Catálogo de publicaciones - libros

Compartir en
redes sociales


Calcium and Phosphate Metabolism Management in Chronic Renal Disease

Chen Hsing Hsu (eds.)

Resumen/Descripción – provisto por la editorial

No disponible.

Palabras clave – provistas por la editorial

Nephrology; Orthopedics; Endocrinology

Disponibilidad
Institución detectada Año de publicación Navegá Descargá Solicitá
No detectada 2006 SpringerLink

Información

Tipo de recurso:

libros

ISBN impreso

978-0-387-33369-4

ISBN electrónico

978-0-387-33370-0

Editor responsable

Springer Nature

País de edición

Reino Unido

Fecha de publicación

Información sobre derechos de publicación

© Springer Science+Business Media, LLC 2006

Tabla de contenidos

Historical Perspective of Calcium Management in Patients with Chronic Renal Diseases

Chen Hsing Hsu

P is a key ion in the body, with important diverse functions. The maintenance of serum P levels is dependent on normal kidney function. As a result, patients with kidney disease are often hyperphosphatemic. Elevations in serum P are associated with increased morbidity and mortality in patients with CKD, may hasten loss of residual renal function, and can cause secondary hyperparathyroidism. Unfortunately, current removal of P with thrice weekly hemodialysis or daily peritoneal dialysis is not adequate for normal dietary intake. As a result, phosphate binders are a mainstay of therapy in patients with CKD.

Pp. 1-11

Disorders of Phosphorous Homeostasis in CKD

Sharon M. Moe

P is a key ion in the body, with important diverse functions. The maintenance of serum P levels is dependent on normal kidney function. As a result, patients with kidney disease are often hyperphosphatemic. Elevations in serum P are associated with increased morbidity and mortality in patients with CKD, may hasten loss of residual renal function, and can cause secondary hyperparathyroidism. Unfortunately, current removal of P with thrice weekly hemodialysis or daily peritoneal dialysis is not adequate for normal dietary intake. As a result, phosphate binders are a mainstay of therapy in patients with CKD.

Pp. 13-28

Pathogenesis and Management of Secondary Hyperparathyroidism

Krishna R. Polu; Ajay K. Singh

Secondary hyperparathyroidism is a universal complication in patients with CKD and occurs early in the development of renal failure. As GFR declines, reduction in serum calcitriol levels, moderate decreases in ionized calcium, and reduced excretion of serum phosphorus contribute to the development of SHPT. Traditional approaches in the treatment of SHPT have focused on phosphorus control, through dietary phosphate restriction, calcium and non-calcium-based phosphate binders, and vitamin D sterols. In cases of severe hyperaparathy-roidism resistant to traditional therapies, parathyroidectomy was the treatment of choice. However, now with the introduction of the calcimimetic agent cinacalcet, additional medical therapy is available as an alternative to surgery. The importance of controlling PTH, serum phosphorus, and calcium goes beyond treatment of bone disease and may have a significant impact on other organ systems and ultimately cardiovascular morbidity and mortality. Prospective, randomized trials to test the value of vitamin D therapies and calcimimetics in reducing cardiovascular and all-cause mortality need to be pursued.

Pp. 29-70

Uremic Toxins in Chronic Renal Failure

Griet Glorieux; Eva Schepers; Raymond Camille Vanholder

P is a key ion in the body, with important diverse functions. The maintenance of serum P levels is dependent on normal kidney function. As a result, patients with kidney disease are often hyperphosphatemic. Elevations in serum P are associated with increased morbidity and mortality in patients with CKD, may hasten loss of residual renal function, and can cause secondary hyperparathyroidism. Unfortunately, current removal of P with thrice weekly hemodialysis or daily peritoneal dialysis is not adequate for normal dietary intake. As a result, phosphate binders are a mainstay of therapy in patients with CKD.

Pp. 71-103

Calcitriol Metabolism and Action in Chronic Renal Disease

Chen Hsing Hsu

P is a key ion in the body, with important diverse functions. The maintenance of serum P levels is dependent on normal kidney function. As a result, patients with kidney disease are often hyperphosphatemic. Elevations in serum P are associated with increased morbidity and mortality in patients with CKD, may hasten loss of residual renal function, and can cause secondary hyperparathyroidism. Unfortunately, current removal of P with thrice weekly hemodialysis or daily peritoneal dialysis is not adequate for normal dietary intake. As a result, phosphate binders are a mainstay of therapy in patients with CKD.

Pp. 105-130

Renal Osteodystrophy

Eric W. Young

P is a key ion in the body, with important diverse functions. The maintenance of serum P levels is dependent on normal kidney function. As a result, patients with kidney disease are often hyperphosphatemic. Elevations in serum P are associated with increased morbidity and mortality in patients with CKD, may hasten loss of residual renal function, and can cause secondary hyperparathyroidism. Unfortunately, current removal of P with thrice weekly hemodialysis or daily peritoneal dialysis is not adequate for normal dietary intake. As a result, phosphate binders are a mainstay of therapy in patients with CKD.

Pp. 131-139

Nephrolithiasis

Melissa A. Cadnapaphornchai; Pravit Cadnapaphornchai

P is a key ion in the body, with important diverse functions. The maintenance of serum P levels is dependent on normal kidney function. As a result, patients with kidney disease are often hyperphosphatemic. Elevations in serum P are associated with increased morbidity and mortality in patients with CKD, may hasten loss of residual renal function, and can cause secondary hyperparathyroidism. Unfortunately, current removal of P with thrice weekly hemodialysis or daily peritoneal dialysis is not adequate for normal dietary intake. As a result, phosphate binders are a mainstay of therapy in patients with CKD.

Pp. 141-178