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Clinicopathological analysis of type I stenosis of autogenous arteriovenous fistula in uremia patients

  • SONG Wen-Jun ,
  • LIANG Li-Ming ,
  • CHEN Qin-Lan ,
  • KONG Xiang-Lei ,
  • XU Dong-Mei
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  • 1Department of Nephrology, Shandong Provincial Qianfoshan Hospital, The First Affiliated Hospital of Shandong First Medical University, Jinan 250014, China; 2Nephrology Research Institute of Shandong Province, Jinan 250014, China

Received date: 2023-02-02

  Revised date: 2023-03-17

  Online published: 2023-06-12

Abstract

Objective  To investigate the clinicopathological characteristics of type I autologous arteriovenous fistula (AVF) stenosis in uremic patients.  Methods  A total of 39 patients who underwent AVF reconstructive surgery for type I stenosis were enrolled in this study. Their clinical data were collected. The stenotic venous tissue cut during the reconstructive surgery and the venous tissue stored during the first AVF constructive surgery were pathologically compared, including HE and masson staining, and immunohistochemistry using antibodies against CD133, CD31, CD68, CD206, iNOS and CD56 to identify the cell types.  Results  The mean age of the 39 patients was 52.7±4.4 years old, 62% were male, and diabetic kidney disease accounted for 43.6% of the patients. HE and Masson staining of the stenotic venous tissues demonstrated typical neointimal hyperplasia (NIH). Pearson correlation analysis showed that NIH was positively correlated with serum phosphorus (r=0.381, P=0.026) and negative correlated with neutrophil count (r=-0.360, P=0.031), but not with serum calcium (r=-0.269, P=0.097) and parathyroid hormone (r=0.007, P=0.971). Immunohistochemical staining showed that positive staining of CD31, CD133, CD206, iNOS, CD68 and CD56 were found in the NIH area in stenotic venous tissues.  Conclusions   Histopathological staining showed an eccentric NIH in the venous tissues from type I AVF stenosis. The thickness of the intimal layer correlated with serum phosphorus level and neutrophil count. Immunohistochemistry showed the presence of abnormally arranged intimal cells, endothelial progenitor cells, M1 and M2 macrophages, and NK cells in NIH areas.

Cite this article

SONG Wen-Jun , LIANG Li-Ming , CHEN Qin-Lan , KONG Xiang-Lei , XU Dong-Mei . Clinicopathological analysis of type I stenosis of autogenous arteriovenous fistula in uremia patients[J]. Chinese Journal of Blood Purification, 2023 , 22(06) : 453 -457 . DOI: 10.3969/j.issn.1671-4091.2023.06.012

References

[1] VACHHARAJANI T J, TALIERCIO J J, ANVARI E. New Devices and Technologies for Hemodialysis Vascular Access: A Review [J]. American Journal of Kidney Diseases, 2021, 78(1): 116-24.
[2] ALPERS C E, IMREY P B, HUDKINS K L, et al. Histopathology of Veins Obtained at Hemodialysis Arteriovenous Fistula Creation Surgery [J]. J Am Soc Nephrol, 2017, 28(10): 3076-88.
[3] CUI J, XU D, MA J, et al. Stenoses in the surgically manipulated segment have better angioplasty response compared to the surgically naive segment in fistulas [J]. J Vasc Access, 2017, 18(3): 192-9.
[4] ROY-CHAUDHURY P, SUKHATME V P, CHEUNG A K. Hemodialysis vascular access dysfunction: a cellular and molecular viewpoint [J]. J Am Soc Nephrol, 2006, 17(4): 1112-27.
[5] DU J, LIANG L, LIU S, et al. Neointimal hyperplasia in the inferior vena cava of adenine-induced chronic kidney disease rats with aortocaval fistulas [J]. Clin Exp Nephrol, 2020, 24(11): 1007-14.
[6] LI Y, CUI W, WANG J, et al. Factors associated with dysfunction of autogenous arteriovenous fistula in patients with maintenance hemodialysis: a retrospective study [J]. Ann Palliat Med, 2021, 10(4): 4047-54.
[7] VILLA-BELLOSTA R. Vascular Calcification: Key Roles of Phosphate and Pyrophosphate [J]. Int J Mol Sci, 2021, 22(24).
[8] BRAHMBHATT A, REMUZZI A, FRANZONI M, et al. The molecular mechanisms of hemodialysis vascular access failure [J]. Kidney Int, 2016, 89(2): 303-16.
[9] SIMONE S, LOVERRE A, CARIELLO M, et al. Arteriovenous fistula stenosis in hemodialysis patients is characterized by an increased adventitial fibrosis [J]. J Nephrol, 2014, 27(5): 555-62.
[10] DUAN Y, YU S, XU P, et al. Co-immobilization of CD133 antibodies, vascular endothelial growth factors, and REDV peptide promotes capture, proliferation, and differentiation of endothelial progenitor cells [J]. Acta Biomaterialia, 2019, 96: 137-48.
[11] BUSSOLATI B, COLLINO F, CAMUSSI G. CD133+ cells as a therapeutic target for kidney diseases [J]. Expert Opin Ther Targets, 2012, 16(2): 157-65.
[12] MAUSE S F, RITZEL E, DECK A, et al. Endothelial Progenitor Cells Modulate the Phenotype of Smooth Muscle Cells and Increase Their Neointimal Accumulation Following Vascular Injury [J]. Thromb Haemost, 2022, 122(3): 456-69.
[13] RATTI S, MAURO R, ROCCHI C, et al. Roles of PI3K/AKT/mTOR Axis in Arteriovenous Fistula [J]. Biomolecules, 2022, 12(3).
[14] MAUSE S F, RITZEL E, DECK A, et al. Engagement of the CXCL12-CXCR4 Axis in the Interaction of Endothelial Progenitor Cell and Smooth Muscle Cell to Promote Phenotype Control and Guard Vascular Homeostasis [J]. Int J Mol Sci, 2022, 23(2).
[15] WYNN T A, CHAWLA A, POLLARD J W. Macrophage biology in development, homeostasis and disease [J]. Nature, 2013, 496(7446): 445-55.
[16] YUNNA C, MENGRU H, LEI W, et al. Macrophage M1/M2 polarization [J]. Eur J Pharmacol, 2020, 877: 173090.
[17] MURRAY P J, ALLEN J E, BISWAS S K, et al. Macrophage activation and polarization: nomenclature and experimental guidelines [J]. Immunity, 2014, 41(1): 14-20.
[18] KRONER A, GREENHALGH A D, ZARRUK J G, et al. TNF and increased intracellular iron alter macrophage polarization to a detrimental M1 phenotype in the injured spinal cord [J]. Neuron, 2014, 83(5): 1098-116.
[19] LASKIN D L, SUNIL V R, GARDNER C R, et al. Macrophages and tissue injury: agents of defense or destruction? [J]. Annu Rev Pharmacol Toxicol, 2011, 51: 267-88.
[20] VODOVOTZ Y, BOGDAN C, PAIK J, et al. Mechanisms of suppression of macrophage nitric oxide release by transforming growth factor beta [J]. J Exp Med, 1993, 178(2): 605-13.
[21] LIU Y C, ZOU X B, CHAI Y F, et al. Macrophage polarization in inflammatory diseases [J]. Int J Biol Sci, 2014, 10(5): 520-9.
[22] MISRA S, KILARI S, YANG B, et al. Anti Human CX3CR1 VHH Molecule Attenuates Venous Neointimal Hyperplasia of Arteriovenous Fistula in Mouse Model [J]. J Am Soc Nephrol, 2021.
[23] FENYO I M, GAFENCU A V. The involvement of the monocytes/macrophages in chronic inflammation associated with atherosclerosis [J]. Immunobiology, 2013, 218(11): 1376-84.
[24] ALEXANDER M R, MOEHLE C W, JOHNSON J L, et al. Genetic inactivation of IL-1 signaling enhances atherosclerotic plaque instability and reduces outward vessel remodeling in advanced atherosclerosis in mice [J]. J Clin Invest, 2012, 122(1): 70-9.
[25] MENG Q H, IRVINE S, TAGALAKIS A D, et al. Inhibition of neointimal hyperplasia in a rabbit vein graft model following non-viral transfection with human iNOS cDNA [J]. Gene Ther, 2013, 20(10): 979-86.
[26] KUWAHARA G, HASHIMOTO T, TSUNEKI M, et al. CD44 Promotes Inflammation and Extracellular Matrix Production During Arteriovenous Fistula Maturation [J]. Arterioscler Thromb Vasc Biol, 2017, 37(6): 1147-56.
[27] DAMMANAHALLI J K, WANG X, SUN Z. Genetic interleukin-10 deficiency causes vascular remodeling via the upregulation of Nox1 [J]. J Hypertens, 2011, 29(11): 2116-25.
[28] SUWANABOL P A, SEEDIAL S M, SHI X, et al. Transforming growth factor-beta increases vascular smooth muscle cell proliferation through the Smad3 and extracellular signal-regulated kinase mitogen-activated protein kinases pathways [J]. J Vasc Surg, 2012, 56(2): 446-54.
[29] MATSUBARA Y, KIWAN G, LIU J, et al. Inhibition of T-Cells by Cyclosporine A Reduces Macrophage Accumulation to Regulate Venous Adaptive Remodeling and Increase Arteriovenous Fistula Maturation [J]. Arterioscler Thromb Vasc Biol, 2021, 41(3): e160-e74.
[30] CHAN J S, WANG Y, CORNEA V, et al. Early Adventitial Activation and Proliferation in a Mouse Model of Arteriovenous Stenosis: Opportunities for Intervention [J]. Int J Mol Sci, 2021, 22(22).
[31] FREUD A G, MUNDY-BOSSE B L, YU J, et al. The Broad Spectrum of Human Natural Killer Cell Diversity [J]. Immunity, 2017, 47(5): 820-33.
[32] HAMIDZADEH K, CHRISTENSEN S M, DALBY E, et al. Macrophages and the Recovery from Acute and Chronic Inflammation [J]. Annu Rev Physiol, 2017, 79: 567-92.
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