Metabolism of Red Blood Cells in Chronic Renal Failure

Dear Colleagues,

In the 1960s, it was discovered that one of the reasons for the development of anemia in chronic kidney disease patients is the shortening of the life of the red blood cell (RBC). Concurrent observations over the next few years demonstrated that the lifespan of uremic erythrocytes is usually half of their physiological longevity.

Red blood cell homeostasis requires multi-level intra- and extracellular regulation to preserve the role of this unit of the organism. It is necessary to continuously supply energy, i.e., to maintain a sufficiently high concentration of ATP and energy charge within the cell. The level of cytoplasmic ATP and "energy chargé" of erythrocytes is not solely determined by the rate of synthesis in the process of anaerobic glycolysis or the reutilization of adenylate nucleotides; the rate of ATPe breakdown and release outside the cell is also important. It is believed that the type of cell death (necrosis or eryptosis) is associated with changes, e.g., in the "red-ox" system, the concentration of intracellular ATP and calcium cations, as well as the activation of several calcium-dependent enzymes necessary for the organization of the membrane structure and the RBC cytoskeleton. Additionally, studies on intracellular calcium homeostasis in CKD patients emphasize the important role of the energy-dependent PMCA calcium pump (mainly the type 4b isoform) anchored in the plasma membrane and involved in the physiological ejection ("exflux") of Ca²⁺ outside the erythrocyte.

This Special Issue is dedicated to the molecular mechanisms in the uremic erythrocyte responsible for the development of anemia in chronic kidney disease. We are seeking original research and reviews which will not only broaden our knowledge in this field, but will also be helpful in understanding how uremic red blood cell metabolism is modeled by :

• Erythropoietin and hypoxia—key incentives for survival, proliferation and differentiation of red blood cells;
• Total and/or functional iron deficiency;
• Inflammation, increased levels of hepcidin;
• Neocytolysis;
• Factors inside and outside the cellular determination process of eryptosis;
• Other changes in metabolic pathways that are worthy of further analysis.

Dr. Dorota Polak-Jonkisz
Dr. Leszek Purzyc
Guest Editors

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