A Practical Approach to the Anaemia of Chronic Kidney Disease: A Mini Review

Abstract

Anaemia is a common complication in chronic kidney disease (CKD) patients. It has a complicated pathophysiology and its management is equally challenging. It is mainly due to impaired erythropoiesis, decreased production of erythropoietin and dysregulated iron metabolism. The primary mechanism of anaemia of CKD and ESRD involves decreased erythropoietin production, decreased gastrointestinal absorption of iron, and decreased life span of red blood cells). It also involves iron and hepcidin dysregulation, chronic inflammation, bone marrow dysfunction, reduced life span of red cells and vitamin B12 or folic acid deficiencies. Another mechanism for anaemia of chronic illness involves cytokines, such as interleukins (IL-1 and IL-6) and tumor necrosis factor (TNF-alpha). These are believed to cause the destruction of RBC precursors and decrease the number of erythropoietin receptors on progenitor cells. Iron deficiency is common in the patients of CKD. It is estimated that the patients on hemodialysis may lose more than 2200 mg of iron per year due to these factors. The disease severity increases with progression of CKD and it is a predictor of adverse outcome including cardiovascular events and mortality. The treatment strategies involve iron supplementation and eryropoeitin stimulating agents (ESAs). The novel therapeutic option such as HIF-poly hydroxylase inhibitors (HIF-PHIs) are emerging as promising interventions. These novel agents target the hypoxia-inducible factor (HIF) pathway to stimulate endogenous EPO production and improve iron utilization.