الفهرس 
Introduction
The pronephros (for kidneys)Only 14 pages are availabe for public view
 |  | from | 104 |  |  |
| | | from | 104 | | |
Abstract
ENDOCRINE ABNORMALITIES IN CHILDREN WITH CHRONIC RENAL FAILURE
Chronic kidney disease is a worldwide public health problem with an increasing incidence and prevalence, poor outcomes, and high cost. Outcomes of chronic kidney disease include complications of decreased kidney function, cardiovascular disease as heart failure and endocrine complications current evidence suggests that some of these adverse outcomes can be prevented or delayed by early detection and treatment of children suffer from CDK.
Chronic kidney disease is defined as either kidney damage or decreased kidney function (decreased GFR) for 3 or more months or glomerular filtration rate (GFR) less than 60ml/min/1.73m2 for 3 months or more) The current definition of CKD encompasses all of the patients who were classified as having chronic renal failure (CRF) and chronic renal insufficiency.
The chief causes of chronic kidney disease in children include the following: Obstructive uropathy, hypoplastic or dysplastic kidneys, reflux nephropathy, focal segmental glomerulosclerosis as a variant of childhood nephritic syndrome, polycystic kidney disease.
Uremia interferes with metabolism and regulation of hormones by various mechanisms. Disturbed endocrine function may arise either from: Inappropriate circulating hormone concentrations and/or, from altered hormone action at the target tissue level.
Growth Hormone: Fasting GH concentrations are variably elevated in uremic children depending on the extent of renal failure. The kidney is a major site of GH degradation. In patients with end-stage renal failure, the metabolic clearance rate of GH is reduced by approximately 50%.
Untreated CRF during early infancy is usually associated with severe growth retardation. Etiology of Growth Failure in Chronic Renal Failure One of the reasons for this growth failure centers on vitamin D, Anutrient that is activated by the kidneys. Activated vitamin D helps the body absorb calcium from foods, and also helps the bones absorb the right amount of calcium that will enable them to grow. When the kidneys are impaired, they are unable to activate vitamin D, and the bones cannot get enough calcium. Consequently, the growth process is interrupted. It’s easy to see how poor nutrition can also contribute to growth failure in young people with CRI. (Guyton Textbook of Medical Physiology 9th edition, WB Saunders, 2008)
Renal Osteodystrophy: Severe metaphyseal skeletal changes are often detected radiologically in patients with chronic renal insufficiency (CRI) and may lead to growth retardation and osseous deformities if left untreated during the critical years of skeletal growth and development. As the longevity of children with CRI increases because of advances in medical management, dialysis, and renal transplantation, the prevention and treatment of renal osteodystrophy should remain a major component in the overall management of these children.
Thyroid Hormone: The thyroid hormone axis plays an important role in the regulation of tissue metabolism. Throughout childhood, thyroid hormone is involved in growth and skeletal maturation, stimulating both cartilage proliferation and epiphyseal differentiation. The plasma levels of total T4 (thyroxin) and T3 (triiodothyronine) are decreased in patients with CRF. Significant depression of T4 and T3 levels usually occurs once the GFR falls below 50%.
Adrenal Androgens: Low plasma levels of dehydroepiandrosterone and dehydroepiandrosterone sulfate, the marker hormones of the zona reticularis, are observed pre- and midpubertal boys on hemodialysis, whereas normal levels are found in patients on conservative treatment. Conversely, levels of androstenedione, an adrenal androgen produced by the ACTH-dependent zona fasciculata, are elevatedxx in patients on conservative treatment, and normal or elevated in hemodialysis patients. A similar elevation of androstenedione level is observed in girls with CRF.
Gonadal Hormones: The onset of puberty is usually delayed in adolescents CRF. In prepubertal children with predialytic renal failure, low total and free testoosterone and dihydrotestosterone (DHT) plasma concentrations have been reported.
Gonadotropins: Plasma LH levels are high normal or elevated in prepubertal and pubertal boys and girls with CRF; follicle-stimulating hormone (FSH) concentrations are also usually elevated in children with CRF. After transplantation, LH levels usually return to normal, whereas plasma FSH frequently remains elevated.
Cortisol: Although normal morning fasting cortisol levels are found in the majority of pediatric patients with CRF 24-hour, integrated mean total and free cortisol concentrations are consistently elevated.
Prolactin: Plasma prolactin levels are elevated in pubertal girls with CRF. Hyperprolactinemia may play a role in the pathogenesis of uremic hypogonadism.
Insulin: Uremia is typically associated with impaired glucose metabolism. Some patients have hyperglycemia in response to oral and intravenous glucose loads, while others are able to maintain normoglycemia by raising plasma insulin levels. Impaired tissue sensitivity to insulin occurs in almost all uremic subjects and is largely responsible for the abnormal glucose metabolism.
Glucagon: Glucagon plasma levels are markedly increased in uremia. This increase is entirely due to decreased metabolic clearance; secretion is normal.
The aim of the article: The definition and classification of chronic renal disease and associated complications may help identify affected individuals possibly resulting in the early detection of endocrine effective therapy which may improve their native kidney function and improve their long-term health.