The effect of hemodialysis on the transport of sodium in erythrocytes from chronic renal failure patients maintained on hemodialysis

Gambhir, Kanwal K.; Parui, Rabindranath; Agarwal, Vaibhav; Cruz, Iluminado A.

doi:10.1016/s0024-3205(02)01855-6

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Misconception #1: Erythropoietin (Epo) and Iron Deficiency A1

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Cited by 3 publications

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“…In HD patients, the RBC cell membrane is poorly deformable and lipid‐peroxidated (18). Many other changes in the composition of RBC membranes and intracellular machinery have been described in ESRD patients, involving Aquaphorin (AQP)‐1 (19), the Na + –K + pump hexokinase (20), lactate dehydrogenase, and adenosine triphosphate (21).…”

Section: Misconception #1: Erythropoietin (Epo) and Iron Deficiency Amentioning

confidence: 99%

Anemia and Iron Management

Besarab

2011

Seminars in Dialysis

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Section: Misconception #1: Erythropoietin (Epo) and Iron Deficiency Amentioning

confidence: 99%

Anemia and Iron Management

Besarab

2011

Seminars in Dialysis

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The biology of hemodialysis

Schmaldienst¹,

Hörl²

2004

Replacement of Renal Function by Dialysis

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Endogenous Cardiotonic Steroids in Kidney Failure: A Review and an Hypothesis

Hamlyn

Manunta

2015

Advances in Chronic Kidney Disease

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In response to progressive nephron loss, volume and humoral signals in the circulation have increasing relevance. These signals, including plasma sodium, angiotensin II and those related to volume status, activate a slow neuromodulatory pathway within the central nervous system (CNS). The slow CNS pathway includes specific receptors for angiotensin II, mineralocorticoids, and endogenous ouabain (EO). Stimulation of the pathway leads to elevated sympathetic nervous system activity (SNA) and increased circulating EO. The sustained elevation of circulating EO (or ouabain) stimulates central and peripheral mechanisms that amplify the impact of SNA on vascular tone. These include: changes in synaptic plasticity in the brain and sympathetic ganglia that increase preganglionic tone and amplify ganglionic transmission, amplification of the impact of SNA on arterial tone in the vascular wall, and the reprogramming of calcium signaling proteins in arterial myocytes. These increase SNA, raise basal and evoked arterial tone, and elevate blood pressure (BP). In the setting of chronic kidney disease, we suggest that sustained elevation of the slow CNS pathway, plasma EO and the cardiotonic steroid marinobufagenin (MBG), comprise a feed-forward system that raises BP and accelerates kidney and cardiac damage. Block of the slow CNS pathway and/or circulating EO and MBG may reduce BP and slow the progression to end stage renal disease.

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The effect of hemodialysis on the transport of sodium in erythrocytes from chronic renal failure patients maintained on hemodialysis

Cited by 3 publications

References 25 publications

Anemia and Iron Management

Anemia and Iron Management

The biology of hemodialysis

Endogenous Cardiotonic Steroids in Kidney Failure: A Review and an Hypothesis

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