Erythrocyte Sodium Sensitivity and Eryptosis in Chronic Hemodialysis Patients

Meyring-Wösten, Anna; Kuntsevich, Viktoriya; Campos, Israel; Williams, Schantel; Ma, Jie; Patel, Samir S.; Ornillo, Chiarra; Thijssen, Stephan; Kotanko, Peter

doi:10.1159/000477608

Cited by 9 publications

(6 citation statements)

References 73 publications

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“…ESA in HD and 4583 I.U. ESA in PD), remained anemic with hemoglobin levels of 10.07 g·dL −1 (HD) and 10.89 g·dL −1 (PD), indicating that anemia is a major complication in CKD . Mounting evidence for a decreased erythrocyte survival in CKD is provided by additional studies .…”

Section: Clinical Conditions Stimulating Eryptosis By Generation Of Omentioning

confidence: 96%

Oxidative stress, eryptosis and anemia: a pivotal mechanistic nexus in systemic diseases

et al. 2018

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The average lifespan of circulating erythrocytes usually exceeds hundred days. Prior to that, however, erythrocytes may be exposed to oxidative stress in the circulation which could cause injury and trigger their suicidal death or eryptosis. Oxidative stress activates Ca -permeable nonselective cation channels in the cell membrane, thus, stimulating Ca entry and subsequent cell membrane scrambling resulting in phosphatidylserine exposure and activation of Ca -sensitive K channels leading to K exit, hyperpolarization, Cl exit, and ultimately cell shrinkage due to loss of KCl and osmotically driven water. While the mechanistic link between oxidative stress and anemia remains ill-defined, several diseases such as diabetes, hepatic failure, malignancy, chronic kidney disease and inflammation have been identified to display both increased oxidative stress as well as eryptosis. Recent compelling evidence suggests that oxidative stress is an important perpetrator in accelerating erythrocyte loss in different systemic conditions and an underlying mechanism for anemia associated with these pathological states. In the present review, we discuss the role of oxidative stress in reducing erythrocyte survival and provide novel insights into the possible use of antioxidants as putative antieryptotic and antianemic agents in a variety of systemic diseases.

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Section: Clinical Conditions Stimulating Eryptosis By Generation Of Omentioning

confidence: 96%

Oxidative stress, eryptosis and anemia: a pivotal mechanistic nexus in systemic diseases

et al. 2018

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“…Accordingly, similar changes in the RBC phenotype of DM patients can be surmised in concomitant conditions such as hypertension and patients with dyslipidemia [ 109 , 125 , 126 ]. Chronic renal failure can aggravate RBC cell death in DM, as uremia and proteinuria have been shown to reduce RBC survival in multiple studies [ 64 , 127 , 128 , 129 , 130 , 131 , 132 ]. Dialysis treatment may further impact RBC survival within DM patients [ 130 , 133 , 134 ].…”

Section: Multifactorial Mechanisms Explaining Shortened Rbc Lifespan ...mentioning

confidence: 99%

“…Chronic renal failure can aggravate RBC cell death in DM, as uremia and proteinuria have been shown to reduce RBC survival in multiple studies [ 64 , 127 , 128 , 129 , 130 , 131 , 132 ]. Dialysis treatment may further impact RBC survival within DM patients [ 130 , 133 , 134 ]. In a previous study, chronic kidney disease was shown to enhance oxidative imbalance and PS exposure in RBCs drawn from T2D patients [ 135 ].…”

Section: Multifactorial Mechanisms Explaining Shortened Rbc Lifespan ...mentioning

confidence: 99%

Pathophysiology of Red Blood Cell Dysfunction in Diabetes and Its Complications

et al. 2023

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Diabetes Mellitus (DM) is a complex metabolic disorder associated with multiple microvascular complications leading to nephropathy, retinopathy, and neuropathy. Mounting evidence suggests that red blood cell (RBC) alterations are both a cause and consequence of disturbances related to DM-associated complications. Importantly, a significant proportion of DM patients develop varying degrees of anemia of confounding etiology, leading to increased morbidity. In chronic hyperglycemia, RBCs display morphological, enzymatic, and biophysical changes, which in turn prime them for swift phagocytic clearance from circulation. A multitude of endogenous factors, such as oxidative and dicarbonyl stress, uremic toxins, extracellular hypertonicity, sorbitol accumulation, and deranged nitric oxide metabolism, have been implicated in pathological RBC changes in DM. This review collates clinical laboratory findings of changes in hematology indices in DM patients and discusses recent reports on the putative mechanisms underpinning shortened RBC survival and disturbed cell membrane architecture within the diabetic milieu. Specifically, RBC cell death signaling, RBC metabolism, procoagulant RBC phenotype, RBC-triggered endothelial cell dysfunction, and changes in RBC deformability and aggregation in the context of DM are discussed. Understanding the mechanisms of RBC alterations in DM provides valuable insights into the clinical significance of the crosstalk between RBCs and microangiopathy in DM.

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“…The question whether the HD therapy ameliorates or triggers eryptosis remains controversial. Results suggesting both an increase (Abed et al, 2014) and a reduction (Meyring-Wösten et al, 2017) of PS exposure post HD session were reported.…”

Section: Eryptosis Pathways: Overviewmentioning

confidence: 93%

The Role of Eryptosis in the Pathogenesis of Renal Anemia: Insights From Basic Research and Mathematical Modeling

Dias

Grobe

Rogg

et al. 2020

Front. Cell Dev. Biol.

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Red blood cells (RBC) are the most abundant cells in the blood. Despite powerful defense systems against chemical and mechanical stressors, their life span is limited to about 120 days in healthy humans and further shortened in patients with kidney failure. Changes in the cell membrane potential and cation permeability trigger a cascade of events that lead to exposure of phosphatidylserine on the outer leaflet of the RBC membrane. The translocation of phosphatidylserine is an important step in a process that eventually results in eryptosis, the programmed death of an RBC. The regulation of eryptosis is complex and involves several cellular pathways, such as the regulation of non-selective cation channels. Increased cytosolic calcium concentration results in scramblase and floppase activation, exposing phosphatidylserine on the cell surface, leading to early clearance of RBCs from the circulation by phagocytic cells. While eryptosis is physiologically meaningful to recycle iron and other RBC constituents in healthy subjects, it is augmented under pathological conditions, such as kidney failure. In chronic kidney disease (CKD) patients, the number of eryptotic RBC is significantly increased, resulting in a shortened RBC life span that further compounds renal anemia. In CKD patients, uremic toxins, oxidative stress, hypoxemia, and inflammation contribute to the increased eryptosis rate. Eryptosis may have an impact on renal anemia, and depending on the degree of shortened RBC life span, the administration of erythropoiesis-stimulating agents is often insufficient to attain desired hemoglobin target levels. The goal of this review is to indicate the importance of eryptosis as a process closely related to life span reduction, aggravating renal anemia.

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Erythrocyte Sodium Sensitivity and Eryptosis in Chronic Hemodialysis Patients

Cited by 9 publications

References 73 publications

Oxidative stress, eryptosis and anemia: a pivotal mechanistic nexus in systemic diseases

Oxidative stress, eryptosis and anemia: a pivotal mechanistic nexus in systemic diseases

Pathophysiology of Red Blood Cell Dysfunction in Diabetes and Its Complications

The Role of Eryptosis in the Pathogenesis of Renal Anemia: Insights From Basic Research and Mathematical Modeling

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