Diabetes and Kidney Disease PDF
Preview Diabetes and Kidney Disease
Diabetes and Kidney Disease Diabetes and Kidney Disease EDITED BY Gunter Wolf MD, MHBA Professor and Chairman Department of Internal Medicine III University of Jena University Hospital Jena, Germany A John Wiley & Sons, Ltd., Publication This edition fi rst published 2013 © 2013 by John Wiley & Sons, Ltd. Wiley-Blackwell is an imprint of John Wiley & Sons, formed by the merger of Wiley’s global Scientifi c, Technical and Medical business with Blackwell Publishing. 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WK 835] LC Classification not assigned 616.4'62–dc23 2012036995 A catalogue record for this book is available from the British Library. Wiley also publishes its books in a variety of electronic formats. Some content that appears in print may not be available in electronic books. Cover image: Courtesy of Hermann J. Kissler, Christiane Rüster, Utz Settmacher Cover design by Garth Stewart Set in 8/12 pt Stone Serif by Toppan Best-set Premedia Limited 1 2013 Contents Contributors, vii 10 Diabetes, pregnancy and the kidney, 129 Preface, x Helmut Kleinwechter and Ute Schäfer-Graf 11 Diabetic nephropathy in children, 143 Kai D Nüsken and Jörg Dötsch Part I Introduction and 12 Diabetes, the kidney and Pathophysiology retinopathy, 153 1 History of diabetic nephropathy: Hans-Peter Hammes a personal account, 3 Eberhard Ritz Part III Prevention and Therapy 2 Epidemiology of chronic kidney disease in diabetes, 14 13 Reducing progression of diabetic Andrea Icks and Michael Koch nephropathy by antihyperglycemic 3 Genetic risk factors for diabetic treatment, 171 nephropathy, 29 Christoph Hasslacher Carsten A. Böger and Peter R. Mertens 14 Dosage of antihyperglycemic drugs in 4 Pathophysiology of diabetic patients with renal insuffi ciency, 186 nephropathy, 45 Alexander Sämann and Ulrich A. Müller Ivonne Loeffl er 15 Reducing progression of diabetic 5 Histology of human diabetic nephropathy by antihypertensive nephropathy, 62 treatment, 202 Kerstin Amann and Christoph Daniel Anita Hansen, Ivo Quack and 6 Natural history and diagnosis of diabetic Lars Christian Rump kidney disease, 70 16 Treatment of the patient with end-stage Bethany Karl and Kumar Sharma diabetic nephropathy, 215 Muriel Ghosn and Fuad N. Ziyadeh 17 Combined pancreas and kidney Part II Special Situations, Risk Factors transplantation or kidney alone and Complications transplantation for patients with diabetic 7 Cardiovascular disease in diabetic nephropathy, 232 nephropathy: pathophysiology and Hermann J. Kissler, Christiane Rüster treatment, 85 and Utz Settmacher Martin Busch 8 Statin therapy in patients with diabetic Index, 253 nephropathy, 101 Color plate section can be found facing Christoph Wanner page 54 9 Diabetes mellitus, bone and kidney, 116 Thomas Neumann and Gabriele Lehmann v Contributors Kerstin Amann MD Hans-Peter Hammes MD Professor of Nephropathology Section Head, Endocrinology Department of Pathology 5th Medical Department Universität Erlangen- Nürnberg UMM– University of Heidelberg Erlangen, Germany Mannheim, Germany Carsten A. Bö ger MD Anita Hansen MD Department of Internal Medicine II Medical Faculty Nephrology Department of Nephrology University Medical Center Regensburg Heinrich-Heine University Dü sseldorf Regensburg, Germany Düsseldorf, Germany Martin Busch MD Christoph Hasslacher Consultant, Nephrologist and Lecturer Professor of Internal Medicine Department of Internal Medicine III Diabetesinstitut Heidelberg Jena University Hospital, Jena, Germany St. Josefskrankenhaus Heidelberg, Germany Christoph Daniel PhD Nephropathology, Department of Pathology Andrea Icks MD DPH MBA Universität Erlangen -Nürnberg Institute of Biometrics and Epidemiology Erlangen, Germany German Diabetes Center; Senior Lecturer Jörg D ötsch MD Department of Public Health Professor of Pediatrics Faculty of Medicine University Hospital of Cologne Heinrich-Heine University Department of Pediatric and Adolescent Düsseldorf, Germany Medicine Cologne, Germany Bethany Karl DO Nephrology Fellow Muriel A. Ghosn MD Center for Renal Translational Medicine Medical Chief Resident University of California Department of Internal Medicine CA, USA American University of Beirut Beirut, Lebanon vii Contributors Hermann J. Kissler MD Thomas Neumann MD Visceral Surgery Fellow Consultant Rheumatologist Department of General, Visceral and Department of Internal Medicine III Vascular Surgery Jena University Hospital Jena University Hospital Jena, Germany Jena, Germany Kai D. N üsken MD Helmut Kleinwechter MD Division of Pediatric Nephrology Specialist in Diabetology Department of Pediatric and Adolescent Diabetologikum Kiel Medicine Diabetes Center and Diabetes Education University Hospital of Cologne Center Cologne, Germany Kiel, Germany Ivo Quack MD Michael Koch MD Medical Faculty Head Department of Nephrology Center of Nephrology Mettmann, Germany; Heinrich-Heine University Dü sseldorf Clinic of Urology and Nephrology Düsseldorf, Germany, Niederberg Hospital Velbert, Germany Eberhard Ritz MD Gabriele Lehmann MD Professor of Nephrology Department of Internal Medicine III Department Internal Medicine Jena University Hospital Division of Nephrology Jena, Germany Nierenzentrum Carola Ruperto University Hospital Ivonne Loeffl er PhD Heidelberg, Germany Postdoctoral Research Fellow Department of Internal Medicine III Lars Christian Rump MD Jena University Hospital Professor of Medicine Jena, Germany Department of Nephrology Heinrich-Heine University Dü sseldorf Peter R. Mertens MD Düsseldorf, Germany Professor of Medicine Director Christiane Rü ster MD Department of Nephrology and Attending Physician, Nephrologist Hypertension, Diabetes and Endocrinology Department of Internal Medicine III Otto-von-Guericke University Magdeburg Jena University Hospital Magdeburg, Germany Jena, Germany Ulrich A. Mü ller MD MSc Alexander Sä mann MD Department of Medicine III Department of Medicine III Jena University Hospital Jena University Hospital Jena, Germany Jena, Germany viii Contributors Ute Sch äfer-Graf MD, PhD Christoph Wanner MD Specialist in Perinatology and Diabetology Professor of Medicine Berlin Diabetes and Pregnancy Center Department of Medicine Department of Gynecology and Obstetrics Division of Nephrology St. Joseph Hospital University of Wü rzburg Berlin, Germany Würzburg, Germany Utz Settmacher MD Fuad N. Ziyadeh MD FASN FACP Professor of Surgery Professor of Medicine and Biochemistry Chairman Chairman, Department of Internal Medicine Department of General, Visceral and American University of Beirut Vascular Surgery Beirut, Lebanon Jena University Hospital Jena, Germany Kumar Sharma MD FAHA Director Center for Renal Translational Medicine Professor of Medicine University of California CA, USA ix Preface In 1801 the English physician Erasmus Darwin more complex relationship between the kidney (1731–1802) recognized some patient with dia- and diabetes. All the contributors to this book betes whose urine could be coagulated by heat, are experts in their fi elds. It covers a wide range indicating proteinuria, and associated this of topics from epidemiology, pathophysiology fi nding with dropsy and general swelling. In and genetics to concrete treatment recommen- 1936, the seminal discovery by Kimmelstiel and dations and algorithms for the practicing physi- Wilson showed the morphologic changes by cian. Furthermore, the reader will also fi nd the description of glomerular lesions in diabet- chapters on topics normally not found in stand- ics with nephropathy. Today, diabetic renal ard books on diabetic nephropathy, such as disease is now worldwide the major cause of diabetic nephropathy in children, the relation- end-stage renal failure. Besides the uncountable ship between retinal and renal diabetic com- individual suffering of patients with diabetic plications and diabetes, bone, and the kidney. nephropathy, there is an increasing economical Therefore, the book is not only for the expert burden for such patients. Patients with diabetic nephrologists and diabetologists, but also for renal disease have a very high cardiovascular general internists and primary care physicians. morbidity and mortality. The spectrum of The authors have put an enormous amount of patients with diabetes and renal disease has work into this book. They would be happy if completely been changed: 25 year ago diabetic this contribution could help to better care for nephropathy was a feature of patients with type patients with diabetes and renal affections. 1 diabetes, type 2 diabetes was considered a rela- Many thanks to Wiley -Blackwell (especially Jen- tively rare even a “normal” process of aging. nifer Seward) for agreeing to start this ambigu- Now, the increasing pandemic of patients with ous projects and for the continuous help while type 2 diabetes makes this group the largest suf- carrying it out. fering from diabetic nephropathy, albeit the incidence of patients with type 1 diabetes has Professor Dr. Gunter Wolf MD, MHBA also increased in recent years. The current book Department of Internal Medicine III provides an up- to-date review of many aspects, University of Jena not only of diabetic nephropathy but of the Jena, Germany x Mesangial expansion and Glomerular basement hemodynamic changes membrane (GBM) Mesangial matrix Glomerulo- Tubular Mesangial cell sclerosis epithelial ceTllusbular basement VED and Hyper-permeability LUMEN membrane (TBM) ROS ECM Endothelial cell TGF-β1 Thickening of Foot processes GBM VEGF MCP1/Cytokines Thickening TUBULE Ang II of TBM Inflammation Podocyte Attenuated (glomerular epithelial cell) tubular reabsorption Podocyte pathology of albumin resident (effacement, apoptosis) fibroblast Tubuloepithelial hypertrophy EMT TGF-β1 Tubular atrophy Tubulointerstitial fibrosis Albuminuria ininnetr erglstoitimaelrular Progression of diabetic nephropaTutihbnyufllaominmteartsitoitnial ECM Masmt cyaeoclfltiibvraotbedlast Plate 4.1 Involvement of different renal cell types in pathogenesis of diabetic nephropathy (DN). Multiple factors contribute to the pathogenesis of DN. Via “crosstalking ” the glomerular cell types (mesangial cells, glomerular endothelial cells, and podocytes) are involved in thickening of the glomerular basement membrane and mesangial expansion as well as via upregulation of various mediators, such as transforming growth factor (TGF)- β1, vascular endothelial growth factor, angiotensin II, reactive oxygen species (ROS), and MCP -1, in glomerular infl ammation, glomerulosclerosis, and vascular endothelial dysfunction (VED). In addition to some of these glomerular changes and the pathology of podocytes, tubules also contribute to the development of albuminuria, a hallmark of DN. Increased extracellular matrix (ECM) production by the renal interstitial cell types (tubular cells, resident fi broblasts, activated myofi broblasts, and mast cells) leads to tubulointerstitial fi brosis, another characteristic feature of DN. See text for details.Reproduced from D’ Agati V, e t al. RAGE, glomerulosclerosis and proteinuria: roles in podocytes and endothelial cells.Trends Endocrinol Metab 2010; 21:50–6. Diabetes and Kidney Disease, First Edition. Edited by Gunter Wolf. © 2013 John Wiley & Sons, Ltd. Published 2013 by John Wiley & Sons, Ltd. Loss of epithelial adhesion Disruption of basement membrane adhesion molecules Induction of mesenchymal markers de novoα-SMA metastable cell synthesis Tubule Tubule Stress Cytokines Extracellular TGF-β1 Matrix basement MMP2 membrane TGF-β1 2) EMT epithelial cells 1) Proliferation resident fibroblast TGF-β1 Fibronectin Collagen I Blood Blood vessel vessel Collagen III 3) EndMT Loss of VE-cadherin and CD31 Induction of endothelial cells mesenchymal markers interstitial myofibroblast de novoα-SMA synthesis Tubulointerstitial 4) Infiltration of circulating bone fibrosis Blood marrow-derived fibrocytes vessel bone marrow-derived fibrocyte Plate 4.2 Hypothesis of progression of tubulointerstitial fi brosis by EMT and EndMT. Interstitial myofi broblasts responsible for synthesis of ECM and contribution to fi brosis have been proposed to be derived from more sources: (1) proliferation/activation of resident fi broblasts, (2) epithelial- to-mesenchymal transition (EMT), (3) endothelial-to-mesenchymal transition (EndMT), and/or (4) infi ltration of circulating bone marrow- derived fi bro- cytes. Initiated by external stimuli (e.g., hyperglycemia, cytokines, extracellular matrix) tubular or endothelial cells lose their cell- cell contacts and start to express mesenchymal markers (e.g. α -smooth muscle actin, vimentin) and undergo EMT and EndMT, respectively. The initially metastable cells, which coexpress tubular/endothelial and mesenchymal markers, disengage themselves from cell connective and transdifferentiate to interstitial myofi brob- lasts. These mesenchymal cells derived from epithelium or endothelium in the tubulointerstitium contribute to progression of DN. Modifi ed and supplemented according to Kizu A, e t al. Endothelial -mesenchymal transition as a novel mechanism for generating myofi broblasts during diabetic nephropathy. A m J Pathol 2009; 175:1371–3, and Barnes JL, e t al. Myofi broblast differentiation during fi brosis: role of NAD(P)H oxidases. K idney Int 2011;79:944–56.
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