摘要: The body's resistance to the actions of insulin (type II diabetes defect) results in compensatory increased production and secretion by pancreas leads hyperinsulinemia order maintain euglycemia. When cannot be adequately I overcome maintaining glucose homeostasis, hyperglycemia intolerance ensues. Insulin has been well recognized patients with advanced chronic kidney diseases (CKD). etiology may involve uremic toxins from protein catabolism, vitamin D deficiency, metabolic acidosis, anemia, poor physical fitness, inflammation, cachexia. Glucose abnormalities nondiabetic CKD are implicated pathogenesis hyperlipidemia represent important risk factors for accelerated atherosclerosis these patients. inadequacy associated growth retardation adolescents CKD. Normal demonstrate an increase as they go into puberty. It seems that puberty spurt both normal health renal failure require one its hormonal requirements. Finally, Whether is antecedent or a consequence impaired function subject debate. goal this review was provide update literature on pathophysiology CKD, current understanding mechanisms, epidemiological association