The iron metabolism is regulated by Hepcidin, a hormone synthesized in the liver, and the inflammatory condition, present in the uremia, stimulates its production. Hepcidin regulates the absorption of iron in the diet and recycled iron from senescent erythrocytes, exerting its function related to the ferroportin protein found in all cells involved in iron homeostasis. Ferroportin is crucial for cellular iron export and is the only iron efflux mechanism. The expression of ferroportin is increased in iron deficiency and hypoxia. (Babitt, 2010; Grotto, 2010). Hepcidin binds to ferroportin, causing its internalization and degradation and in turn affecting the release of iron for hemoglobin synthesis. In patients with CKD, there is an accumulation of
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The presence of serum ferritin lower than 30mg / dl is indicative of iron deficiency and predictive of absence of iron stores in the bone marrow. However, serum ferritin greater than 30mg / dl does not necessarily indicate adequate iron stores in the bone marrow. (KDIGO, 2012). For patients with CKD, serum ferritin levels greater than 100 mg / dl are considered sufficient and ideal, above 300mg / dl (KDIGO, 2012).
KDIGO recommends using iron supplementation to maintain ferritin levels greater than 200 mg / dl for patients on hemodialysis, greater than 100 mg / dl for those not on dialysis or peritoneal dialysis, and for all, transferrin saturation above 20% . (KDIGO, 2012)
The human body has no specific mechanism for eliminating excess iron absorbed or accumulated after macrophage recycling. This excess is usually eliminated by bodily secretions, desquamation of intestinal and epidermal cells or menstrual bleeding. Hence, iron replacement in situations in which ferritin > 500 and transferrin saturation > 30% lead to the risk of iron overload in the parenchyma tissue. (Babitt et al., 2010; Grotto, 2010; KDIGO,
The presence of serum ferritin lower than 30mg / dl is indicative of iron deficiency and predictive of absence of iron stores in the bone marrow. However, serum ferritin greater than 30mg / dl does not necessarily indicate adequate iron stores in the bone marrow. (KDIGO, 2012). For patients with CKD, serum ferritin levels greater than 100 mg / dl are considered sufficient and ideal, above 300mg / dl (KDIGO, 2012).
KDIGO recommends using iron supplementation to maintain ferritin levels greater than 200 mg / dl for patients on hemodialysis, greater than 100 mg / dl for those not on dialysis or peritoneal dialysis, and for all, transferrin saturation above 20% . (KDIGO, 2012)
The human body has no specific mechanism for eliminating excess iron absorbed or accumulated after macrophage recycling. This excess is usually eliminated by bodily secretions, desquamation of intestinal and epidermal cells or menstrual bleeding. Hence, iron replacement in situations in which ferritin > 500 and transferrin saturation > 30% lead to the risk of iron overload in the parenchyma tissue. (Babitt et al., 2010; Grotto, 2010; KDIGO,