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Kyoung Chan Doh,
Sun Woo Lim,
Shang Guo Piao,
Long Jin,
Seong Beom Heo,
Yu Fen Zheng,
Soo Kyung Bae,
Gyu Hyun Hwang,
Kyoung Il Min,
Byung Ha Chung, Chul Woo Yang
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ABSTRACT: Background: This study was performed to investigate whether ginseng extract has a protective effect in an experimental mouse model of chronic cyclosporine (CsA) nephropathy. Methods: Mice were treated with CsA (30 mg/kg/day, subcutaneously) with or without Korean red ginseng extract (KRG) (0.2, 0.4 g/kg/day, orally) on a 0.01% salt diet for 4 weeks. The effect of KRG on CsA-induced renal injury was evaluated by assessing renal function and pathology, mediators of inflammation, tubulointerstitial fibrosis and apoptotic cell death. Using an in vitro model, we also examined the effect of KRG on CsA-treated proximal tubular cells (HK-2). Oxidative stress was measured by assessing 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels in 24-hour urine, tissue sections, and culture media. Results: Four weeks of CsA treatment caused renal dysfunction, typical pathologic lesions and apoptotic cell death. KRG treatment reduced serum creatinine and blood urea nitrogen and histopathology and increased creatinine clearance. Proinflammatory and profibrotic molecules such as induced nitric oxide synthase, cytokines, transforming growth factor (TGF)-β1 and TGF-β1-inducible gene h3 and apoptotic cell death, also decreased with KRG treatment. Consistent with these results, in vitro studies showed that addition of KRG protected against CsA-induced morphological changes, cytotoxicity, inflammation, and apoptotic cell death as demonstrated by annexin V binding. These changes were accompanied by decrease in the level of 8-OHdG in urine and culture supernatant after KRG treatment. Conclusion: The results of our in vivo and in vitro studies demonstrate that KRG has a protective effect in CsA-induced renal injury via reducing oxidative stress.
American Journal of Nephrology 04/2013; 37(5):421-433. · 2.54 Impact Factor
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ABSTRACT: Background: The aim of this study is to investigate the clinical characteristics and our experience of treating patients with IgA nephropathy (IgAN) and IgA nephropathy with hepatitis B surface antigen (HBs-IgAN). Methods: From 1996 to 2011, biopsy-proven IgAN was diagnosed in 477 patients and 22 (4.6%) had hepatitis B surface antigen (HBsAg). Of these, we included 360 patients who had more than 6-month follow-up period, and compared clinical characteristics and renal function decline between the patients with IgAN and HBs-IgAN. Results: Of 360 patients, 22 were classified as HBs-IgAN. There were no differences in the clinical characteristics and renal function decline between idiopathic IgAN and HBs-IgAN (-0.01 vs. -0.17 mL/min per 1.73 m(2)/month, p = 0.319). Of 22 patients with HBs-IgAN, nine had hepatitis B virus (HBV) replication marker (RM), of which six were treated with anti-viral agents. However, there were no differences in renal function decline and urinary protein excretion between patients who did or did not receive anti-viral therapy. Five patients with HBs-IgAN received corticosteroid therapy. Of these, three without HBV RM and one with HBV RM who received entecavir did not exhibit active viral replication, whereas the other patients with HBV RM experienced viral replication after lamivudine was discontinued. Conclusion: There were no differences in the clinical characteristics and prognosis between the patients with IgAN and HBs-IgAN. Further, there were no differences in renal function decline and urinary protein excretion between patients with and without anti-viral therapy. Anti-viral therapy may be considered for treating patients with HBs-IgAN receiving immunosuppressants according to HBV RM.
Renal Failure 03/2013; · 0.82 Impact Factor
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ABSTRACT: Plasma cell infiltration into a renal allograft comprises a spectrum of lesions from acute rejection to posttransplant lymphoproliferative disease. We report an unusual case of plasma cell infiltration into a renal allograft with monoclonal gammopathy. A 42-year-old woman was admitted because of graft dysfunction after noncompliance with immunosuppressive therapy for 5 months. A graft biopsy showed acute T-cell-mediated rejection and massive plasma cell infiltration. Despite initial treatment with steroids and antithymocyte globulin, there was persistence of graft dysfunction, monoclonal gammopathy, and plasma cell infiltration. Subsequent treatment with bortezomib improved graft function and caused the monoclonal gammopathy to resolve. Immunohistochemical evaluation of markers of B cells (CD20 and CD138) and the ratio of kappa-to-lambda light chain (15:1) showed that infiltrating cells were plasma cells producing kappa light chain. This suggested that plasma cell-rich acute rejection with monoclonal gammopathy in this patient might have been in an early stage of kappa light chain-producing posttransplant lymphoproliferative disease confined to the renal allograft, and that bortezomib may be effective in treating a patient with this condition.
Experimental and clinical transplantation : official journal of the Middle East Society for Organ Transplantation. 03/2013;
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Sun Ryoung Choi,
Ji Hee Lim,
Min Young Kim,
Yu-Ah Hong,
Byung Ha Chung,
Sungjin Chung,
Bum Soon Choi, Chul Woo Yang,
Yong-Soo Kim,
Yoon Sik Chang,
Cheol Whee Park
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ABSTRACT: Background: Secondary hyperparathyroidism (SHPT) in patients on hemodialysis is strongly associated with cardio-vascular morbidity and mortality. Treatment of SHPT with cinacalcet decreases circulating parathyroid hormone (PTH) concentrations and lowers serum calcium and phosphorus concentrations. Therefore, we investigated the cardiovascular effects of cinacalcet in hemodialysis patients with SHPT. Methods: We studied 12 hemodialysis patients with SPHT [serum intact PTH (iPTH) >300 pg/ml]. The study consisted of three phases: an initial run-in period of 16 weeks, including a wash-out period of 4 weeks (pretreatment), a cinacalcet treatment period of 20 weeks (treatment), and 20-week follow-up after suspension of cinacalcet treatment (posttreatment). In this study, vitamin D sterols were not prescribed to all the study subjects for at least 1 year during the pretreatment period. Results: Cinacalcet significantly decreased serum iPTH (pretreatment vs. treatment; 628.2 ± 250.8 vs. 251.7 ± 237.4 pg/ml, p < 0.01), calcium, phosphorus, and calcium × phosphorus product (p < 0.01), all of which returned to baseline levels after treatment. There was no change in C-reactive protein during the study period. There was significantly improvement in brachial flow-mediated dilatation (p < 0.01) and enhanced cardio-ankle vascular index (p < 0.01) with cinacalcet treatment. Moreover, cinacalcet significantly improved diastolic function (E/e' ratio, p < 0.05) and the left ventricular mass index (p < 0.05). Cinacalcet also increased serum NO x (p < 0.05) and decreased serum isoprostane (p < 0.05) and soluble intercellular adhesion molecule-1 concentrations (p < 0.05). All of these biochemical parameters returned to their pretreatment concentrations after withdrawal of cinacalcet. Conclusions: Cinacalcet hydrochloride without vitamin D might ameliorate endothelial dysfunction, diastolic dysfunction, and cardiac hypertrophy by decreasing oxidative stress and increasing the serum nitric oxide production in hemodialysis patients with SHPT.
Nephron Clinical Practice 03/2013; 122(1-2):1-8. · 2.04 Impact Factor
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Thrombosis Research 01/2013; · 2.44 Impact Factor
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ABSTRACT: BACKGROUND: Rifampin is one of the most important drugs in first-line therapies for tuberculosis. The renal toxicity of rifampin has been reported sporadically and acute tubulointerstitial nephritis (ATIN) is a frequent histological finding. We describe for the first time a case of ATIN and Fanconi syndrome presenting as hypokalemic paralysis, associated with the use of rifampin. CASE PRESENTATION: A 42-year-old man was admitted with sudden-onset lower extremity paralysis and mild renal insufficiency. He had been treated for pulmonary tuberculosis with isoniazid, rifampin, and ethambutol for 2 months. Laboratory tests revealed proteinuria, profound hypokalemia, hyperchloremic metabolic acidosis with a normal anion gap, positive urine anion gap, hypophosphatemia with hyperphosphaturia, hypouricemia with hyperuricosuria, glycosuria with normal serum glucose level, generalized aminoaciduria, and beta2-microglobulinuria. A kidney biopsy revealed findings typical of ATIN and focal granular deposits of immunoglubulin A and complement 3 in the glomeruli and tubules. Electron microscopy showed epithelial foot process effacement and electron-dense deposits in the subendothelial and mesangial spaces. Cessation of rifampin resolved the patient's clinical presentation of Fanconi syndrome, and improved his renal function and proteinuria. CONCLUSION: This case demonstrates that rifampin therapy can be associated with Fanconi syndrome presenting as hypokalemic paralysis, which is a manifestation of ATIN. Kidney function and the markers of proximal tubular injury should be carefully monitored in patients receiving rifampin.
BMC Nephrology 01/2013; 14(1):13. · 2.18 Impact Factor
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ABSTRACT: The timing of referral to a nephrologist may influence the outcome of chronic kidney disease patients, but its impact has not been evaluated thoroughly. The results of a recent study showing an association between early referral and patient survival are still being debated. A total of 1028 patients newly diagnosed as end-stage renal disease (ESRD) from July 2008 to October 2011 were enrolled. Early referral (ER) was defined as patients meeting with a nephrologist more than a year before dialysis and dialysis education were provided, and all others were considered late referral (LR). The relationship of referral pattern with mortality in ESRD patients was explored using a Cox proportional hazards regression models. Time from referral to dialysis was significantly longer in 599 ER patients than in 429 LR patients (62.3±58.9 versus 2.9±3.4 months, P<0.001). Emergency HD using a temporary vascular catheter was required in 485 (47.2%) out of all patients and in 262 (43.7%) of ER compared with 223 (52.0%) of LR (P = 0.009). After 2 years of follow-up, the survival rate in ER was better than that in LR (hazard ratio [HR] 2.38, 95% confidence interval [CI] 1.27-4.45, P = 0.007). In patients with diabetes nephropathy, patient survival was also significantly higher in ER than in LR (HR 4.74, 95% CI 1.73-13.00, P = 0.002). With increasing age, HR also increased. Timely referral to a nephrologist in the predialytic stage is associated with reduced mortality.
PLoS ONE 01/2013; 8(1):e55323. · 4.09 Impact Factor
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ABSTRACT: The aim of this study was to investigate whether hATMSCs protect against cyclosporine (CsA)-induced renal injury. CsA (7.5 mg/kg) and hATMSCs (3×10(6)/5 mL) were administered alone and together to rats for 4 weeks. The effect of hATMSCs on CsA-induced renal injury was evaluated by assessing renal function, interstitial fibrosis, infiltration of inflammatory cells, and apoptotic cell death. Four weeks of CsA-treatment produced typical chronic CsA-nephropathy. Combined treatment with CsA and hATMSCs did not prevent these effects and showed a trend toward further renal deterioration. To evaluate why hATMSCs aggravated CsA-induced renal injury, we measured oxidative stress, a major mechanism of CsA-induced renal injury. Both urine and serum 8-hydroxydeoxyguanosine(8-OHdG) levels were higher in the CsA+hATMSCs group than in the CsA group (P<0.05). An in vitro study showed similar results. Although the rate of apoptosis did not differ significantly between HK-2 cells cultured in hATMSCs-conditioned medium and those cultured in DMEM, addition of CsA resulted in greater apoptosis in HK-2 cells cultured in hATMSCs-conditioned medium. Addition of CsA increased oxidative stress in the hATMSCs-conditioned medium. The results of our study suggest that treatment with hATMSCs may aggravate CsA-induced renal injury because hATMSCs cause oxidative stress in the presence of CsA.
PLoS ONE 01/2013; 8(3):e59693. · 4.09 Impact Factor
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ABSTRACT: Objective: This study evaluated the prognostic value of the aortic calcification index (ACI), an estimate of abdominal aortic calcification by plain abdominal computed tomography (CT), in terms of left ventricular (LV) diastolic dysfunction, mortality, and nonfatal cardiovascular (CV) events in peritoneal dialysis (PD) patients. Method: PD patients who received both abdominal CT and echocardiography were divided into a low-ACI group (n=46) and a high-ACI group (n=46). Results: During follow-up (median, 35.2 months; range, 3.6 - 111.3), 30 patients (32.6%) died and 10 patients (10.9%) developed nonfatal cardiovascular (CV) events. The 5-year event-free survival rates for mortality and nonfatal CV events were significantly lower in the high-ACI group compared with those in the low-ACI group (35.7% vs. 64.1%, P = 0.01). The ACI was positively correlated with left atrial diameter and ratio of peak early transmitral flow velocity to peak early diastolic mitral annular velocity (E/E' ratio; a marker of left ventricular diastolic function). Using multivariate analyses, the high-ACI group (vs. low-ACI group, HR 5.25, 95% CI 1.77 - 15.58, P = 0.003) and increased E/E' ratio (HR 1.16, 95% CI 1.03 - 1.31, P = 0.013) were independent predictors for mortality and CV events. The ACI provided a higher predictive value for adverse outcomes (AUC = 0.755, P = 0.002) than the E/E' ratio (AUC = 0.543, P = 0.61). Conclusion: The ACI was significantly associated with left ventricular diastolic dysfunction and predicted all-cause mortality and nonfatal CV events in PD patients.
International journal of medical sciences 01/2013; 10(5):617-23. · 2.24 Impact Factor
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ABSTRACT: The aim of this study is to investigate the usefulness of the GFR-estimating equations to predict renal function in kidney donors before and after transplantation. We compared the performance of 24-hour-urine-based creatinine clearance (24 hr urine-CrCl), the Cockcroft-Gault formula (eGFRCG), the Modification of Diet in Renal Disease equation (eGFRMDRD), and the Chronic Kidney Disease Epidemiology Collaboration equation (eGFRCKD-EPI) with technetium-diethylenetriaminepentaacetic acid ((99m)Tc-DTPA) clearance (mGFR) in 207 potential kidney donors and 108 uninephric donors. Before donation, eGFRCKD-EPI showed minimal bias and did not show a significant difference from mGFR (P = 0.65, respectively) while 24 hr urine-CrCl and eGFRMDRD significantly underestimated mGFR (P<0.001 for each). Precision and accuracy was highest in eGFRCKD-EPI and this better performance was more dominant when renal function is higher than 90 mL·min(-1)·1.73 m(-2). After kidney donation, eGFRMDRD was superior to other equations in precision and accuracy in contrast to before donation. Within individual analysis, eGFRMDRD showed better performance at post-donation compared to pre-donation, but eGFRCKD-EPI and eGFRCG showed inferior performance at post-donation. In conclusion, eGFRCKD-EPI showed better performance compared to other equations before donation. In a uninephric donor, however, eGFRMDRD is more appropriate for the estimation of renal function than eGFRCKD-EPI.
PLoS ONE 01/2013; 8(4):e60720. · 4.09 Impact Factor
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Hyeon Seok Hwang,
Keum Jin Yang,
Ki Cheol Park,
Hyun Soo Choi,
So Hee Kim,
Sung Youp Hong,
Byeong Hwa Jeon,
Yoon Kyung Chang,
Cheol Whee Park,
Suk Young Kim,
Sang Ju Lee, Chul Woo Yang
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ABSTRACT: Background
The effect of paricalcitol on renal ischemia-reperfusion injury (IRI) has not been investigated. We examined whether paricalcitol is effective in preventing inflammation in a mouse model of IRI, and evaluated the cyclooxygenase-2 (COX-2) and prostaglandin E2 (PGE2) pathways as a protective mechanism of paricalcitol.Methods
Paricalcitol (0.3 μg/kg) was administered to male C57BL/6 mice 24 h before IRI. Bilateral kidneys were subjected to 23 min of ischemia, and mice were killed 72 h after IRI. The effects of paricalcitol on renal IRI were evaluated in terms of renal function, tubular necrosis, apoptotic cell death, inflammatory cell infiltration and inflammatory cytokines. The effects of paricalcitol on COX-2, PGE2 and its receptors were investigated.ResultsParicalcitol pretreatment improved renal function (decreased blood urea nitrogen and serum creatinine levels), tubular necrosis and apoptotic cell death in IRI-mice kidneys. The infiltration of inflammatory cells (T cells and macrophages), and the production of proinflammatory cytokines (RANTES, tumor necrosis factor-α, interleukin-1β and interferon-γ) were reduced in paricalcitol-treated mice with IRI. Paricalcitol up-regulated COX-2 expression, PGE2 synthesis and mRNA expression of receptor subtype EP4 in post-ischemic renal tissue. The cotreatment of a selective COX-2 inhibitor with paricalcitol restored functional injury and tubular necrosis in paricalcitol-treated mice with IRI.Conclusions
Our study demonstrates that paricalcitol pretreatment prevents renal IRI via the inhibition of renal inflammation, and the up-regulation of COX-2 and PGE2 is one of the protective mechanisms of paricalcitol in renal IRI.
Nephrology Dialysis Transplantation 12/2012; · 3.40 Impact Factor
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Hee Yeon Kim,
Mi-La Cho,
Joo Yeon Jhun,
Jae Kyeong Byun,
Eun-Kyung Kim,
Ye Been Yim,
Byung Ha Chung,
Seung Kew Yoon,
Si Hyun Bae,
Dong Goo Kim, Chul Woo Yang,
Jong Young Choi
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ABSTRACT: There is limited clinical research regarding the changes in peripheral lymphocytes subsets during the early postoperative period of liver transplantation. Serial changes of T cells and B cells in living donor liver transplantation (LDLT) recipients during the early posttransplantion period were prospectively investigated. From June 2010 to February 2011, 27 consecutive LDLT recipients were enrolled. Percentages of Th1 (interferon-γ-producing), Th2 (interleukin-4-producing), Th17 (interleukin-17-producing), Treg (CD4(+) CD25(+) FOXP3(+) ), memory B (CD19(+) CD24(hi) CD38(-) ) and mature B (CD19(+) CD24(int) CD38(int) ) cells were measured using fluorescence-activated cell sorting. Patients were followed up for a median of 9.9 months (range 6.8-15.5 months) after transplantation. Serial monitoring of immunological profiles showed no significant suppression of Th1, Th2, Th17, mature B or memory B cells, whereas frequencies of Tregs significantly decreased. IL-17 production by T(CM) or T(EM) was not suppressed during the early postoperative period. The continuous production of IL-17 by the memory T cells may contribute to the persistence of Th17 cells. This prospective study demonstrated that current immunosuppression maintained the effector T or memory B cells during the early posttransplantation period, however, significantly suppressed Tregs. Serial immune monitoring may suggest clues for optimal or individualized immunosuppression during the early postoperative period in clinical practice. © 2012 The Authors. Immunology © 2012 Blackwell Publishing Ltd.
Immunology 12/2012; · 3.32 Impact Factor
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The Korean Journal of Internal Medicine 12/2012; 27(4):470-3.
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ABSTRACT: Chronic hepatitis B infection is a common cause of secondary membranous nephropathy (MN) in endemic areas. Lamivudine treatment improves renal outcome in patients with hepatitis B virus-associated MN (HBV-MN), but prolonged use leads to the emergence of lamivudine-resistant variants. We describe our experience treating lamivudine-resistant and other strains of HBV-MN with new antiviral drugs.
Of the 89 patients biopsied and diagnosed with MN from 1996 to 2011, 10 positive for hepatitis B surface antigen were recruited for this study. We investigated the clinical courses, therapeutic responses, and prognoses of patients with HBV-MN.
The incidence of HBV-MN among the original 89 patients was 11.2%. Of these patients, four were treated with supportive care and six with antiviral drugs. One of the four patients treated with supportive care had a spontaneous remission. Four of the six patients treated with antiviral drugs were given lamivudine, and the other two were given entecavir. Two of the four patients treated with lamivudine achieved complete remission with seroconversion (i.e., development of anti-hepatitis B e antigen antibodies), whereas the other two had lamivudine-resistant strains, which were detected at 22 and 23 months after lamivudine treatment, respectively. We added adefovir to the treatment regimen for one of these patients, and for the other patient we substituted clevudine for lamivudine. Both of these patients experienced complete remission, as did the two patients initially treated with entecavir, neither of whom showed resistance to the drug.
New nucleoside analogues, such as entecavir, adefovir, and clevudine, can be effective for treatment of HBV-MN, including lamivudine-resistant strains.
The Korean Journal of Internal Medicine 12/2012; 27(4):411-6.
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ABSTRACT: A 27-year-old man presented at the emergency room with hemoptysis. His blood pressure was 180/100 mm Hg, and he had no history of hypertension. Chest radiographs showed bilateral infiltration, suggestive of alveolar hemorrhage. His laboratory data were consistent with acute kidney injury. His serum creatinine level increased abruptly; therefore, renal biopsy was performed. Steroid pulse therapy was administered because of a strong suspicion of immune-mediated pulmonary renal syndrome. Renal biopsy showed proliferative endarteritis, fibrinoid necrosis, and intraluminal thrombi in the vessels without crescent formation or necrotizing lesions. Steroid pulse therapy rapidly tapered and stopped. His serum creatinine level gradually decreased with strict blood pressure control. Ten months after discharge, his blood pressure was approximately 120/80 mm Hg with a serum creatinine level of 1.98 mg/dL. Pulmonary renal syndrome is generally caused by an immune-mediated mechanism. However, malignant hypertension accompanying renal insufficiency and heart dysfunction causing end-organ damage can create a pulmonary hemorrhage, similar to pulmonary renal syndrome caused by an immune-mediated mechanism. The present case shows that hypertension, a common disease, can possibly cause pulmonary renal syndrome, a rare condition.
Yonsei medical journal 11/2012; 53(6):1224-7. · 0.77 Impact Factor
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ABSTRACT: Background: We recently reported that long-term cyclosporine (CsA)-induced oxidative stress is associated with decreased expression of klotho, an anti-aging gene. This study evaluated whether the antioxidant effect of statin might upregulate klotho expression in CsA-induced renal injury. Methods: Two separate experiments were performed. First, the dose-dependent effect of statin on klotho expression was evaluated in normal mouse kidneys. Second, the effect of statin on klotho expression was evaluated in experimental chronic CsA nephropathy in mice. We performed immunohistochemistry and immunoblotting for klotho, Forkhead box O transcription factors [FoxOs; phosphorylated FoxO1 (p-FoxO1) and FoxO3a (p-FoxO3a)] and their target molecules, manganese superoxide dismutase (MnSOD), Bim and hemeoxygenase-1. Results: Statin treatment upregulated klotho expression in a dose-dependent manner in the normal mouse kidney and alleviated the decrease in klotho expression in kidneys exhibiting CsA nephropathy. CsA administration increased p-FoxO1 expression and decreased p-FoxO3a expression, whereas concurrent statin treatment reversed these changes, increased the expression of the antioxidant enzymes MnSOD and hemeoxygenase-1 and decreased the expression of the pro-apoptotic protein Bim. Conclusion: Statin-mediated upregulation of klotho expression and differential regulation of FoxO expression promote resistance to CsA-induced oxidative stress.
Nephron Experimental Nephrology 09/2012; 120(4):e123-e133. · 1.86 Impact Factor
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In O Sun,
Yu Ah Hong,
Hoon Suk Park,
Sun Ryoung Choi,
Seok Hui Kang,
Byung Ha Chung,
Bum Soon Choi,
Yeong Jin Choi, Chul Woo Yang,
Yong Soo Kim,
Cheol Whee Park
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ABSTRACT: Renal involvement in the form of glomerulonephritis in Sjögren's syndrome (SS) is less common and usually a latent sequel in the course of the disease. We report a patient with Type III membarnoproliferative glomerulonephritis (MPGN) with hypothyroidism, which precedes the onset of the clinical manifestation of SS. She received immunosuppressions consisting of i.v. cyclophosphamide and high-dose corticosteroid and subsequently oral corticosteroid resulting in complete remission of nephrotic syndrome. To our knowledge, this is the first report of successfully treated Type III MPGN associated with SS.
Clinical nephrology 09/2012; · 1.17 Impact Factor
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ABSTRACT: Vascular calcification of the coronary arteries or aorta is an independent risk factor for cardiovascular outcome, but clinical significance of arterial micro-calcification (AMC) of vascular access is unclear in hemodialysis (HD) patients. Sixty-five patients awaiting vascular access operation were enrolled. We compared surrogate markers of cardiovascular morbidity such as aortic arch calcification (AoAC) by chest radiography, arterial stiffness by brachial-ankle pulse wave velocity (baPWV) and endothelial dysfunction by flow-mediated dilatation (FMD) between patients with and without AMC of vascular access on von Kossa staining. AMC of vascular access was detected in 36 (55.4%). The AMC-positive group had significantly higher incidence of AoAC (63.9% vs. 20.7%, p < 0.001) and higher baPWV (26.5 ± 9.4 m/s vs. 19.8 ± 6.6 m/s, p = 0.006) than the AMC-negative group. There was no significant difference in FMD between the two groups (5.4 ± 2.6% vs. 5.7 ± 3.5%, p = 0.764). The AMC-positive group had higher incidence of diabetes mellitus, higher systolic blood pressure and wider pulse pressure than the AMC-negative group. This study suggests that AMC of vascular access may be associated with cardiovascular morbidity via AoAC and arterial stiffness in HD patients.
Seminars in Dialysis 08/2012; · 2.27 Impact Factor
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ABSTRACT: This study evaluated the significance of aortic calcification index (ACI), an estimate of abdominal aortic calcification by plain abdominal computed tomography (CT), in terms of left ventricular (LV) diastolic dysfunction, mortality, and nonfatal cardiovascular (CV) events in chronic hemodialysis patients. Hemodialysis patients who took both an abdominal CT and echocardiography were divided into a low-ACI group (n = 64) and a high-ACI group (n = 64). The high-ACI group was significantly older, had a longer dialysis vintage and higher comorbidity indices, and more patients had a previous history of CV disease than the low-ACI group. The ACI was negatively correlated with LV end-diastolic volume or LV stroke volume, and was positively correlated with the ratio of peak early transmitral flow velocity to peak early diastolic mitral annular velocity (E/E' ratio), a marker of LV diastolic function. The E/E' ratio was independently associated with the ACI. The event-free survival rates for mortality and nonfatal CV events were significantly lower in the high-ACI group compared with those in the low-ACI group, and the ACI was an independent predictor for all-cause deaths and nonfatal CV events. In conclusion, ACI is significantly associated with diastolic dysfunction and predicts all-cause mortality and nonfatal CV events in hemodialysis patients.
Journal of Korean medical science 08/2012; 27(8):870-5. · 0.84 Impact Factor
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ABSTRACT: The adequate rituximab (RTX) dosage in ABO-incompatible transplantation (ABO-IKT) remains undetermined. We used two kinds of RTX dosage groups [low RTX (100 mg/m(2)) and typical RTX (375 mg/m(2)) dosage groups] according to immunologic risks and investigated the change of B-cell, anti-ABO antibodies, and the clinical outcome in ABO-IKT according to the RTX dose. Fifteen patients with high immunologic risk [panel reactive antibody (PRA) > 50%, retransplant, AB to O transplant] were assigned to typical RTX group and 17 patients without risk were assigned to low RTX group. We compared the changes of B-cell, anti-ABO antibody titer, required number of plasmapheresis (PP), and the clinical outcome after transplantation between the two groups. After infusion of RTX, peripheral blood B-cell counts were successfully depleted to <1% in both groups. Before kidney transplantation (KT), the minimal number of PP to achieve the target titer (1:16) (2.6 ± 2.7 vs. 2.2 ± 2.5; p = 0.66) and the titer reduction rate of anti-ABO antibodies did not differ between the two groups (low RTX: 1.52 ± 1.21 vs. typical RTX: 1.53 ± 1.20, p = 0.94). After KT, anti-ABO antibody titer was suppressed less than 1:32 in both groups up to posttransplant 1 year. The allograft function and infectious complication did not differ between the two groups as well. In ABO-IKT, low RTX is comparable with typical RTX dosing with respect to B-cell depletion, antibody rebound suppression, the effect on clinical outcome in patients with low immunologic risk.
Renal Failure 07/2012; 34(8):974-9. · 0.82 Impact Factor
