The Relationship between Serum TWEAK Levels and Carotid Intima-media Thickness in Patients with Fabry Disease.
Journal
Saudi journal of kidney diseases and transplantation : an official publication of the Saudi Center for Organ Transplantation, Saudi Arabia
ISSN: 1319-2442
Titre abrégé: Saudi J Kidney Dis Transpl
Pays: Saudi Arabia
ID NLM: 9436968
Informations de publication
Date de publication:
01 Sep 2023
01 Sep 2023
Historique:
medline:
12
7
2024
pubmed:
12
7
2024
entrez:
12
7
2024
Statut:
ppublish
Résumé
Fabry disease (FD) is associated with inflammation, proteinuria, and chronic kidney disease. Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) plays an important role in inflammation in diabetic nephropathy and lupus nephritis. Since there is a close relationship linking serum TWEAK (sTWEAK), inflammation, and carotid intima-media thickness (CIMT) in various kidney diseases, we aimed to determine the relationship between sTWEAK levels and CIMT in subjects with and without proteinuria in a cross-sectional study involving 15 FD patients (seven females, eight males) and seven healthy controls (four females, three males). There were no differences in age, sex, estimated glomerular filtration rate, and biochemical parameters (serum glucose, albumin, creatinine, uric acid, C-reactive protein (CRP), low-density lipoprotein, and high-density lipoprotein) between FD patients and healthy controls. The spot urine protein-creatinine ratios of healthy controls and FD patients were 90 mg/g and 185 mg/g, respectively (P = 0.022). STWEAK levels were higher in FD patients than in healthy controls (P = 0.007). The CIMT of FD patients and healthy controls was 0.55 ± 0.14 mm and 0.42 ± 0.04 mm, respectively (P = 0.007). STWEAK was positively correlated with CRP and CIMT, and negatively with proteinuria (P = 0.005, P = 0.013, and P = 0.018, respectively). In the multivariate analysis, only sTWEAK was an independent variable of increased CIMT. We demonstrated that sTWEAK and CIMT were increased in FD patients. STWEAK might have a role in the pathogenesis of subclinical atherosclerosis in FD.
Identifiants
pubmed: 38995299
doi: 10.4103/1319-2442.397202
pii: 00936703-202334050-00004
doi:
Substances chimiques
Cytokine TWEAK
0
TNFSF12 protein, human
0
Biomarkers
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
406-415Informations de copyright
Copyright © 2023 Copyright: © 2023 Saudi Journal of Kidney Diseases and Transplantation.
Références
Aerts JM, Groener JE, Kuiper S, et al. Elevated globotriaosylsphingosine is a hallmark of fabry disease. Proc Natl Acad Sci U S A 2008;105:2812-7.
Vitner EB, Platt FM, Futerman AH. Common and uncommon pathogenic cascades in lysosomal storage diseases. J Biol Chem 2010;285:20423-7.
Turkmen K, Guclu A, Sahin G, et al. The prevalence of fabry disease in patients with chronic kidney disease in Turkey: The turkfab study. Kidney Blood Press Res 2016;41:1016-24.
Castaneda JA, Lim MJ, Cooper JD, Pearce DA. Immune system irregularities in lysosomal storage disorders. Acta Neuropathol 2008;115:159-74.
Yalin SF, Eren N, Sinangil A, et al. Fabry disease prevalence in renal replacement therapy in Turkey. Nephron 2019;142:26-33.
Sanchez-Niño MD, Carpio D, Sanz AB, Ruiz- Ortega M, Mezzano S, Ortiz A. Lyso-gb3 activates notch1 in human podocytes. Hum Mol Genet 2015;24:5720-32.
Rozenfeld P, Feriozzi S. Contribution of inflammatory pathways to fabry disease pathogenesis. Mol Genet Metab 2017;122:19-27.
Chicheportiche Y, Bourdon PR, Xu H, et al. TWEAK, a new secreted ligand in the tumor necrosis factor family that weakly induces apoptosis. J Biol Chem 1997;272:32401-10.
Ortiz A, Sanz AB, Muñoz García B, et al. Considering TWEAK as a target for therapy in renal and vascular injury. Cytokine Growth Factor Rev 2009;20:251-8.
Blanco-Colio LM, Martín-Ventura JL, Muñóz- García B, et al. Identification of soluble tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) as a possible biomarker of subclinical atherosclerosis. Arterioscler Thromb Vasc Biol 2007;27:916-22.
Turkmen K, Tonbul HZ, Erdur FM, et al. Soluble TWEAK independently predicts atherosclerosis in renal transplant patients. BMC Nephrol 2013;14:144.
Sanz AB, Justo P, Sanchez-Niño MD, Blanco-, et al. The cytokine TWEAK modulates renal tubulointerstitial inflammation. J Am Soc Nephrol 2008;19:695-703.
Yilmaz MI, Carrero JJ, Ortiz A, et al. Soluble TWEAK plasma levels as a novel biomarker of endothelial function in patients with chronic kidney disease. Clin J Am Soc Nephrol 2009;4:1716-23.
Burkly LC, Michaelson JS, Zheng TS. TWEAK/Fn14 pathway: An immunological switch for shaping tissue responses. Immunol Rev 2011;244:99-114.
Chamoles NA, Blanco M, Gaggioli D. Fabry disease: Enzymatic diagnosis in dried blood spots on filter paper. Clin Chim Acta 2001;308:195-6.
Friedewald WT, Levy RI, Fredrickson DS. Estimation of the concentration of low-density lipoprotein cholesterol in plasma, without use of the preparative ultracentrifuge. Clin Chem 1972;18:499-502.
Levey AS, Berg RL, Gassman JJ, Hall PM, Walker WG. Creatinine filtration, secretion and excretion during progressive renal disease. Modification of Diet in Renal Disease (MDRD) study group. Kidney Int Suppl 1989;27:S73-80.
Pereira CS, Azevedo O, Maia ML, Dias AF, Sa- Miranda C, Macedo MF. Invariant natural killer T cells are phenotypically and functionally altered in fabry disease. Mol Genet Metab 2013;108:241-8.
Biancini GB, Vanzin CS, Rodrigues DB, et al. Globotriaosylceramide is correlated with oxidative stress and inflammation in fabry patients treated with enzyme replacement therapy. Biochim Biophys Acta 2012;1822:226-32.
De Francesco PN, Mucci JM, Ceci R, Fossati CA, Rozenfeld PA. Fabry disease peripheral blood immune cells release inflammatory cytokines: Role of globotriaosylceramide. Mol Genet Metab 2013;109:93-9.
Justo P, Sanz AB, Sanchez-Nino MD, al. Cytokine cooperation in renal tubular cell injury: the role of TWEAK. Kidney Int 2006;70:1750-8.
Icli A, Cure MC, Cure E, et al. Soluble Tumor Necrosis Factor (TNF)-like weak inducer of apoptosis (Tweak) independently predicts subclinical atherosclerosis in behcet's disease. Acta Medica (Hradec Kralove) 2018;61:86-92.
Muñoz-García B, Moreno JA, López-Franco O, et al. Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) enhances vascular and renal damage induced by hyperlipidemic diet in ApoE-knockout mice. Arterioscler Thromb Vasc Biol 2009;29:2061-8.
Sanz AB, Sanchez-Niño MD, Izquierdo MC, et al. Tweak induces proliferation in renal tubular epithelium: A role in uninephrectomy induced renal hyperplasia. J Cell Mol Med 2009;13:3329-42.
Zhao Z, Burkly LC, Campbell S, et al. TWEAK/Fn14 interactions are instrumental in the pathogenesis of nephritis in the chronic graft-versus-host model of systemic lupus erythematosus. J Immunol 2007;179:7949-58.
Ucero AC, Benito-Martin A, Fuentes-Calvo I, et al. TNF-related weak inducer of apoptosis (TWEAK) promotes kidney fibrosis and ras-dependent proliferation of cultured renal fibroblast. Biochim Biophys Acta 2013;1832:1744-55.
Hurst RT, Ng DW, Kendall C, Khandheria B. Clinical use of carotid intima-media thickness: Review of the literature. J Am Soc Echocardiogr 2007;20:907-14.
Hagège A, Réant P, Habib G, et al. Fabry disease in cardiology practice: Literature review and expert point of view. Arch Cardiovasc Dis 2019;112:278-87.
Puccio D, Coppola G, Corrado E, et al. Non invasive evaluation of endothelial function in patients with anderson-fabry disease. Int Angiol 2005;24:295-9.
Collin C, Briet M, Tran TC, et al. Long-term changes in arterial structure and function and left ventricular geometry after enzyme replacement therapy in patients affected with fabry disease. Eur J Prev Cardiol 2012;19:43-54.
Rombach SM, van den Bogaard B, de Groot E, et al. Vascular aspects of fabry disease in relation to clinical manifestations and elevations in plasma globotriaosylsphingosine. Hypertension 2012;60:998-1005.
Blanco-Colio LM, Martín-Ventura JL, Munoz- Garcia B, et al. TWEAK and Fn14. New players in the pathogenesis of atherosclerosis. Front Biosci 2007;12:3648-55.
Chen T, Guo ZP, Li L, et al. TWEAK enhances E-selectin and ICAM-1 expression, and may contribute to the development of cutaneous vasculitis. PLoS One 2013;8:e56830.
Li H, Mittal A, Paul PK, et al. Tumor necrosis factor-related weak inducer of apoptosis augments matrix metalloproteinase 9 (MMP-9) production in skeletal muscle through the activation of nuclear factor-kappaB-inducing kinase and p38 mitogen-activated protein kinase: A potential role of MMP-9 in myopathy. J Biol Chem 2009;284:4439-50.
Taslipinar A, Yaman H, Yilmaz MI, et al. The relationship between inflammation, endothelial dysfunction and proteinuria in patients with diabetic nephropathy. Scand J Clin Lab Invest 2011;71:606-12.
Sanz AB, Izquierdo MC, Sanchez-Niño MD, et al. TWEAK and the progression of renal disease: Clinical translation. Nephrol Dial Transplant 2014;29 Suppl 1:i54-62.
Dong XW, Zheng ZH, Ding J, et al. Combined detection of uMCP-1 and uTWEAK for rapid discrimination of severe lupus nephritis. Lupus 2018;27:971-81.