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• W2048309822 abstract "Heme oxygenase-1 (HO-1) is a rate-limiting enzyme in heme degradation, producing carbon monoxide (CO), which carries potent antiproliferative and anti-inflammatory effects in the vascular walls. Transcription of the HO-1 gene is regulated by the length polymorphism of dinucleotide guanosine thymine repeat (GT)n in the promoter region, which was measured in this study to determine its association with arteriovenous fistula (AVF) failure in Chinese hemodialysis (HD) patients in Taiwan. L allele means (GT)n≥30 and S allele means (GT)n<30. Therefore, there are two L alleles for L/L genotype, one L and one S allele for L/S genotype, and two S alleles for S/S genotype. Among the 603 HD patients who were enrolled in this study, 178 patients had history of AVF failure, while 425 patients did not. Significant associations were found between AVF failure and the following factors (hazard ratio): longer HD duration (1.004 month), lower pump flow (0.993 ml/min), higher dynamic venous pressure (1.010 mmHg), location of AVF on the right side (1.587 vs left side) and upper arm (2.242 vs forearm), and L/L and L/S genotypes of HO-1 (2.040 vs S/S genotype). The proportion of AVF failure increased from 20.3% in S/S genotype and 31.0% in L/S genotype to 35.4% in L/L genotype (P=0.011). Relative incidences were 1/87.6 (1 episode per 87.6 patient-months), 1/129, and 1/224.9 for HD patients with L/L, L/S, and S/S genotypes, respectively (P<0.002). The unassisted patency of AVF at 5 years decreased significantly from 83.8% (124/148) to 75.1% (223/297) and 69% (109/158) in S/S, L/S, and L/L genotypes, respectively (P<0.0001). In comparison with HD patients with S/S genotype, those with L/L genotype had a higher prevalence of coronary artery disease (29.1 vs 14.2%; P=0.005). A longer length polymorphism with (GT)n ≥30 in the HO-1 gene was associated with a higher frequency of access failure and a poorer patency of AVF in HD patients. The longer GT repeat in the HO-1 promoter might inhibit gene transcription, and consequently offset the CO-mediated protective effect against vascular injury. Heme oxygenase-1 (HO-1) is a rate-limiting enzyme in heme degradation, producing carbon monoxide (CO), which carries potent antiproliferative and anti-inflammatory effects in the vascular walls. Transcription of the HO-1 gene is regulated by the length polymorphism of dinucleotide guanosine thymine repeat (GT)n in the promoter region, which was measured in this study to determine its association with arteriovenous fistula (AVF) failure in Chinese hemodialysis (HD) patients in Taiwan. L allele means (GT)n≥30 and S allele means (GT)n<30. Therefore, there are two L alleles for L/L genotype, one L and one S allele for L/S genotype, and two S alleles for S/S genotype. Among the 603 HD patients who were enrolled in this study, 178 patients had history of AVF failure, while 425 patients did not. Significant associations were found between AVF failure and the following factors (hazard ratio): longer HD duration (1.004 month), lower pump flow (0.993 ml/min), higher dynamic venous pressure (1.010 mmHg), location of AVF on the right side (1.587 vs left side) and upper arm (2.242 vs forearm), and L/L and L/S genotypes of HO-1 (2.040 vs S/S genotype). The proportion of AVF failure increased from 20.3% in S/S genotype and 31.0% in L/S genotype to 35.4% in L/L genotype (P=0.011). Relative incidences were 1/87.6 (1 episode per 87.6 patient-months), 1/129, and 1/224.9 for HD patients with L/L, L/S, and S/S genotypes, respectively (P<0.002). The unassisted patency of AVF at 5 years decreased significantly from 83.8% (124/148) to 75.1% (223/297) and 69% (109/158) in S/S, L/S, and L/L genotypes, respectively (P<0.0001). In comparison with HD patients with S/S genotype, those with L/L genotype had a higher prevalence of coronary artery disease (29.1 vs 14.2%; P=0.005). A longer length polymorphism with (GT)n ≥30 in the HO-1 gene was associated with a higher frequency of access failure and a poorer patency of AVF in HD patients. The longer GT repeat in the HO-1 promoter might inhibit gene transcription, and consequently offset the CO-mediated protective effect against vascular injury. In Taiwan, more than 85% of patients with end-stage renal disease undergo maintenance hemodialysis (HD). A well-functioning vascular access is necessary for HD, and long-term technical survival is best for native arteriovenous fistula (AVF), which accounts for a prevalence of more than 80% of the vascular access in our patients. About 17–25% of HD patient hospitalizations in the USA result from vascular access complications, at a cost of US $1 billion annually.1.Feldman H.I. Kobrin S. Wasserstein A. Hemodialysis vascular access morbidity.J Am Soc Nephrol. 1996; 7: 523-535PubMed Google Scholar Failure of dialysis access can result from either inadequate blood flow on account of stenosis of the venous outflow tract or complete occlusion due to thrombosis.2.Paun M. Beach K. Ahmad S. et al.New ultrasound approaches to dialysis access monitoring.Am J Kidney Dis. 2000; 35: 477-481Abstract Full Text Full Text PDF PubMed Scopus (20) Google Scholar About 80–85% of arteriovenous (AV) access failures come from AV access thromboses, more than 80% of which result from AVF stenoses.3.Windus D.W. Permanent vascular access: a nephrologist's view.Am J Kidney Dis. 1993; 21: 457-471Abstract Full Text PDF PubMed Scopus (278) Google Scholar Decreased access flow (Qa) is associated with an increased risk of access thrombosis. Qa less than 500 ml/min was demonstrated to be predictive of poorer unassisted patency of native AVF by variable pump flow-based Doppler ultrasound method in our previous study.4.Lin C.C. Chang C.F. Chiou H.J. et al.Variable pump flow-based Doppler ultrasound method: a novel approach to the measurement of access flow in hemodialysis patients.J Am Soc Nephrol. 2005; 16: 229-236Crossref PubMed Scopus (17) Google Scholar In addition to Qa, some mechanical factors, such as the surgical skill, the puncture technique, and the shear stress on vascular endothelia, influence AVF patency. Several medical factors have also been identified to be associated with AVF stenosis in HD patients, including endothelial cell injury, stasis, hypercoagulability, medications, and red cell mass.5.Abularrage C.J. Sidawy A.N. Weiswasser J.M. et al.Medical factors affecting patency of arteriovenous access.Semin Vasc Surg. 2004; 17: 25-31Abstract Full Text Full Text PDF PubMed Scopus (15) Google Scholar Many factors lead to endothelial cell injury or dysfunction, such as oxidative stress, hyperhomocysteinemia, activated platelets, tumor necrosis factor-α, calcium/phosphate deposition, and pre-existing intimal hyperplasia. The pathological features of stenosis of vascular access consist of intimal hyperplasia, vascular smooth muscle cell (VSMC) proliferation in the media with subsequent migration to intima, and excessive accumulation of extracellular matrix.6.Weiss M.F. Scivittaro V. Anderson J.M. Oxidative stress and increased expression of growth factors in lesions of failed hemodialysis access.Am J Kidney Dis. 2001; 37: 970-980Abstract Full Text PDF PubMed Scopus (155) Google Scholar In spite of the above findings, the causes for development of stenoses still remain unknown in a significant proportion of HD patients. This interindividual variation may relate to genetic differences among patients. In this regard, AV fistula patency has been reported to be associated with specific genotype polymorphisms of transforming growth factor β1 (TGF-β1)7.Heine G.H. Ulrich C. Sester U. et al.Transforming growth factor beta1 genotype polymorphisms determine AV fistula patency in hemodialysis patients.Kidney Int. 2003; 64: 1101-1107Abstract Full Text Full Text PDF PubMed Scopus (57) Google Scholar and methylene tetrahydrofolate reductase (MTHFR).8.Fukasawa M. Matsushita K. Kamiyama M. et al.The methylenetetrahydrofolate reductase C677T point mutation is a risk factor for vascular access thrombosis in hemodialysis patients.Am J Kidney Dis. 2003; 41: 637-642Abstract Full Text Full Text PDF PubMed Scopus (48) Google Scholar In addition to the above factors, the activity of heme oxygenase-1 (HO-1) is another factor associated with higher risk of developing some vascular diseases. HO-1, an enzyme playing an important role in heme degradation, results in the production of biliverdin, free iron, and carbon monoxide (CO).9.Maines M.D. The heme oxygenase system: a regulator of second messenger gases.Annu Rev Pharmacol Toxicol. 1997; 37: 517-554Crossref PubMed Scopus (2133) Google Scholar This enzyme is associated with oxidative stress, platelet activation, and VSMC proliferation, as VSMC proliferation, migration, and extracellular matrix synthesis may be regulated by its reaction product, CO.10.Durante W. Heme oxygenase-1 in growth control and its clinical application to vascular disease.J Cell Physiol. 2003; 195: 373-382Crossref PubMed Scopus (148) Google Scholar The human HO-1 gene was located at chromosome 22q12, and a (guanidinium thiocyanate (GT)n) dinucleotide repeat of different length was identified in the proximal promoter region.11.Lavrovsky Y. Schwartzman M.C. Levere R.D. Identification of binding sites for transcription factors NF-κB and AP-2 in the promoter region of the human heme oxygenase-1 gene.Proc Natl Acad Sci USA. 1994; 91: 5987-5991Crossref PubMed Scopus (340) Google Scholar However, the actions of HO-1 are highly variable and may reflect a role for HO-1 in maintaining tissue homeostasis. Kaneda et al.12.Kaneda H. Ohno M. Taguchi J. Heme oxygenase-1 gene promoter polymorphism is associated with coronary artery disease in Japanese patients with coronary risk factors.Arterioscler Thromb Vasc Biol. 2002; 22: 1680-1685Crossref PubMed Scopus (149) Google Scholar and Chen et al.13.Chen Y.H. Lin S.J. Lin M.W. et al.Microsatellite polymorphism in promoter of heme oxygenase-1 gene is associated with susceptibility to coronary artery disease in type 2 diabetic patients.Hum Genet. 2002; 111: 1-8Crossref PubMed Scopus (265) Google Scholar have shown that the (GT)n repeat is highly polymorphic, and a longer (GT)n repeat exhibits lower transcriptional activity and is associated with susceptibility to coronary artery disease (CAD). Chen et al.14.Chen Y.H. Chau L.Y. Lin M.W. et al.Heme oxygenase-1 gene promoter microsatellite polymorphism is associated with angiographic restenosis after coronary stenting.Eur Heart J. 2004; 25: 39-47Crossref PubMed Scopus (83) Google Scholar also showed that genetic variation influencing HO-1 expression would interact with traditional risk factors and contribute to the development of restenosis after placement of coronary stents. However, little information is available on the role of genetic background of HO-1 in the development of AVF stenosis. This study was designed to determine whether the length polymorphism of the dinucleotide (GT)n repeats in the HO-1 gene promoter region would be an independent factor for predicting patency of AVF in HD patients. The demographic and clinical characteristics of the patients are summarized in Table 1. A total of 603 patients were enrolled in the study. Among them, 425 patients did not have any episode of AV fistula failure, but 178 patients did. Compared with HD patients without AV fistula failure, those with AV fistula failure had a longer HD duration (89.2±65.6 vs 62.5±53.0 months, P<0.001), a higher prevalence of AV fistula at the right upper extremity (32 vs 18.6%, P<0.001) and upper arm (27 vs. 9.2%, P<0.001), higher dynamic venous pressure (148.2±29.5 vs 140.9±29.9 mmHg, P<0.001), lower prevalence of hypertension (45.5 vs 56%, P=0.019), and borderline higher prevalence of cardiovascular disease (32.6 vs 24.9%, P=0.05). The allele frequencies of the dinucleotide length polymorphism (GT)n in the HO-1 gene promoter found in the studied individuals are shown in Figure 1. The repeat numbers ranged from 16 to 39, with (GT)23 and (GT)30 being the two most common alleles in our study population (allele frequencies are 20.6% for (GT)23 and 30.1% for (GT)30). We assigned those with GT repeats ≥30 as allele class L (long) and those with GT repeats <30 as allele class S (short) owing to two reasons. First, Yamada et al.15.Yamada N. Yamaya M. Okinaga S. Microsatellite polymorphism in the heme oxygenase-1 gene promoter is associated with susceptibility to emphysema.Am J Hum Genet. 2000; 66: 187-195Abstract Full Text Full Text PDF PubMed Scopus (489) Google Scholar also defined an allele with the number of GT repeats ≥30 as a long allele (class L) in the Japanese population, which, like our Chinese population, is a part of eastern Asian people. Second, the alleles with GT repeats ≥30 accounted for about 50% of all the alleles of HD patients and controls in our study. The genotype of the study individual was defined as (1) class L/L if both allele lengths of GT repeats were ≥30, (2) class L/S if one GT repeat was ≥30 and the other was <30, and (3) class S/S if both allele lengths of GT repeats were <30. Therefore, the case number in any genotype group will not be too small to allow appropriate statistical analysis. The distribution of allele and genotype classes did not differ between whole HD patients and healthy controls (Table 2).Table 1Clinical characteristics of HD patients by the presence of failure of AV fistulaOverall (n=603)No AVF failure (n=425)AVF failure (n=178)P-valueMale (%)52.651.355.60.33Age (years)60.0±14.559.8±14.060.6±15.80.57HD duration (months)70.3±58.262.5±53.089.2±65.6<0.001Site of AV fistula Right side (%)22.618.632<0.001 Left side (%)77.481.468Location of AV fistula Upper arm (%)14.49.227<0.001 Forearm (%)85.690.873Survival of AV fistula (months)56.5±53.364.3±52.938.1±49.6<0.001Time between creation of AV fistula and initial HD (months)1.64±4.211.79±6.951.29±3.870.368Dynamic venous pressure under pump flow at 250 ml/min (mmHg)142.6±29.9140.9±29.9148.20±29.5<0.001Maximal pump flow (ml/min)271.9±33.3273.2±34.4268.8±30.10.14Hypertension (%)52.95645.50.019Diabetes mellitus (%)30.530.430.90.894Cerebral infarction (%)8.67.810.70.246Peripheral arterial obstructive disease (%)4.63.86.70.113Coronary artery disease (%)21.119.524.70.154Cardiovascular disease (%)27.224.932.60.054 Open table in a new tab Table 2Comparison of HO-1 promoter genotypes and allele frequencies among controls, total and subgroups of hemodialysis patients (with and without AVF failure)ControlsTotal HD patientsHD patients without AVF failureHD patients with AVF failureP-valueAlleles, n (%)n=572n=1206n=850n=356 S (short)285 (49.8%)593 (49.2%)441 (51.9%)152 (42.7%)NS*Signifies the P-value for the comparison between controls and HD patients L (long)287 (50.2%)613 (50.8%)409 (48.1%)204 (57.3%)0.004#signifies the P-value for the comparison between HD patients with and without AVF failure.Genotypes, n (%)n=286n=603n=425n=178 S/S61 (21.3%)148 (24.5%)118 (27.8%)30 (16.8%)NS*Signifies the P-value for the comparison between controls and HD patients L/S163 (57%)297 (49.3%)205 (48.2%)92 (51.7%)0.011#signifies the P-value for the comparison between HD patients with and without AVF failure. L/L62 (21.7%)158 (26.2%)102 (24%)56 (31.5%)The alleles were classified into two subgroups according to the number of GT repeats: the S group with repeat number <30, and the L group with ≥30 GT repeats; the genotypes were classified into three subgroups according to the number of GT repeats at both chromosomes: the S/S group with both repeat numbers <30, L/S group with one repeat number <30 and one repeat number ≥30, and L/L group with both repeat numbers ≥30. NS=nonsignificant.* Signifies the P-value for the comparison between controls and HD patients# signifies the P-value for the comparison between HD patients with and without AVF failure. Open table in a new tab The alleles were classified into two subgroups according to the number of GT repeats: the S group with repeat number <30, and the L group with ≥30 GT repeats; the genotypes were classified into three subgroups according to the number of GT repeats at both chromosomes: the S/S group with both repeat numbers <30, L/S group with one repeat number <30 and one repeat number ≥30, and L/L group with both repeat numbers ≥30. NS=nonsignificant. As shown in Table 2, the proportion of L allele frequency (57.3 vs 48.1%; P=0.004) and the proportion of L/L genotype frequency (31.5 vs 24%; P=0.011) were significantly higher in HD patients with AVF failure than in those without AVF failure. With regard to the frequencies of HD patients with AVF failure in different classes of genotypes, the proportion of AVF failure increases from 20.3% in class S/S to 31.0% in class L/S and 35.4% in class L/L (Table 3; P=0.011).Table 3HO-1 genotypes and vascular diseases in hemodialysis patientsGenotype, case number (n)S/S n=148L/S n=297L/L n=158P-valueHypertension (%)51.452.954.4NSDiabetes mellitus (%)25.731.632.9NSCerebral infarction (%)7.49.87.6NSPeripheral arterial obstructive disease (%)3.44.75.7NSCoronary artery disease (%)14.220.229.10.005Cardiovascular disease (%)20.327.333.50.033AVF failure (%)20.331.035.40.011 Open table in a new tab In comparison with HD patients with S/S genotype of HO-1, those with L/L genotype had a significantly higher prevalence of CAD (29.1 vs 14.2%; P=0.005) and cardiovascular disease (33.5 vs 20.3%; P=0.033), but similar frequencies of hypertension, DM, cerebral infarction, and PAODs (Table 3). Table 4 shows the Cox regression model for the association of AVF failure with the selected parameters carrying obvious or borderline statistical significances from Table 1. There was a significant correlation between increasing incidence of AVF failure and longer HD duration, lower pump flow, higher dynamic venous pressure, location of AVF at the right side and upper arm, and L/L and L/S genotypes of HO-1. HO-1 genotype polymorphism was a strongly relevant factor and showed a significant difference, with a hazard ratio of 2.040 and a 95% confidence interval between 1.295 and 3.215 (P=0.002).Table 4Cox regression model of factors associated with AVF failure in HD patientsSignificanceHazard ratio95% CI lower95% CI upperHD duration (months)0.0061.0041.0011.008Pump flow (ml/min)0.0060.9930.9880.998Maximal venous pressure (mmHg)<0.0011.0101.0041.015Right vs left side0.0051.5871.1472.197Upper arm vs forearm<0.0012.2421.5573.228HO-1 genotype (L/L+L/S vs S/S)0.0022.0401.2953.215Cardiovascular disease0.2241.4240.8052.517Hypertension0.8580.9450.5071.760 Open table in a new tab Some patients experienced multiple episodes of AVF failure during observation. Thus, HO-1 genotypes and the relative incidence of AVF failure (number of incidences per patient-months of follow-up) were calculated. Table 5 lists the relative incidence of AVF failure in HD patients according to the three different HO-1 genotypes. Relative incidences were 1 episode per 87.6 patient-months, 1 episode per 129 patient-months, and 1 episode per 224.9 patient-months for HD patients with L/L, L/S, and S/S genotypes, respectively. The relative incidence in the subgroup of L/L genotype (1 episode per 87.6 patient-months) was significantly greater than that in the subgroup of S/S genotype (1 episode per 224.9 patient-months; P<0.002; Table 5).Table 5HO-1 genotypes and relative incidence of AVF failure in HD patientsGenotypeTotal observations (patient-months)Episodes (times)Episodes/patient-monthsS/S10794.7481/224.9P<0.002S/L20513.61591/129.0L/L11035.21261/87.6Total42343.53331/127.2 Open table in a new tab Of the 148 patients with S/S genotypes, fistula failure occurred in 30 patients after 46.4±54.3 months, whereas the remaining 118 patients without fistula failure were followed for 65.1±54.2 months (P=0.09). Among the 297 HD patients with L/S genotypes, 92 patients developed AV fistula failure after a mean time of 37.2±45.2 months. The remaining 205 patients without fistula failure were followed for 63.2±53.6 months (P<0.001). Among the 158 patients with L/L genotypes, 56 patients had fistula failure that occurred after 35.0±54.1 months. The 102 patients who had no fistula failure had a mean follow-up of 65.7±50.4 months (P<0.001). The time of follow-up in patients without fistula failure did not differ significantly among the three genotype subgroups (S/S, L/S, and L/L). We evaluated the effect of different genotypes of HO-1 on AVF patency for all the HD patients in this study. As shown in Figure 2, AV fistula patency differed significantly when patients were classified according to their HO-1 genotypes. The unassisted patency of AV fistulae at 5 years decreased significantly from 83.8% (124/148) in patients with S/S genotypes to 75.1% (223/297) in patients with L/S genotypes and further to 69% (109/158) in patients with L/L genotypes (P<0.0001 by log-rank test; Figure 2). According to the recommendation of the Disease Outcomes Quality Initiative (DOQI) guidelines, creation of native AV fistulas at the upper extremity is preferable to placement of AV graft account of lower morbidity and higher long-term patency. Nevertheless, stenosis remains the most frequent complication for native AV fistulas and may predispose to thrombosis and subsequent AVF failure. In this study, both univariate and multivariate analyses showed that the presence of AVF failure could be significantly correlated with several clinical factors, including HD duration, location of AV fistula at the upper arm (cephalic vein-to-brachial artery anastomosis) or right upper extremity, and dynamic venous pressure. As to the preferable location of vascular access, usually the first native AV fistula will be created at the forearm of the nondominant hand. Since more than 95% of our HD patients use the right hand as their dominant hand, the desirable location of AVF placement should be the left forearm (brachiocephalic vein-to-radial artery anastomosis at wrist). Henceforth, the generalized vascular quality was usually poorer in these HD patients, with location of their first AVF at the upper arm (cephalic vein to brachial artery at elbow) or right side because a suitable vein for the creation of AVF was not available at the left forearm. It is reasonable that HD patients with poorer vascular condition may also have higher risk of AVF failure. Patients with AVF stenosis usually have a higher dynamic venous pressure than those without stenosis. From univariate analysis, hypertension was a significant factor in decreasing the frequency of AVF failure. As we know, hypotension may increase the risk of access failure because reducing Qa may predispose to clotting in a dialyzer. HD patients with hypertension should be less prone to hypotension, and therefore may have a lower prevalence of AVF failure than those without hypotension. In comparison with HD patients without hypertension, however, those with hypertension had a lower frequency of location of AVF at the upper arm (11.9 vs 18.2%, P<0.05). As location of AVF at the upper arm is a risk factor of AVF failure by our results, its lower frequency might reduce the risk of AVF failure in those with hypertension. Therefore, hypertension was no more significant in reducing the frequency of AVF failure after the confounding effect of AVF location was removed by multivariate analysis. On the contrary, maximal pump flow was not significant in univariate analysis, but was significant in multivariate analysis, which might be caused by higher prevalence of location of AVF at the upper arm in those with AVF failure. The Qa of AVF at the upper arm is usually higher than that of AVF at the forearm. A higher Qa usually permits a higher maximal pump flow. Consequently, the maximal pump flow may increase more in those with AVF failure than in those without AVF failure under the above-mentioned confounding effect between these variables. After adjusting for the confounding effect arising from location of AVF at the upper arm, maximal pump flow was significantly lower in those with AVF failure by multivariate analysis. In our study, both older age and a history of diabetes mellitus (DM) were not significant risk factors for AVF failure, which is similar to the results of some large-scale single-center16.Konner K. Hulbert-Shearon T.E. Roys E.C. Port F.K. Tailoring the initial vascular access for dialysis patients.Kidney Int. 2002; 62: 329-338Abstract Full Text Full Text PDF PubMed Scopus (166) Google Scholar and multi-center8.Fukasawa M. Matsushita K. Kamiyama M. et al.The methylenetetrahydrofolate reductase C677T point mutation is a risk factor for vascular access thrombosis in hemodialysis patients.Am J Kidney Dis. 2003; 41: 637-642Abstract Full Text Full Text PDF PubMed Scopus (48) Google Scholar, 17.Saran R. Dykstra D.M. Wolfe R.A. Association between vascular access failure and the use of specific drugs: The Dialysis Outcomes and Practice Patterns Study (DOPPS).Am J Kidney Dis. 2002; 40: 1255-1263Abstract Full Text Full Text PDF PubMed Scopus (144) Google Scholar studies on AVF survival. Only a few earlier single-center studies, including smaller case numbers, reported a significantly reduced AVF survival in HD patients with old age or DM.18.Golledge J. Smith C.J. Emery J. Outcome of primary radiocephalic fistula for haemodialysis.Br J Surg. 1999; 86: 211-216Crossref PubMed Scopus (101) Google Scholar However, these two characteristics were risk factors for failure of synthetic AV grafts in HD patients.17.Saran R. Dykstra D.M. Wolfe R.A. Association between vascular access failure and the use of specific drugs: The Dialysis Outcomes and Practice Patterns Study (DOPPS).Am J Kidney Dis. 2002; 40: 1255-1263Abstract Full Text Full Text PDF PubMed Scopus (144) Google Scholar Moreover, our study revealed that there was no correlation between cardiovascular disease and AVF failure, which is similar to the studies reporting no association of AVF failure with a history of any vascular disease, including CAD,8.Fukasawa M. Matsushita K. Kamiyama M. et al.The methylenetetrahydrofolate reductase C677T point mutation is a risk factor for vascular access thrombosis in hemodialysis patients.Am J Kidney Dis. 2003; 41: 637-642Abstract Full Text Full Text PDF PubMed Scopus (48) Google Scholar, 19.Dixon B.S. Novak L. Fangman J. Hemodialysis vascular access survival: upper-arm native arteriovenous fistula.Am J Kidney Dis. 2002; 39: 92-101Abstract Full Text Full Text PDF PubMed Scopus (231) Google Scholar cerebral vascular disease,8.Fukasawa M. Matsushita K. Kamiyama M. et al.The methylenetetrahydrofolate reductase C677T point mutation is a risk factor for vascular access thrombosis in hemodialysis patients.Am J Kidney Dis. 2003; 41: 637-642Abstract Full Text Full Text PDF PubMed Scopus (48) Google Scholar or peripheral vascular disease.19.Dixon B.S. Novak L. Fangman J. Hemodialysis vascular access survival: upper-arm native arteriovenous fistula.Am J Kidney Dis. 2002; 39: 92-101Abstract Full Text Full Text PDF PubMed Scopus (231) Google Scholar Cardiovascular diseases are more greatly characterized by inflammatory response and endothelial dysfunction than AVF stenosis. In addition, the main pathological feature of AVF stenosis is intimal hyperplasia, which is different from the atherosclerotic lesions specific to cardiovascular diseases. Although the above-mentioned risk factors of AVF failure have been identified in this study, stenosis still develops with wide individual variation. As the stenotic lesions are characterized by intimal hyperplasia originating from VSMC migration, proliferation, and exuberant synthesis of extracellular matrix,20.Lemson M.S. Tordoir J.H. Daemen M.J. Kitslaar P.J. Intimal hyperplasia in vascular grafts.Eur J Vasc Endovasc Surg. 2000; 19: 336-350Abstract Full Text PDF PubMed Scopus (139) Google Scholar some factors (such as TGF-β and homocysteine) were associated with these pathologic characteristics. Further, according to the genetic reports by Heine et al.7.Heine G.H. Ulrich C. Sester U. et al.Transforming growth factor beta1 genotype polymorphisms determine AV fistula patency in hemodialysis patients.Kidney Int. 2003; 64: 1101-1107Abstract Full Text Full Text PDF PubMed Scopus (57) Google Scholar and Fukasawa et al.,8.Fukasawa M. Matsushita K. Kamiyama M. et al.The methylenetetrahydrofolate reductase C677T point mutation is a risk factor for vascular access thrombosis in hemodialysis patients.Am J Kidney Dis. 2003; 41: 637-642Abstract Full Text Full Text PDF PubMed Scopus (48) Google Scholar genotype polymorphisms of TGF-β and MTHFR are independent factors for predicting AVF stenosis and patency. We investigated HO, another genetic factor other than TGF-β and homocysteine, possibly contributing to the pathophysiologic features of AVF stenosis. HO catalyzes the rate-limiting step in the degradation of heme by cleaving the α-meso carbon bridge of heme, leading to the generation of equimolar quantities of CO, free iron, and biliverdin.21.Tenhunen R. Marver H.S. Schmidt R. The enzymatic conversion of heme to bilirubin by microsomal heme oxgyenase.Proc Natl Acad Sci USA. 1968; 244: 6388-6394Google Scholar There are three isoforms of HO: (i) HO-1, an inducible 32-kDa protein, is ubiquitously distributed, and its encoding gene is located at chromosome 22q12;11.Lavrovsky Y. Schwartzman M.C. Levere R.D. Identification of binding sites for transcription factors NF-κB and AP-2 in the promoter region of the human heme oxygenase-1 gene.Proc Natl Acad Sci USA. 1994; 91: 5987-5991Crossref PubMed Scopus (340) Google Scholar (ii) HO-2, a constitutively expressed 36-kDa protein, is present in high levels in the brain and testes, and its encoding gene is located at" @default.
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• W2048309822 title "Length polymorphism in heme oxygenase-1 is associated with arteriovenous fistula patency in hemodialysis patients" @default.
• W2048309822 cites W1524392242 @default.
• W2048309822 cites W1829187584 @default.
• W2048309822 cites W1972340186 @default.
• W2048309822 cites W1979672764 @default.
• W2048309822 cites W1988329029 @default.
• W2048309822 cites W1990557868 @default.
• W2048309822 cites W2010572306 @default.
• W2048309822 cites W2013790946 @default.
• W2048309822 cites W2014002468 @default.
• W2048309822 cites W2019545491 @default.
• W2048309822 cites W2021030855 @default.
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• W2048309822 cites W2059625939 @default.
• W2048309822 cites W2061755142 @default.
• W2048309822 cites W2071425400 @default.
• W2048309822 cites W2078199018 @default.
• W2048309822 cites W2084001563 @default.
• W2048309822 cites W2086805237 @default.
• W2048309822 cites W2096238897 @default.
• W2048309822 cites W2105529372 @default.
• W2048309822 cites W2120981783 @default.
• W2048309822 cites W2124433916 @default.
• W2048309822 cites W2144630241 @default.
• W2048309822 cites W2145530136 @default.
• W2048309822 cites W2149167244 @default.
• W2048309822 cites W2151815632 @default.
• W2048309822 cites W2156465612 @default.
• W2048309822 cites W2156570713 @default.
• W2048309822 cites W2161790711 @default.
• W2048309822 cites W2166427090 @default.
• W2048309822 cites W2170662335 @default.
• W2048309822 cites W2254934747 @default.
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