This volume is the first of a biannual series entitled Contemporary Nephrology. The series intends to provide the reader with a broad, authoritative review of the important developments that have occurred during the previous two years in the major areas of both basic and clinical nephrology. We have been fortunate to enlist a distinguished group of scientists, teachers, and clinicians to serve as members of the Editorial Board of this series. We are grateful to them for the outstand ing contributions they have made to this first volume of Contemporary Nephrology. This volume has fifteen chapters. The first four chapters deal with more basic aspects of nephrology: Membrane Transport (Schafer); Renal Physiology (Knox and Spielman); Renal Metabolism (School werth); and Renal Prostaglandins (Dunn). Chapters 5-10 are more pathophysiologically oriented, and each contains an "appropriate mix" of basic and clinical information. This group of chapters includes Acid-Base Physiology and Pathophysiology (Arruda and Kurtzman); Mineral Metabolism in Health and Disease (Agus, Goldfarb, and Was serstein); Hypertension and the Renin-Angiotensin-Aldosterone Axis (Williams and Hollenberg); Immunologically Mediated Renal Disease (Glassock); Acute Renal Failure and Toxic Nephropathy (Anderson and Gross); and the Kidney in Systemic Disease (Martinez-Maldonado). The last five chapters, which are more clinically oriented, include Uremia (Friedman and Lundin); Nutrition in Renal Disease (Mitch); Dialysis (Maher); Renal Transplantation (Strom); and, finally, Drugs and the Kidney (Bennett).
Shaul G. Massry Division of Nephrology, The University of Southern California, School of Medicine Los Angeles, California In the last two decades evidence has accumulated indicating that parathyroid hormone may exert a multitude of effects on many cells and a variety of organs beyond its classical targets: the kidney and the bone. These efforts have been spearheaded by nephrologists. The interest of this group of clinicians-scientists stems from the fact that patients with renal failure have secondary hyperparathyroidism and markedly elevated blood levels of PTH (1,2). If this hormone does act on various organs, it becomes plausible that excess blood levels of PTH may be harmful in these patients. Indeed, in an Editorial published in 1977, Massry suggested that the elevated blood levels of PTH in patients with renal failure may exert deleterious effects on many systems and as such may participate in the genesis of many of the manifestations of the uremic syndrome (3). Thus, the essence of the Massry hypothesis is the notion that PTH may act as a major uremic toxin. The search for uremic toxins did not yield successful results. In the last three decades many compounds have been implicated as uremic toxins. However, a cause and effect relationship between these compounds and the manifestations of the uremic syndrome has not been established in most cases.
Shaul G. Massry Division of Nephrology, The University of Southern California, School of Medicine Los Angeles, California In the last two decades evidence has accumulated indicating that parathyroid hormone may exert a multitude of effects on many cells and a variety of organs beyond its classical targets: the kidney and the bone. These efforts have been spearheaded by nephrologists. The interest of this group of clinicians-scientists stems from the fact that patients with renal failure have secondary hyperparathyroidism and markedly elevated blood levels of PTH (1,2). If this hormone does act on various organs, it becomes plausible that excess blood levels of PTH may be harmful in these patients. Indeed, in an Editorial published in 1977, Massry suggested that the elevated blood levels of PTH in patients with renal failure may exert deleterious effects on many systems and as such may participate in the genesis of many of the manifestations of the uremic syndrome (3). Thus, the essence of the Massry hypothesis is the notion that PTH may act as a major uremic toxin. The search for uremic toxins did not yield successful results. In the last three decades many compounds have been implicated as uremic toxins. However, a cause and effect relationship between these compounds and the manifestations of the uremic syndrome has not been established in most cases.
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