Pathogenesis and Treatment in IgA Nephropathy
- 342pagine
- 12 ore di lettura




Primary IgA nephropathy, identified nearly 40 years ago, is an immune-complex-mediated glomerulonephritis marked by granular deposits of IgA (primarily IgA1) and C3 in the glomerular mesangial areas. This condition is characterized by proliferative changes in glomerular mesangial cells and an increase in mesangial matrices. It ranks as one of the most prevalent forms of chronic glomerulonephritis and is a leading cause of end-stage renal disease. Despite ongoing research clarifying various aspects of its pathogenesis, no specific treatment is currently available. This publication features contributions from international nephrologists and basic scientists, presenting the latest findings on IgA nephropathy. It begins with clinical reviews covering topics like clinico-pathological classification, novel treatment strategies, and the significance of renal biopsies. The focus then transitions to basic reviews discussing candidate genes, the role of IgA receptors, and immune complex formation. The second part of the book provides updates on clinical and basic advances, including the impact of obesity and various therapeutic approaches. This comprehensive resource offers valuable insights for nephrologists, general practitioners, residents, and interns seeking to understand this complex disease.
Type-2 diabetic nephropathy is one of the major long-term microvascular complications occurring in nearly 40% of diabetic patients in Japan. The purpose of this book is to review recent work on the genetic background, pathogenesis and treatment of this disorder and to provide the most up-to-date findings on these subjects in Japan. The pathogenesis of diabetic nephropathy includes both metabolic and / or hemodynamic factors, as well as renal hypertrophy. Hyperglycemia is necessary, but not sufficient, for its initiation and progression: The toxicity of persistent hyperglycemia results from glucose overutilization and multiple secondary effects. Moreover, diabetic nephropathy is generally considered to alter the chemical composition of the glomerular basement membrane and mesangium. At present, it is supposed that the increases in extracellular matrix accumulation due to TGF-beta activation might be related to the glomerular sclerosis in diabetic nephropathy. Although large numbers of candidate genes have been analyzed, those related to initiation and progression are still obscure in patients with type-2 diabetic nephropathy. Presenting clinical findings and issues related to laboratory analysis, this book will be of interest for nephrologists, diabetologists, pathologists, biochemists, general physicians and residents.
Research on renal diseases is progressing at a rapid pace, bringing with it a major change in the research techniques used: There has been a shift from urine and blood analysis or histological examinations by light microscopy to immunohistochemical assays at the protein levels, and studies are now being performed at the molecular and gene levels.