TY - JOUR

T1 - Alterations in Erythrocyte Deformability and Functions Associated with End-Stage Renal Disease

AU - Sudnitsyna, J. S.

AU - Skverchinskaya, E. A.

AU - Zubina, I. M.

AU - Suglobova, E. D.

AU - Vlasov, T. D.

AU - Smirnov , A. V.

AU - Vasiliev, A. N.

AU - Ruzhnikova, T. O.

AU - Kaljuzhnyi, B. A.

AU - Mindukshev, I. V.

AU - Borisov, Yu. A.

N1 - Publisher Copyright: © 2022, Pleiades Publishing, Ltd.

PY - 2022/3

Y1 - 2022/3

N2 - End-stage renal disease (ESRD) is associated with a variety of erythron alterations including structural and functional changes in circulating erythrocytes (RBCs), which are potential risk factors to cause RBC malfunctions and corresponding anemia of different severity. However, the mechanisms of such changes in RBCs remain understudied. Here we used flow cytometry to estimate intracellular esterase activity, phosphatidylserine externalization, and reticulocyte count and state, laser diffraction for osmotic and ammonium stress tests, and spectrophotometry to evaluate the generation of unstable hemoglobin (Hb) forms in RBCs of patients with ESRD before and after the hemodialysis (HD) session. RBCs in ESRD were more osmotically fragile and had an increased swelling rate in the ammonium stress test. HD did not affect RBC deformability but led to Hb oxidation to ferryl forms and triggered such apoptosis-like events, as a decrease in intracellular esterase activity and an increase in the number of annexin-V-positive cells. Our data indicate that uremic syndrome, combined with the mechanical and chemical effects of HD therapy, challenges the erythron of HD patients and contributes to a multifactorial decrease in RBC function and aggravation of renal anemia.

AB - End-stage renal disease (ESRD) is associated with a variety of erythron alterations including structural and functional changes in circulating erythrocytes (RBCs), which are potential risk factors to cause RBC malfunctions and corresponding anemia of different severity. However, the mechanisms of such changes in RBCs remain understudied. Here we used flow cytometry to estimate intracellular esterase activity, phosphatidylserine externalization, and reticulocyte count and state, laser diffraction for osmotic and ammonium stress tests, and spectrophotometry to evaluate the generation of unstable hemoglobin (Hb) forms in RBCs of patients with ESRD before and after the hemodialysis (HD) session. RBCs in ESRD were more osmotically fragile and had an increased swelling rate in the ammonium stress test. HD did not affect RBC deformability but led to Hb oxidation to ferryl forms and triggered such apoptosis-like events, as a decrease in intracellular esterase activity and an increase in the number of annexin-V-positive cells. Our data indicate that uremic syndrome, combined with the mechanical and chemical effects of HD therapy, challenges the erythron of HD patients and contributes to a multifactorial decrease in RBC function and aggravation of renal anemia.

KW - erythrocytes

KW - end-stage renal disease (ESRD)

KW - oxidative stress

KW - Ammonium stress

KW - osmotic fragility test

KW - ammonium stress

KW - HEMOGLOBIN

KW - OXIDATIVE STRESS

KW - MECHANISM

KW - UREMIC TOXINS

KW - AMMONIUM

KW - TRANSPORT

KW - RED-BLOOD-CELLS

KW - ANEMIA

KW - CHRONIC KIDNEY-DISEASE

KW - MODULATION

UR - http://www.scopus.com/inward/record.url?scp=85124967369&partnerID=8YFLogxK

UR - https://www.mendeley.com/catalogue/98725c53-5e4f-3614-a599-f40635e5b267/

U2 - 10.1134/s1990747821060118

DO - 10.1134/s1990747821060118

M3 - Article

VL - 16

SP - 79

EP - 90

JO - Biochemistry (Moscow) Supplement Series A: Membrane and Cell Biology

JF - Biochemistry (Moscow) Supplement Series A: Membrane and Cell Biology

SN - 1990-7478

IS - 1

ER -