By D. Silverberg

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This protective antieryptotic mechanism may ameliorate erythrocyte death in vivo, resulting in increased lifespan of circulating cells. 7. Conclusion The human red blood cell, by lacking nucleus or any other subcellular organelle, represents the final differentiation stage of the erythroid series. After a limited period in circulation, aged cells become sequestered and removed by macrophages from the reticuloendothelial system. This fate implies that erythrocyte life and death should be well regulated.

Change in hematocrit and risk of mortality. J Am Soc Nephrol. 1998;9(suppl A):204A. [142] Collins AJ, Li S, St Peter W, et al. Death, hospitalization, and economic associations among incident hemodialysis patients with hematocrit values of 36 to 39%. 2001;12: 2465-2473. [143] Collins A, Ma JZ, Ebben J, et al. Impact of hematocrit on morbidity and mortality. Semin Nephrol. 2000;20:345-349. [144] Eschbach JW, Abdulhadi MH, Browne JK, et al. Recombinant human erythropoietin in anemic patients with end-stage renal disease: results of a phase III multicenter clinical trial.

32 Anemia Considering that senescence represents the time-dependent induction of erythrocyte selfdestruction process, premature cell death due to proeryptotic factors could greatly contribute to the development of anemia. Energy depletion, oxidative stress, and osmotic shock are the most common events that can produce erythrocyte damage, leading to premature eryptosis (Fig. 2). The common feature is the increased intracellular calcium concentration due to either calcium channel activation or depressed calcium pump.

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