Part I. Pathogenesis -- Chapter 1. Is IgA nephropathy the same disease/a homogenous disease? -- Chapter 2. Genetic variations of IgA nephropathy -- Chapter 3. Is IgA nephropathy a familial or sporadic disease? -- Chapter 4. Heterogeneity of GdIgA1 -- Chapter 5. Differences of histological classification between the Japanese guideline and the Oxford classification -- Chapter 6. Podocyte injury and the role of megalin -- Chapter 7. Complement activation -- Part II. Treatment -- Chapter 8. How different are the current understandings of treatments for IgA nephropathy? -- Chapter 9. Differences in etiology and treatment in China -- Chapter 10. Differences in etiology and treatment in Korea -- Chapter 11. Differences in etiology and treatment in Japan -- Chapter 12. The VALIGA study: Differences in treatment approaches within the EU -- Chapter 13. Differences in etiology and treatment in Scandinavian countries -- Chapter14 The Implication of the KDIGO Clinical Practice Guidelines on management of IgA Nephropathy -- Chapter15 Japanese Clinical Practice Guidelines for IgA Nephropathy: Difference from KDIGO Guidelines -- Chapter16 Limitations of RAS blockade in IgA nephropathy -- Chapter17 What is the goal for proteinuria in IgA nephropathy? -- Chapter 18. Rationale of tonsillectomy and steroid pulse therapy (TSP): Is it race dependent? -- Chapter 19. Is tonsillectomy a possible treatment for IgA nephropathy from RCT? -- Chapter 20. Is tonsillectomy a possible treatment for IgA nephrology from a retrospective analysis?.

This book discusses the latest findings on the pathogenesis and treatment of IgA nephropathy. It particularly focuses on recently recognized initiation and progression factors and the varying treatment strategies in different regions, such as Asia, Europe, and the United States. More than 40 years have passed since Dr. Jean Berger first described primary IgA nephropathy (“Nephropathy with mesangial IgA-IgG deposits”) as a new disease entity. Immunohistopathologically, IgA nephropathy is characterized by the granular deposition of IgA (IgA1) and C3 in the glomerular mesangial areas with mesangial cell proliferation and the expansion of mesangial matrices. It is clear that IgA nephropathy is one of the most common types of chronic glomerulonephritis in the world. This disease may lead to end-stage kidney disease, with its enormous economic impact on healthcare everywhere. Efforts by many investigators around the world have gradually clarified various aspects of the pathogenesis and treatment of IgA nephropathy. However, there are many controversial strategies for the treatment of patients with IgA nephropathy throughout the world, as there are several limitations for treatment in each country. This volume provides nephrologists everywhere with an overview and comparison of both global and regional findings in basic and clinical fields in IgA nephropathy. It covers genetic variation, aberrant IgA1 production, and classification etiology, guidelines, and treatment goals, with all chapters written by top international researchers.