Altered RBC deformability in diabetes: clinical characteristics and RBC pathophysiology.


Journal

Cardiovascular diabetology
ISSN: 1475-2840
Titre abrégé: Cardiovasc Diabetol
Pays: England
ID NLM: 101147637

Informations de publication

Date de publication:
18 Oct 2024
Historique:
received: 22 06 2024
accepted: 23 09 2024
medline: 19 10 2024
pubmed: 19 10 2024
entrez: 18 10 2024
Statut: epublish

Résumé

Reduced red blood cell deformability (RBCD) is associated with diabetic vascular complications, but early pathophysiological RBC changes and predictive demographic and clinical factors in populations with diabetes are unclear. An understanding of early diabetes-specific RBC changes associated with impaired RBCD is essential in investigating mechanisms that predispose to diabetic vascular complications. We conducted an outpatient cross-sectional study of participants in a well-controlled diabetes cohort (N81) and nondiabetic controls (N78) at the National Institutes of Health. First, between-group differences in RBCD measures were assessed with shear stress-gradient ektacytometry. Differences in structural RBC parameters were assessed using osmotic gradient ektacytometry and NaCl osmotic fragility. Functional RBC changes were assessed using hemoglobin-oxygen dissociation: p50. All shear-stress gradient RBCD measures were significantly altered in the diabetes cohort vs. nondiabetic controls, even after adjustment for confounding covariates (p < 0.001). Adjusted for diabetes-status and demographic factors, significant predictors of reduced RBCD included older age, Black race, male gender, hyperglycemia, and vascular complications (all p < 0.05). Reduced RBCD was also associated with aberrant osmotic-gradient parameters, with a left-shift on osmotic gradient profile indicative of dehydrated RBCs in diabetes. A structure-function relationship was observed with reduced RBCD associated with reduced osmotic fragility (P < 0.001) and increased hemoglobin-oxygen dissociation (P < 0.01). Findings suggest impaired RBCD incurs similar demographic and clinical risk factors as diabetic vascular disease, with early pathophysiological RBC changes indicative of disordered RBC hydration in diabetes. Findings provide strong evidence for disordered oxygen release as a functional consequence of reduced RBCD. NCT00071526.

Sections du résumé

BACKGROUND BACKGROUND
Reduced red blood cell deformability (RBCD) is associated with diabetic vascular complications, but early pathophysiological RBC changes and predictive demographic and clinical factors in populations with diabetes are unclear. An understanding of early diabetes-specific RBC changes associated with impaired RBCD is essential in investigating mechanisms that predispose to diabetic vascular complications.
METHODS METHODS
We conducted an outpatient cross-sectional study of participants in a well-controlled diabetes cohort (N81) and nondiabetic controls (N78) at the National Institutes of Health. First, between-group differences in RBCD measures were assessed with shear stress-gradient ektacytometry. Differences in structural RBC parameters were assessed using osmotic gradient ektacytometry and NaCl osmotic fragility. Functional RBC changes were assessed using hemoglobin-oxygen dissociation: p50.
RESULTS RESULTS
All shear-stress gradient RBCD measures were significantly altered in the diabetes cohort vs. nondiabetic controls, even after adjustment for confounding covariates (p < 0.001). Adjusted for diabetes-status and demographic factors, significant predictors of reduced RBCD included older age, Black race, male gender, hyperglycemia, and vascular complications (all p < 0.05). Reduced RBCD was also associated with aberrant osmotic-gradient parameters, with a left-shift on osmotic gradient profile indicative of dehydrated RBCs in diabetes. A structure-function relationship was observed with reduced RBCD associated with reduced osmotic fragility (P < 0.001) and increased hemoglobin-oxygen dissociation (P < 0.01).
CONCLUSIONS CONCLUSIONS
Findings suggest impaired RBCD incurs similar demographic and clinical risk factors as diabetic vascular disease, with early pathophysiological RBC changes indicative of disordered RBC hydration in diabetes. Findings provide strong evidence for disordered oxygen release as a functional consequence of reduced RBCD.
CLINICAL TRIAL NUMBER BACKGROUND
NCT00071526.

Identifiants

pubmed: 39425096
doi: 10.1186/s12933-024-02453-2
pii: 10.1186/s12933-024-02453-2
doi:

Banques de données

ClinicalTrials.gov
['NCT00071526']

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

370

Informations de copyright

© 2024. This is a U.S. Government work and not under copyright protection in the US; foreign copyright protection may apply.

Références

Shin S, et al. Progressive impairment of erythrocyte deformability as indicator of microangiopathy in type 2 diabetes mellitus. Clin Hemorheol Microcirc. 2007;36:253–61.
pubmed: 17361027
Keymel S, Heiss C, Kleinbongard P, Kelm M, Lauer T. Impaired red blood cell deformability in patients with coronary artery disease and diabetes mellitus. Horm Metab Res. 2011;43:760–5.
pubmed: 22009370 doi: 10.1055/s-0031-1286325
Brown CD, Ghali HS, Zhao Z, Thomas LL, Friedman EA. Association of reduced red blood cell deformability and diabetic nephropathy. Kidney Int. 2005;67:295–300.
pubmed: 15610255 doi: 10.1111/j.1523-1755.2005.00082.x
Moon JS, et al. Impaired RBC deformability is associated with diabetic retinopathy in patients with type 2 diabetes. Diabetes Metab. 2016;42:448–52.
pubmed: 27209441 doi: 10.1016/j.diabet.2016.04.008
Diamantopoulos EJ, Raptis SA, Moulopoulos SD. Red blood cell deformability index in diabetic retinopathy. Horm Metab Res. 1987;19:569–73.
pubmed: 3428873 doi: 10.1055/s-2007-1011884
Mcmillan DE, Utterbach NG, Lapuma J. Reduced erythrocyte deformability in diabetes. Biorheology. 1978;15:487–487.
Tan JKS, et al. Altered red blood cell deformability-A novel hypothesis for retinal microangiopathy in diabetic retinopathy. Microcirculation. 2020;27:e12649.
pubmed: 32663357 doi: 10.1111/micc.12649
Cahn A, et al. Diabetic foot disease is associated with reduced erythrocyte deformability. Int Wound J. 2016;13:500–4.
pubmed: 26018868 doi: 10.1111/iwj.12466
Schwartz RS, Madsen JW, Rybicki AC, Nagel RL. Oxidation of Spectrin and deformability defects in Diabetic erythrocytes. Diabetes. 1991;40:701–8.
pubmed: 2040386 doi: 10.2337/diab.40.6.701
Shin S, Ku YH, Suh JS, Singh M. Rheological characteristics of erythrocytes incubated in glucose media. Clin Hemorheol Microcirc. 2008;38:153–61.
pubmed: 18239257
Mazzanti L, et al. Sialic acid, diabetes, and aging: a study on the erythrocyte membrane. Metabolism. 1997;46:59–61.
pubmed: 9005970 doi: 10.1016/S0026-0495(97)90168-2
Babu N, Singh M. Influence of hyperglycemia on aggregation, deformability and shape parameters of erythrocytes. Clin Hemorheol Microcirc. 2004;31:273–80.
pubmed: 15567897
Parrow NL et al. Measuring deformability and red cell heterogeneity in blood by Ektacytometry. Jove-J Vis Exp (2018).
Hardeman MR, Goedhart PT, Dobbe JGG, Lettinga KP. Laser-assisted optical rotational cell analyzer (Lorca).1. A new instrument for measurement of various structural hemorheological parameters. Clin Hemorheol. 1994;14:605–18.
Da Costa L, et al. Diagnostic tool for red blood cell membrane disorders: assessment of a new generation ektacytometer. Blood Cell Mol Dis. 2016;56:9–22.
doi: 10.1016/j.bcmd.2015.09.001
Jain SK. Hyperglycemia can cause membrane lipid-peroxidation and osmotic fragility in human red blood-cells. J Biol Chem. 1989;264:21340–5.
pubmed: 2592379 doi: 10.1016/S0021-9258(19)30085-7
Tu H et al., Low red blood cell vitamin c concentrations induce red blood cell fragility: a link to diabetes via glucose, glucose transporters, and dehydroascorbic acid. EBioMedicine. 2015;2:1735–1750.
Shin S, Ku Y, Babu N, Singh M. Erythrocyte deformability and its variation in diabetes mellitus. Indian J Exp Biol. 2007;45:121–8.
pubmed: 17249336
Renoux C et al. Impact of surface-area-to-volume ratio, internal viscosity and membrane viscoelasticity on red blood cell deformability measured in isotonic condition. Sci Rep-Uk 9; 2019.
Parrow NL, et al. Measurements of red cell deformability and hydration reflect HbF and HbA(2) in blood from patients with sickle cell anemia. Blood Cells Mol Dis. 2017;65:41–50.
pubmed: 28472705 doi: 10.1016/j.bcmd.2017.04.005
Gutierrez M, et al. Characterizing bulk rigidity of rigid red blood cell populations in sickle-cell disease patients. Sci Rep. 2021;11:7909.
pubmed: 33846383 pmcid: 8041827 doi: 10.1038/s41598-021-86582-8
Zaninoni A, et al. Use of laser assisted optical rotational cell analyzer (LoRRca MaxSis) in the diagnosis of RBC membrane disorders, enzyme defects, and congenital dyserythropoietic anemias: a monocentric study on 202 patients. Front Physiol. 2018;9:451.
pubmed: 29755372 pmcid: 5934481 doi: 10.3389/fphys.2018.00451
Clark MR, Mohandas N, Shohet SB. Osmotic gradient ektacytometry: comprehensive characterization of red cell volume and surface maintenance. Blood. 1983;61:899–910.
pubmed: 6831052 doi: 10.1182/blood.V61.5.899.899
Baskurt OK, et al. New guidelines for hemorheological laboratory techniques. Clin Hemorheol Microcirc. 2009;42:75–97.
pubmed: 19433882 doi: 10.3233/CH-2009-1202
Gallagher PG. Disorders of erythrocyte hydration. Blood. 2017;130:2699–708.
pubmed: 29051181 pmcid: 5746162 doi: 10.1182/blood-2017-04-590810
Parpart AK, Lorenz PB, Parpart ER, Gregg JR, Chase AM. The osmotic resistance (fragility) of human red cells. J Clin Invest. 1947;26:636–40.
pubmed: 20255641 pmcid: 439273 doi: 10.1172/JCI101847
Guarnone R, Centenara E, Barosi G. Performance characteristics of hemox-analyzer for assessment of the hemoglobin dissociation curve. Haematologica. 1995;80:426–30.
pubmed: 8566883
Zeger SL, Liang KY. Longitudinal data analysis for discrete and continuous outcomes. Biometrics. 1986;42:121–30.
pubmed: 3719049 doi: 10.2307/2531248
Ziegler A, Kastner C, Blettner M. The generalised estimating equations: an annotated bibliography. Biom J. 1998;40:115–39.
doi: 10.1002/(SICI)1521-4036(199806)40:2<115::AID-BIMJ115>3.0.CO;2-6
Zhao LP, Prentice RL, Self SG. Multivariate mean parameter estimation by using a partly exponential model. J Royal Stat Soc Ser B (Methodological). 1992;54:805–11.
doi: 10.1111/j.2517-6161.1992.tb01453.x
Lee SB, et al. Use of RBC deformability index as an early marker of diabetic nephropathy. Clin Hemorheol Micro. 2019;72:75–84.
Cho YI, Cho DJ. Hemorheology and microvascular disorders. Korean Circ J. 2011;41:287–95.
pubmed: 21779279 pmcid: 3132688 doi: 10.4070/kcj.2011.41.6.287
Houston BL, et al. Refinement of the hereditary xerocytosis locus on chromosome 16q in a large Canadian kindred. Blood Cells Mol Dis. 2011;47:226–31.
pubmed: 21944700 doi: 10.1016/j.bcmd.2011.08.001
Porro B, et al. Red blood cell morphodynamics: a new potential marker in high-risk patients. Front Physiol. 2020;11:603633.
pubmed: 33519509 doi: 10.3389/fphys.2020.603633
Tsai WC, et al. Risk factors for development and progression of chronic kidney disease: a systematic review and exploratory meta-analysis. Med (Baltim). 2016;95:e3013.
doi: 10.1097/MD.0000000000003013
Sorber R, Abularrage CJ. Diabetic foot ulcers: epidemiology and the role of multidisciplinary care teams. Semin Vasc Surg. 2021;34:47–53.
pubmed: 33757635 doi: 10.1053/j.semvascsurg.2021.02.006
Stratton IM, et al. Association of glycaemia with macrovascular and microvascular complications of type 2 diabetes (UKPDS 35): prospective observational study. BMJ. 2000;321:405–12.
pubmed: 10938048 pmcid: 27454 doi: 10.1136/bmj.321.7258.405
Selvin E, Erlinger TP. Prevalence of and risk factors for peripheral arterial disease in the United States: results from the National Health and Nutrition Examination Survey, 1999–2000. Circulation. 2004;110:738–43.
pubmed: 15262830 doi: 10.1161/01.CIR.0000137913.26087.F0
Ostchega Y, Paulose-Ram R, Dillon CF, Gu Q, Hughes JP. Prevalence of peripheral arterial disease and risk factors in persons aged 60 and older: data from the National Health and Nutrition Examination Survey 1999–2004. J Am Geriatr Soc. 2007;55:583–9.
pubmed: 17397438 doi: 10.1111/j.1532-5415.2007.01123.x
McDermott K, Fang M, Boulton AJM, Selvin E, Hicks CW. Etiology, epidemiology, and disparities in the burden of diabetic foot ulcers. Diabetes Care. 2023;46:209–21.
pubmed: 36548709 doi: 10.2337/dci22-0043
Li H, Fang K, Peng H, He L, Wang Y. The relationship between glycosylated hemoglobin level and red blood cell storage lesion in blood donors. Transfusion. 2022;62:663–74.
pubmed: 35137967 doi: 10.1111/trf.16815
Sparrow RL. Red blood cell components: time to revisit the sources of variability. Blood Transfus. 2017;15:116–25.
pubmed: 28263168 pmcid: 5336332
Kanias T, et al. Ethnicity, sex, and age are determinants of red blood cell storage and stress hemolysis: results of the REDS-III RBC-Omics study. Blood Adv. 2017;1:1132–41.
pubmed: 29034365 pmcid: 5638435 doi: 10.1182/bloodadvances.2017004820
Bizjak DA, Brinkmann C, Bloch W, Grau M. Increase in red blood cell-nitric oxide synthase dependent nitric oxide production during red blood cell aging in health and disease: a study on age dependent changes of rheologic and enzymatic properties in red blood cells. PLoS ONE. 2015;10:e0125206.
pubmed: 25902315 pmcid: 4406474 doi: 10.1371/journal.pone.0125206
Turpin C, et al. Enhanced oxidative stress and damage in glycated erythrocytes. PLoS ONE. 2020;15:e0235335.
pubmed: 32628695 pmcid: 7337333 doi: 10.1371/journal.pone.0235335
Statistical Power Analysis for the Behavioral-Sciences. Cohen J Percept Motor Skill. 1988;67:1007–1007.

Auteurs

Ifechukwude Ebenuwa (I)

Molecular and Clinical Nutrition Section, Digestive Diseases Branch, Intramural Research Program, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, 20892, USA. Ebenuwaic@nih.gov.

Pierre-Christian Violet (PC)

Molecular and Clinical Nutrition Section, Digestive Diseases Branch, Intramural Research Program, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, 20892, USA.

Hongbin Tu (H)

Molecular and Clinical Nutrition Section, Digestive Diseases Branch, Intramural Research Program, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, 20892, USA.

Casey Lee (C)

Molecular and Clinical Nutrition Section, Digestive Diseases Branch, Intramural Research Program, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, 20892, USA.

Nicholas Munyan (N)

Molecular and Clinical Nutrition Section, Digestive Diseases Branch, Intramural Research Program, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, 20892, USA.

Yu Wang (Y)

Molecular and Clinical Nutrition Section, Digestive Diseases Branch, Intramural Research Program, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, 20892, USA.

Mahtab Niyyati (M)

Molecular and Clinical Nutrition Section, Digestive Diseases Branch, Intramural Research Program, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, 20892, USA.

Kartick Patra (K)

Molecular and Clinical Nutrition Section, Digestive Diseases Branch, Intramural Research Program, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, 20892, USA.

Kenneth J Wilkins (KJ)

Biostatistics Program, Office of Clinical Research Support, Office of the Director, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, 20892, USA.

Nermi Parrow (N)

Molecular and Clinical Nutrition Section, Digestive Diseases Branch, Intramural Research Program, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, 20892, USA.

Mark Levine (M)

Molecular and Clinical Nutrition Section, Digestive Diseases Branch, Intramural Research Program, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, 20892, USA. MarkL@nih.gov.

Articles similaires

[Redispensing of expensive oral anticancer medicines: a practical application].

Lisanne N van Merendonk, Kübra Akgöl, Bastiaan Nuijen
1.00
Humans Antineoplastic Agents Administration, Oral Drug Costs Counterfeit Drugs

Smoking Cessation and Incident Cardiovascular Disease.

Jun Hwan Cho, Seung Yong Shin, Hoseob Kim et al.
1.00
Humans Male Smoking Cessation Cardiovascular Diseases Female
Humans United States Aged Cross-Sectional Studies Medicare Part C
1.00
Humans Yoga Low Back Pain Female Male

Classifications MeSH