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ABSTRACT: BACKGROUND & AIMS: The efficacy of homocysteine-lowering therapy with folic acid to lower homocysteine levels in an effort to reduce cardiovascular disease (CVD) risk in patients with kidney disease remains inconclusive. We conducted a meta-analysis of relevant randomized trials to further examine this issue. METHODS: This meta-analysis included 8234 patients with kidney disease from nine qualified randomized trials using folic acid therapy, and with CVD reported as one of the endpoints. Relative risk (RR) was used to measure the effect of folic acid supplementation on risk of CVD using a random effects model. RESULTS: When pooling the nine randomized trials, folic acid therapy reduced the risk of CVD by 10%（RR = 0.90; 95% CI:0.81-1.00, P = 0.046). A greater beneficial effect was observed among those trials without a history of grain fortification with folic acid (0.82; 0.70-0.96, P = 0.01), with lower percent baseline diabetes (<30% (median), 0.80; 0.65-0.99, P = 0.04), and in patients with end-stage renal disease (ESRD) or advanced chronic kidney disease (ACKD) (0.85; 0.77-0.94, P = 0.002). Furthermore, a meta-regression analysis suggested a positive dose-response relationship between percent baseline diabetes and log-RR for CVD risk associated with folic acid supplementation (P = 0.007). Most importantly, even the inclusion of three subgroup results did not substantially affect the results (n = 11032, RR: 0.93; 95% CI:0.87-0.99, P = 0.03). CONCLUSIONS: Our meta-analysis indicates that folic acid supplementation may be effective for CVD prevention in patients with kidney disease, particularly in trials among patients without a history of grain fortification with folic acid, with lower percent baseline diabetes, and in patients with ESRD or ACKD.
Clinical nutrition (Edinburgh, Scotland) 12/2012; · 3.27 Impact Factor
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Jianping Jiang,
Pingyan Chen,
Jianghua Chen,
Xueqing Yu,
Di Xie,
Changlin Mei,
Fei Xiong,
Wei Shi,
Wei Zhou,
Xusheng Liu, [......],
Xinling Liang,
Zhimin Zhang,
Qizhan Lin,
Yan Yu,
Toshio Miyata,
Jianwei Tian,
Min Liang,
Weihong Luo,
Xin Xu, Fanfan Hou
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ABSTRACT: Accumulation of tissue advanced glycation end products (AGEs) is a marker of cumulative glycemic and/or oxidative stress. Cutaneous AGEs levels measured by skin autofluorescence correlate well with cardiovascular outcomes in diabetes and hemodialysis (HD) patients. The present study aimed to compare tissue AGEs levels with peritoneal dialysis (PD) and HD patients and to evaluate the relationship between skin autofluorescence and cardiovascular morbidity in patients on PD.
A total of 2388 maintenance dialysis patients (613 PD and 1775 HD) were enrolled in this cross-sectional study. Skin autofluorescence was measured non-invasively with an autofluorescence reader. Cardiovascular morbidity was defined as clinically diagnosed ischemic heart disease, heart failure, stroke or peripheral vascular disease from initiation of dialysis.
More than 90% of patients on both PD and HD had met current dialysis adequacy targets. Compared to HD group, PD patients receiving conventional glucose-containing dialyzate had significantly higher skin autofluorescence values in each category of age and dialysis duration, irrespective of the presence or absence of diabetes. In PD patients, skin autofluorescence values were strongly correlated with the duration of PD and glucose exposure dose and independently associated with cardiovascular morbidity. Multivariate analysis revealed that glucose exposure dose and skin autofluorescence were the strongest risk factors for cardiovascular morbidity in PD patients after adjustment by age, gender, and other classic- or uremic-related risk factors.
Accumulation of tissue AGEs provides a potential link between PD exposure of metabolic stress and progression of cardiovascular disease in patients on PD.
Atherosclerosis 07/2012; 224(1):187-94. · 3.79 Impact Factor
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ABSTRACT: Acute worsening of renal function, an independent risk factor for adverse outcomes in acute decompensated heart failure (ADHF), occurs as a consequence of new onset kidney injury (AKI) or acute deterioration of pre-existed chronic kidney disease (CKD) (acute-on-chronic kidney injury, ACKI). However, the possible difference in prognostic implication between AKI and ACKI has not been well established.
We studied all consecutive patients hospitalized with ADHF from 2003 through 2010 in Nanfang Hospital. We classified patients as with or without pre-existed CKD based on the mean estimated glomerular filtration rate (eGFR) over a six-month period before hospitalization. AKI and ACKI were defined by RIFLE criteria according to the increase of the index serum creatinine.
A total of 1,005 patients were enrolled. The incidence of ACKI was higher than that of AKI. The proportion of patients with diuretic resistance was higher among patients with pre-existed CKD than among those without CKD (16.9% vs. 9.9%, P = 0.002). Compared with AKI, ACKI was associated with higher risk for in-hospital mortality, long hospital stay, and failure in renal function recovery. Pre-existed CKD and development of acute worsening of renal function during hospitalization were the independent risk factors for in-hospital death after adjustment by the other risk factors. The RIFLE classification predicted all-cause and cardiac mortality in both AKI and ACKI.
Patients with ACKI were at greatest risk of adverse short-term outcomes in ADHF. Monitoring eGFR and identifying CKD should not be ignored in patients with cardiovascular disease.
BMC Nephrology 07/2012; 13:51. · 2.18 Impact Factor
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Qiugen Zhou,
Shengjie Wu,
Jianping Jiang,
Jianwei Tian,
Jianghua Chen,
Xueqing Yu,
Pingyan Chen,
Changlin Mei,
Fei Xiong,
Wei Shi,
Wei Zhou,
Xusheng Liu,
Shiren Sun,
D I Xie,
Jun Liu,
Xin Xu,
Min Liang, Fanfan Hou
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ABSTRACT: Whether the burden of advanced oxidation protein products (AOPP) accumulation, a marker of oxidative stress, is affected by dialysis modality remains unclear. We compared the serum levels of AOPP in patients on haemodialysis (HD) and continuous ambulatory peritoneal dialysis (CAPD) and tested the hypothesis that an accumulation of AOPP was an independent risk factor for cardiovascular disease.
This was a cross-section study. A total of 2095 patients (1539 HD, 556 CAPD) were recruited from the nine largest dialysis centres in China. Persons in medical centres for disease screening were selected as controls. Patients maintained on HD were dialyzed twice or thrice weekly. CAPD patients used lactate-buffered, glucose-containing solutions. The patients' data were abstracted from the medical record. The serum levels of AOPP were determined by spectrophotometric detection.
The levels of AOPP were significantly elevated in both HD and CAPD patients compared to healthy controls. Accumulation of AOPP was more significant in HD compared to CAPD population. Meanwhile, AOPP accumulation was associated with the presence of ischaemic heart disease (IHD) only in HD, but not CAPD patients. A higher proportion of IHD was found in the HD population among those with higher levels of AOPP in each category of age and irrespective of the presence or absence of high triglyceride. Multivariate regression analysis indicated that accumulation of AOPP was an independent risk factor for IHD in HD population.
Accumulation of AOPP was more significant in HD compared to CAPD patients. The level of AOPP was independently associated with IHD only in HD patients.
Nephrology 06/2012; 17(7):642-9. · 1.31 Impact Factor
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ABSTRACT: Advanced oxidation protein products (AOPP) as a biomarker of oxidative stress has been demonstrated in chronic kidney disease (CKD) patients; however, current methods to detect the accumulation of AOPP in serum and in tissues are limited and unreliable. This study generated a monoclonal antibody (mAb) designated 3F2, that reacts specifically with hypochlorous acid (HOCl)-modified proteins, but not with the native forms or with other types of oxidative modifications. Notably, mAb 3F2 recognizes the AOPP deposited in renal tissues of AOPP-treated rats and of patients with different kinds of CKD. Moreover, this mAb can almost completely inhibit the production of reactive oxygen species in RAW264.7 cells induced by AOPP (p < 0.001). In conclusion, mAb 3F2 can be used to detect AOPP specifically in serum and in tissues, and this antibody can potentially provide an important tool and new insight into research on diseases related to oxidative stress.
Free radical research 03/2011; 45(6):662-71. · 2.22 Impact Factor
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ABSTRACT: The efficacy of folic acid therapy to lower homocysteine (Hcy) levels in an effort to reduce cardiovascular disease (CVD) risk in patients with ESRD or advanced chronic kidney disease (ACKD; creatinine clearance, <30 ml/min) remains inconclusive. We conducted a meta-analysis of relevant randomized trials to further examine this issue.
This meta-analysis included 3886 patients with ESRD/ACKD from seven qualified randomized trials using folic acid therapy and with CVD reported as one of the end points.
When pooling the seven trials, folic acid therapy reduced the risk of CVD by 15% (RR, 0.85; 95% CI, 0.76 to 0.96; P = 0.009). A greater beneficial effect was observed among those trials with a treatment duration >24 months (RR, 0.84; 95% CI, 0.72 to 0.98; P = 0.02), a decrease in Hcy level >20% (RR, 0.83; 95% CI, 0.73 to 0.95; P = 0.007), and no or partial folic acid fortification (RR, 0.80; 95% CI, 0.65 to 0.99; P = 0.04). The beneficial effect also was seen when Hcy levels decreased >20%, even in the presence of folic acid fortification (RR, 0.85; 95% CI, 0.73 to 0.99; P = 0.04). In the corresponding comparison groups, the estimated RRs were attenuated and insignificant.
Folic acid therapy can reduce CVD risk in patients with ESRD/ACKD by 15%. A greater beneficial effect was observed among those trials with no or partial folic acid fortification or a decrease in Hcy level >20% regardless of folic acid fortification.
Clinical Journal of the American Society of Nephrology 11/2010; 6(3):482-8. · 5.23 Impact Factor
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ABSTRACT: Accumulation of plasma advanced oxidation protein products (AOPPs) promotes progression of proteinuria and glomerulosclerosis. To investigate the molecular basis of AOPPs-induced proteinuria, normal Sprague-Dawley rats were treated with AOPPs-modified rat serum albumin. The expression of glomerular podocyte slit diaphragm (PSD)-associated proteins, nephrin and podocin, was significantly decreased coincident with the onset of albuminuria in rats treated with AOPPs. Chronic inhibition of NADPH oxidase by apocynin prevented down-regulation of nephrin and podocin and decreased albuminuria in AOPPs-challenged rats. This suggested that accumulation of AOPPs promotes proteinuria, possibly via down-regulating the expression of PSD-associated proteins.
Science China. Life sciences 01/2010; 53(1):68-77. · 2.02 Impact Factor
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Yu Wang,
Luxia Zhang,
Xiaomei Li,
Yulan Xu,
Min Yang,
Jiaqi Qian,
Lining Wang,
Nan Chen,
Yong Gu,
Mangmang Chen, [......],
Guodong Huang,
Qing Zhang,
Rong Wang,
Li Wang,
Changlin Mei,
Youyun Li,
Zhihong Liu,
Liancheng Zhao,
Yangfeng Wu,
Hai Yan Wang
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ABSTRACT: Controlling hypertension is important to protect renal function and prevent cardiovascular disease in chronic kidney disease (CKD) patients. However, data on hypertension awareness, treatment and control among CKD patients are limited. Two nationwide surveys were conducted in China in 1999-2000 and 2004-2005 among, respectively, 1328 and 1244 adult, non-dialysis, hypertensive CKD patients, to assess the status of hypertension awareness, treatment and control and associated factors. A standard questionnaire was adopted, and blood pressure (BP) was measured by trained staff according to a standard protocol in both surveys. Compared with the data from 1999-2000, the data from 2004-2005 showed increased awareness (87.2 vs. 75.7%, P<0.001), treatment (85.9 vs. 80.4%, P=0.001) and control (30.0 vs. 21.1%, P<0.001, by the general threshold of BP<140/90 mm Hg; 7.7 vs. 5.9%, P=0.075, by an optimal threshold of BP<130/80 mm Hg) of hypertension. The odds ratios for general BP control were 1.4 (95% confidence index (CI), 1.1-1.7) for female gender, 1.1 (95% CI, 1.0-1.1) for high estimated glomerular filtration rate, 1.3 (95% CI, 1.1-1.6) for treatment in a local hospital, 2.8 (95% CI, 2.0-3.9) for hypertension awareness and 1.7 (95% CI, 1.4-1.9) for combined treatment. General physicians from local hospitals made greater contributions to the total improvement. Lack of treatment was mainly due to patients not recognizing the necessity for it. This is the first report of hypertension awareness, treatment and control among hypertensive CKD patients from a developing country. Improvement of awareness and general control of hypertension were demonstrated. Education of both physicians and patients regarding optimal BP control should be reinforced in the future.
Hypertension Research 06/2009; 32(6):444-9. · 2.58 Impact Factor
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ABSTRACT: To observe the effects of flavone from leaves of Diospyros kaki on adventitial fibroblasts proliferation by advanced oxidation protein products (AOPP) in vitro.
NIH-3T3 cells were cultured in vitro and treated with AOPP and flavone from leaves of Diospyros kaki, respectively, and observed in comparison with the control group. The ratio of cell proliferation was determined by non-radioactive MTS/PES assay.
The ratio of cell proliferation was 1.789 +/- 0.299 in the control group, and 2.064 +/- 0.141, 2.149 +/- 0.218, 2.108 +/- 0.165, 2.124 +/- 0.131 and 2.087 +/- 0.125 in AOPP groups corresponding to AOPP concentrations of 100, 50, 10, 1 and 0.1 microg/ml, respectively. It showed that AOPP significantly induced the fibroblasts proliferation when the concentration was above 100 ng/ml (P < 0.05). The ratio of cell proliferation was 1.714 +/- 0.179 in flavone from leaves of Diospyros kaki group corresponding to concentration of 50 microg/ml. It also showed that flavone from leaves of Diospyros kaki alone had no effect on fibroblasts proliferation (P > 0.05). With AOPP stimulation, flavone from leaves of Diospyros kaki significantly inhibited fibroblasts proliferation (P < 0.05).
Flavone from leaves of Diospyros kaki can significantly inhibit the adventitial fibroblasts proliferation stimulated by AOPP in vitro.
Zhong yao cai = Zhongyaocai = Journal of Chinese medicinal materials 04/2004; 27(3):186-8.
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ABSTRACT: To compare the value of ATN-ISI (acute tubular necrosis-individual severity index) and APACHE II (acute physiology and chronic health evaluation) score models in predicting mortality and renal outcome in patients with acute renal failure (ARF).
422 in-hospital patients with ARF were retrospectively analysed, the value in predicting prognosis and renal outcome of these two score models was compared. Renal outcome was observed three times, i.e. >or= 30 days, >or= 45 days and >or= 60 days after the occurrence of ARF and discriminant analysis was used in the study.
The scores of the two models both correlated significantly with the mortality of patients with ARF. When ATN-ISI scores were >or= 0.85, the mortality was 100% and it was the same with APACHE II when the scores were >or= 35. The areas under ROC curve of APACHE II and ATN-ISI were 0.817 +/- 0.021 and 0.880 +/- 0.018 respectively, suggesting good model discriminantion. For the correctly classificated rate of renal outcome, ATN-ISI was better than APACHE II at any time. When ATN-ISI scores were >or= 0.75, patients were dialysis dependent. When the scores were >or= 0.58 but less than 0.75, the patient's renal function did not recover but was not dialysis dependent; when the scores were < 0.58, the patients's renal function would recover. When APACHE II scores were >or= 26, patients were dialysis dependent. There was no cut-off score point to separate renal function recovery from renal dysfunction. However, when APACHE II scores were <or= 22, 19.6% of the patients had renal dysfunction and 80.4% of them had renal function recovered.
Both the score models are of value in predicting mortality and renal outcome in patients with ARF. ATN-ISI score model was better than APACHE II.
Zhonghua nei ke za zhi [Chinese journal of internal medicine] 11/2002; 41(11):769-72.
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ABSTRACT: To study the effect of advanced glycation end products (AGE) modified protein on nitric oxide (NO) production by human endothelial cells and the possible role of signal transduction pathway in this pathological procedure.
Human umbilical vein endothelial cells (HUVECs) and HUVEC-derived cell line (ECV304) were cultured in vitro with AGE modified human serum albumin (AGE-HSA) or AGE modified bovine serum albumin (AGE-BSA) of the concentrations of 12.5, 25, and 50 micro g/ml for 2, 4, 8, 12, and 24 hours. NO levels in the supernatant at each time point were determined by using Griess reagents. HUVECs and ECV304 cells incubated with HAS or BSA of the same concentrations were used as controls. The phosphorylation activity of cellular p38 mitogen-activated protein kinase (p38-MAPK) was analyzed by Western blot using a phospho-specific antibody after the cells were incubated with AGE-HAS or AGE-BSA of the concentration of 12.5, 25, 50, and 100 micro g/ml for 5, 15, 30, 60, and 120 minutes. HUVECs were incubated with SB 203580, a specific inhibitor of p38, of the concentrations of 0.075, 0.15, and 0.3 micro mol/L for 4 hours, then the culture with SB 203580 was extracted. The endothelial cells were cleansed with RPMI 1640 culture and then were incubated with AGE-HAS or AGE-BSA for 8 hours. The No level in this supernatant was examined after the above-mentioned method.
The NO level in the supernatant of culture of HUVECs incubated with AGE-HAS or AGE-HAS for 2 hours were 92.2% +/- 10.1% and 94.1% +/- 12.5% of the controls respectively. The NO levels reached the lowest values, 72.4% +/- 7.14% and 68.3% +/- 10.9% of the values of the controls respectively after 8-hour incubation with AGE-HAS or AGE-HAS. AGE-HSA and AGE-BSA decreased the NO levels in the supernatant in a dose and time-dependant manner. The unmodified HSA and BSA did not influence the NO production by HUVECs or ECV304 cells. There was no difference in inhibition effect on NO production between AGE-HSA and AGE-BSA (P > 0.05). There was no difference in response to AGE-HSA and AGE-BSA between HUVECs and ECV304 cells (P > 0.05). In the culture of HUVECs or of ECV304 cells incubated with AGE-HSA or AGE-BSA, the p38 phosphorylation activity was obviously enhanced 10 minutes after dose-dependently, reached its peak 30 minutes after, and returned to its basic level in 120 minutes. SB203580 of the concentration of 0.3 micro mol/L completely abolished the inhibitive effect of AGE-albumin on NO production by endothelial cells.
AGE modified protein inhibits the production of NO by human endothelial cells through activation of the p38 signal pathway. This AGE modification-induced pathobiological cascade may be involved in the pathogenesis of atherosclerosis seen in AGE-associated diseases.
Zhonghua yi xue za zhi 10/2002; 82(19):1328-31.
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ABSTRACT: To elucidate the relationship between the expression of receptors for AGE (RAGE) at the surface of monocyte and the plasma levels of tumor necrosis factor alpha (TNFalpha) and interleukin-1beta (IL-1beta), proinflammatory cytokines in patients with chronic renal failure (CRF) undergoing hemodialysis (HD).
Human serum albumin modified with AGE (AGE-HSA) was prepared in vitro and was radiolabeled with (125)I. Human peripheral blood monocytes were isolated from 59 CRF patients (37 of which underwent hemodialysis) and 30 normal volunteers by Ficoll-hypaque centrifugation technique. Specific binding of AGE-HSA to monocytes was analyzed by radioactive ligand-receptor binding assay. The degradation to AGE-HSA by monocytes was measured by trichloroacetic acid precipitation method. The expression of REGE in monocytes was determined by flow cytometry. The levels of TNFalpha and IL-1beta were detected by a sandwich enzyme immunoassay.
The specific binding of (125)I-AGE-HSA to monocytes was 41.4 fmol/10(5) cells +/- 2.2 fmol/10(5) cells, significantly higher than that in normal controls (31.6 fmol/10(5) cells +/- 4.1 fmol/10(5) cells, P < 0.05). The number of AGE conjugated protein at the monocytes' surface of CRF patients undergoing HD was 2.42 +/- 0.21 x 10(5)/cells, significantly higher than that in normal controls (1.74 +/- 0.29 x 10(5)/cells, P < 0.001), and the affinity constant (Kd) of the monocytes of CRF patients undergoing HD was 228 nmol/L +/- 100 nmol/L, not significantly different from that in normal controls (262 nmol/L +/- 108 nmol/L, P > 0.05). The degration rate of AGE-HAS by monocytes in CRF patients undergoing HD was 25.24% +/- 4.35%, significantly higher than that in normal controls (18% +/- 0.6%, P < 0.05). The fluorescent intensity of RAGE at the surface of monocytes in CRF patients undergoing HD was 3.68 +/- 0.42, significantly higher than that in normal controls (1.09 +/- 0.37, P < 0.05), When the monocytes were incubated in vitro with 50 microgram/ml of AGE-HSA, the levels of TNFalpha and IL-1beta in the supernatants of CRF patients undergoing HD were 197 +/- 98 ng/L and 357.0 +/- 140.1 ng/L respectively, both significantly higher than those in the normal controls (111 +/- 77 ng/L and 184 +/- 118 ng/L respectively, both P < 0.05). The secretion of proinflammatory cytokines was inhibited when the monocytes were preincubated with anti-RAGE. Increased RAGE level was accompanied by higher plasma levels of TNFalpha and IL-1beta.
The expression of AGE receptors in monocytes is up-regulated in patients with CRF. This may contribute to the enhanced plasma level of proinflammatory cytokines seen in HD patients.
Zhonghua yi xue za zhi 09/2002; 82(17):1168-72.
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ABSTRACT: To determine whether atherosclerosis may be accelerated by hyperhomocysteinemia in patients with chronic renal failure (CRF).
One hundred and ninety-seven CRF patients and 53 healthy volunteers were included in this study. Plasma total homocysteine (tHcy) levels were measured by using fluorescence polarization immunoassay. Intima-media thickness (IMT) and prevalence atherosclerotic plaques of the extracranial common carotid artery were determined by high-resolution B-mode ultrasonography. The changes in brachial artery diameter during reactive hyperemia (D(h)) and after administration of sublingual nitroglycerin (D(n)) were analyzed during ultrasonic examination.
The prevalence of hyperhomocysteinemia was 84.4% in the CRF patients. The mean level of tHcy (23.56 +/- 11.91) micro mol/L was significantly higher in the CRF patients than that in the healthy controls (7.97 +/- 2.65) micro mol/L (P < 0.01). The prevalence of atherosclerotic plaques and the mean IMT value of carotid artery were significantly increased in CRF patients compared with that in age-matched controls. Furthermore, arterial dilating function sush as D(h) and D(n) was significantly decreased in CRF patients [(D(h)) (4.05 +/- 3.81)% and (D(n)) (4.94 +/- 4.28)%] compared with that in controls [(D(h)) (8.81 +/- 6.15)% and (D(n)) (11.72 +/- 7.64)%] (P < 0.01). The levels of plasma tHcy were coherent with intensity of atherosclerosis in the CRF patients. Multiple stepwise regression analysis showed that in CRF patients, independent risk factors associated with value of IMT were level of tHcy, age, and duration of dialysis (RR = 0.484, P < 0.001), while those associated with D(h) arterial dilatation were plasma tHcy level, age, duration of dialysis and total cholesterol (RR = 0.263, P < 0.001) and those associated with D(n) were age and tHcy level (RR = 0.211, P < 0.001).
The results indicate that atherosclerosis and dysfunction of arterial vasodilation in CRF patients are associated with increase of plasma tHcy. Hyperhomocysteinemia may be an independent risk factor for atherosclerosis seen in CRF patients.
Zhonghua nei ke za zhi [Chinese journal of internal medicine] 09/2002; 41(8):517-21.
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ABSTRACT: Previous studies have demonstrated the accumulation of advanced glycation end products (AGE) in patients with chronic renal failure (CRF), but the mechanism is not completely understood. This study was performed to elucidate the effect of heparin on binding of AGE to its receptors on human monocytes.
Human serum albumin (HSA) modified with AGE was prepared in vitro and was radioiodinated with carrier-free [(125)I]. Human peripheral blood monocytes obtained from dialysis patients and normal volunteers were isolated by Ficoll-hypaque centrifugation technique. Specific binding (125)I-AGE-HSA to the AGE-receptor on human monocytes was measured by radioactive ligand-receptor binding assay.
The binding of (125)I-AGE-HSA to its receptors in dialysis patients was inhibited by 27% 15 minutes after starting of hemodialysis using heparin as anti-coagulant. These effects continued 6 hours and resume to the levels of predialysis after 24 hours. There was no differences in binding of (125)I-AGE-HSA to monocytes between pre-and post-dialysis session when low-molecule weight heparin (LMWH) was used as the anti-coagulant. In vitro study further demonstrated that exposure of normal monocytes to heparin-containing media inhibited the binding of (125)I-AGE-HSA to its receptor with a dose-dependent manner. LMWH did not inhibit such binding.
Heparin blocks the binding of AGE to its receptors on monocytes and may therefore interrupt the clearance and degradation of AGE. This may be one of the mechanisms by which AGE accumulation occurs in patients with hemodialysis.
Zhonghua nei ke za zhi [Chinese journal of internal medicine] 02/2002; 41(1):43-6.
