22. 61. Kadziela J, Prejbisz A, Michalowska I, et al. Relationship between hemodynamic parameters of renal artery stenosis and the changes of kidney function after renal artery stenting in patients with hypertension and preserved renal function. Blood Press. 2015;24:30–4. 62. Naghi J, Palakodeti S, Ang L, Reeves R, Patel M, Mahmud E. Renal frame count: a measure of renal flow that predicts success of renal artery stenting in hypertensive patients. Catheter Cardiovasc Interv. 2015;86:304–9. 63. Lim SW, Chrysochou C, Buckley DL, Kalra PA, Sourbron SP. Prediction and assessment of responses to renal artery revascularization with dynamic contrast-enhanced magnetic resonance imaging: a pilot study. Am J Physiol Renal Physiol. 2013;305:F672–8. 64. Gloviczki ML, Saad A, Textor SC. Blood oxygen level-dependent (BOLD) MRI analysis in atherosclerotic renal artery stenosis. Curr Opin Nephrol Hypertens. 2013;22:519–24.

Part II

Therapeutic Considerations with Revascularization in Chronic Kidney Disease

Chapter 5

Therapeutic Considerations with Revascularization in Chronic Kidney Disease: Radial Versus Femoral Arterial Access Giuseppe Andò, Felice Gragnano, Paolo Calabrò, and Marco Valgimigli

Abbreviations AKI Acute kidney injury AV Arteriovenous CI Confidence interval CABG Coronary artery bypass grafting CIN Contrast-induced nephropathy CKD Chronic kidney disease eGFR Estimated glomerular filtration rate MATRIX Minimizing Adverse Haemorrhagic Events by Transradial Access Site and Systemic Implementation of AngioX PCI Percutaneous coronary intervention sCr Serum creatinine TFA Transfemoral approach TRA Transradial approach

G. Andò Azienda Ospedaliera Universitaria Policlinico “Gaetano Martino”, Department of Clinical and Experimental Medicine, University of Messina, Messina, Italy e-mail: [email protected] F. Gragnano · P. Calabrò Division of Clinical Cardiology, A.O.R.N. Sant’Anna e San Sebastiano, Caserta, Italy Department of Cardiothoracic and Respiratory Sciences, University of Campania “Luigi Vanvitelli”, Naples, Italy e-mail: [email protected]; [email protected] M. Valgimigli (*) Department of Cardiology, Bern University Hospital, University of Bern, Bern, Switzerland e-mail: [email protected] © Springer Nature Switzerland AG 2020 J. Rangaswami et al. (eds.), Kidney Disease in the Cardiac Catheterization Laboratory, https://doi.org/10.1007/978-3-030-45414-2_5

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 ascular Access for Coronary Angiography and Percutaneous V Coronary Interventions: General Considerations Both diagnostic coronary angiography and percutaneous coronary interventions (PCIs) have been almost exclusively performed via the transfemoral approach (TFA)) until the late 1980s, when the transradial approach (TRA)) demonstrated similar feasibility and safety [1], gaining more space in catheterization laboratories [2–4]. In Europe, the utilization of the TRA is growing exponentially, with a current usage rate of TRA in more than 80% of cases [5]. The radial artery is a terminal branch of the brachial artery, originating below the elbow. Its course becomes more superficial in its 3–5­cm distal portion, which is considered the puncture site. The relative absence of satellite nerves and major veins limits possible iatrogenic injury, making the technique very safe [6]. TRA is feasible in both stable and urgent settings to manage simple and complex coronary lesions, with 5-, 6-, or 7-French (Fr) guiding catheters and compatible devices for angioplasty balloons, stents, rotational atherectomy, and thrombectomy. After an initial learning curve, the procedural success rates increase rapidly, becoming similar to those of the transfemoral procedures [5, 7]. The recent development of highly effective antiplatelet agents has reducing thrombotic events post PCI but has contributed to the higher risk of serious femoral access site-related bleeding, which is associated with poor outcomes [2]. Because of anatomic and procedural considerations, the TRA has been associated with virtually no major access site-related bleeding and has been shown to improve clinical outcomes (including mortality) in recent randomized trials [2].

 adial Access for Coronary Artery Interventions: Rationale R for Renal Protection Acute kidney injury (AKI) is a major complication of percutaneous coronary angiography and interventions, affecting hospitalization duration as well as short- and long-term prognosis [8–10]. It refers to an abrupt decrease in kidney function, defined by an increase in serum creatinine (sCr) by 50% within 7 days of the index event or an increase in sCr by 0.3 mg/dl within 2 days or oliguria development [11]. Its course is usually transient; however, a subset of patients develop irreversible injury, leading to progressive function impairment and renal failure [12, 13], which is associated with increased long-term risk of cardiovascular events [14]. The presence of pre-procedural CKD is a major determinant of post-procedural AKI [15]. Although less established, several other parameters have also been associated with an increased risk [16–18]. These include patient characteristics such as age, sex, diabetes mellitus, heart failure, hypotension, volume status, and concomitant nephrotoxic drug use [19, 15]. Procedure-related risk factors for AKI include contrast volume, type and administration route, operator experience, and procedure complexity [8, 13, 17].

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No effective treatment is currently available in patients with established post-­ catheterization AKI.  Reduction of AKI burden related to cardiac catheterization largely rests on the employment of preventative strategies. Prophylactic venous hydration with isotonic saline (1.0–1.5 mL/kg/h), 6 hours before and after the procedure, represents presently the only highly recommended preventive measure in patients at intermediate to high risk for contrast-induced AKI (CI-AKI) [20, 21], with significant relative risk reduction in the rates of post-catheterization AKI achieved with left ventricular end-diastolic pressure (LVEDP)-guided fluid therapy compared to a fixed fluid prescription [22]. The injection of contrast media into the intra-arterial circuit is followed by a period of sustained renal arteriolar vasoconstriction and cellular damage predominantly to the proximal tubular epithelium [23], triggering tubulo-glomerular feedback (TGF) which further reduces single-nephron glomerular filtration rates (GFR) [17]. Therefore, all efforts should be made to minimize contrast volume as far as possible including avoidance of left ventriculography and aortography in patients at high risk for AKI, adopting intracoronary imaging guidance for PCI (e.g., IVUS) [24] and using renal function-adjusted contrast volume (CV) determination (CV/eGFR) [25]. A growing awareness about the role of potential strategies that are nephroprotective is emerging in the literature, mostly for the categories of patients considered at higher risk such as in advanced CKD, as demonstrated by the use of “zero contrast” PCIs in patients with advanced CKD [26]. The reader is also referred to the appropriate chapters in this textbook that detail the evidence behind specific contrast-based renal optimization strategies. However, the possibility of adopting and implementing preventive strategies is limited [27], especially for patients requiring urgent PCI. In addition, AKI after PCI is a multicausal phenomenon with several confounding operative factors and comorbidities existing in patients undergoing catheter-based procedures with intra-arterial iodinated contrast administration [17, 18]. Such other mechanisms not related to contrast media include periprocedural bleedings, systemic and renal hemodynamic instability, imbalance between vasodilation and vasoconstriction stimuli, and direct cholesterol embolization which are involved in iatrogenic renal damage during cardiac catheterization. Moreover, several cardiovascular medications might exert a protective (e.g., statins) or detrimental (renin-angiotensin inhibitors and diuretics) effect on renal function at the time of the procedure, and their careful administration is of critical importance in patients managed invasively [28, 29]. In this backdrop, it has been hypothesized that vascular access site for cardiac catheterization and PCI may impact the occurrence of renal complications, largely by reducing the risk of periprocedural bleeding and renal atheroembolic disease [30]. The clinical advantages of the radial over femoral approach have been recently described, mainly resulting from the favorable modulation of periprocedural determinants of AKI distinct from contrast administration [10]. The following sections describe the impact of periprocedural bleeding and atheroembolic disease on AKI after cardiac catheterization and summarize the evolution of evidence in favor of the TRA toward reduction of post-­ catheterization AKI.

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 nemia, Bleeding, and Hypotension: The Hypoperfusion A Hypothesis Periprocedural bleeding and anemia are established risk factors for the development of adverse cardiovascular and renal outcomes [15, 31]. Blood loss, periprocedural hypotension, and hemodilution (often resulting from intensive fluid replacement therapy after bleeding) are all potential causes of periprocedural impairment in renal perfusion. Patients with CKD undergoing cardiac catheterization are more frequently anemic and may experience excessive bleeding [32]. This is a consequence of profound impairment of coagulation and fibrinolytic systems altering the physiologic interaction between the coagulation factors, platelets and the vessel wall in the background of CKD [32]. The use of coagulation-modifying drugs during PCI in these patients, and their altered pharmacokinetic profile in the setting of renal dysfunction, makes them even more prone to bleeding events and consequently renal injury [32]. These pathophysiological alterations have been consistently confirmed in clinical practice. In patients undergoing PCI, Nikolsky et al. [15] firstly reported that each 3% reduction in the hematocrit level at the baseline resulted in a significant increase in the occurrence of contrast-induced nephropathy (CIN), which was higher in CKD than non-CKD patients (23% and 11%, respectively). In patients with low pre-procedural hematocrit (5.9%) was associated with double rates of CIN compared with milder reduction (0.5 mg/ dl or 50% within 72 hours

Creatinine 6743 increase of ≥0.3 mg/ dl or 1.5- to two-fold

Cortese [47]

Kooiman [3]

Damluji [49]

Steinvil [48]

Study

AKI definition

5624

641

73,310

494

64.3

62

63.9

63.1

65.2

60

65.1

64.8

34.9

32

38.4

21.4

38.2

41

36.8

22.9

NR

16

20.1

NR

NR

28

24.4

NR

14.8

12

14.1

NR

16.3

15

15.5

NR

Number of Mean/median Chronic kidney Congestive heart patie­nts Radial Femoral age (years) Diabetes (%) disease (%) failure (%) Radial Femoral Radial Femoral Radial Femoral Radial Femoral

51

NR

NR

47

44

NR

NR

46

NR

NR

7.7

100

NR

NR

16.8

100

Mean left ventricular ejection fraction STEMI (%) (%) ∗any ACS Radial Femoral Radial Femoral

162

180

NR

207

154

165

NR

189

2.7

4.5

13.1

1.4

2.5

4.7

(continued)

16.9

8.1

Mean/median contrast volume Incidence of (ml) AKI (%) Radial Femoral Radial Femoral

Table 5.1  Overview of studies evaluating the occurrence of AKI after cardiac catheterization and/or percutaneous coronary intervention using transradial as compared to transfemoral approach

5  Therapeutic Considerations with Revascularization in Chronic Kidney Disease… 91

2176

1141

4109

Creatinine 7529 increase >0.5 mg/ dl or 25% within 48–72 hours

Feldkamp Creatinine 2937 [46] increase >0.3 mg/ dl or 50% within 48 hours

Creatinine 8210 increase >0.5 mg/ dl or 25%

Pan­choly [45]

4101

1796

5353

857

65.5

71

62.0

59.8

65.9

73

66.0

60.2

22.8

25.0

32

20.0

22.4

28.7

33

19.7

NR

20.8

NR

1.6

NR

28.5

NR

2.3

8.6

37.6

10.0

NR

AKI acute kidney injury, NR not reported, STEMI ST-segment elevation myocardial infarction

Andò [29]

305

Creatinine 1162 increase >0.5 mg/ dl or 25% within 48 hours

Kolte [44]

Study

AKI definition

9.2

42.8

9.2

NR

Number of Mean/median Chronic kidney Congestive heart patie­nts Radial Femoral age (years) Diabetes (%) disease (%) failure (%) Radial Femoral Radial Femoral Radial Femoral Radial Femoral

Table 5.1 (continued)

NR

NR

NR

50

NR

NR

NR

50

19.4∗

28.1∗

48.2

74∗

83∗

48.1

100

100

Mean left ventricular ejection fraction STEMI (%) (%) ∗any ACS Radial Femoral Radial Femoral

203

180

190

181

204

180

220

212

15.9

17.4

15.4

2.4

7.0

10.1

1.1

5.9

Mean/median contrast volume Incidence of (ml) AKI (%) Radial Femoral Radial Femoral

92 G. Andò et al.

5  Therapeutic Considerations with Revascularization in Chronic Kidney Disease…

93

the results of the PRIPITENA (Primary PCI from Tevere to Navigli) study, which was a retrospective investigation of the role of TRA for emergent PCI in the setting of ST-segment elevation myocardial infarction (STEMI) [48]. After a propensity-­ matched analysis, the occurrence of AKI was lower in patients treated with radial versus femoral primary PCI (8.4% vs. 16.9%, P = 0.007), and, in the multivariate analysis, TFA was an independent predictor of AKI (odds ratio 1.654, 95% CI 1.084–2.524, P  =  0.042). In 2017, a propensity score analysis of a large, single-­ center, real-world registry [49] substantially confirmed previous findings, showing that TRA reduced post-PCI AKI (defined by creatinine increase of ≥0.3 mg/dL during hospitalization) in both univariate- (4.3% vs. 10.4%, P