BACKGROUND: Herein, the significance of post-transplant glomerulonephritis (PTGN) has been revisited to investigate whether PTGN induces allograft failure. The aim of this study was to identify the incidence of PTGN and its association with allograft failure, as well as to analyze the risk factors for PTGN. METHODS: Among the 996 Korean patients who underwent kidney transplantation in a multicenter cohort from 1995 to 2010, 764 patients were enrolled in this study. RESULTS: The incidence rate of PTGN was 9.7% and 17.0% at 5 and 10 years of follow-up, respectively. PTGN was diagnosed in 17.8% of the recipients with results of biopsy tests or clinical diagnosis identifying glomerular diseases as the underlying cause, compared with 0.0%, 4.4%, 4.9%, 5.5%, and 5.7% of the recipients with renal vascular diseases, renal interstitial diseases/pyelonephritis/uropathy, diabetic renal disease, hereditary renal diseases, and diseases with unknown etiologies, respectively. Allograft survival was significantly decreased in patients with PTGN. PTGN was associated with a fourfold increase in graft failure with a hazard ratio of 7.11 for both acute rejection and PTGN. Results of the risk factor analysis for PTGN revealed that the underlying glomerular renal diseases and treatment methods using drugs such as tacrolimus and basiliximab significantly increased PTGN development, after adjusting for other risk factors. CONCLUSION: We conclude that PTGN is strongly associated with poor kidney allograft survival. Therefore, optimal management of recurrent or de novo GN should be the critical focus of post-transplant care.
Antibodies, Monoclonal ; Biopsy ; Cohort Studies ; Follow-Up Studies ; Genetic Diseases, Inborn ; Glomerulonephritis ; Graft Survival ; Humans ; Incidence ; Kidney ; Kidney Transplantation ; Recombinant Fusion Proteins ; Rejection (Psychology) ; Risk Factors ; Tacrolimus ; Transplantation, Homologous ; Transplants ; Vascular Diseases

PURPOSE: We conducted a multi-center randomized double-blind study to determine the effects of 6-month therapy with sulodexide on urinary protein excretion in patients with idiopathic Immunoglobulin A (IgA) nephropathy. MATERIALS AND METHODS: A total of seventy-seven patients participated in the study. They were randomly allocated to one of three groups: sulodexide 75 mg or 150 mg daily or the placebo for 6 months. The primary end point was the achievement, at 6 months, of at least 50% reduction in urine protein/creatinine ratio (UPCR) from the baseline value. RESULTS: At 6 months, the primary end point was achieved by 12.5% of the patients assigned to the placebo, 4.0% of the patients assigned to sulodexide 75 mg daily and 21.4% of those assigned to 150 mg (p=0.308). Treatment with sulodexide 150 mg daily for 6 months significantly reduced log UPCR from 6.38+/-0.77 at baseline to 5.98+/-0.94 at 6 months (p=0.045), while treatment with sulodexide 75 mg daily and placebo did not. CONCLUSION: A 6-month treatment with sulodexide did not achieve 50% reduction of urinary protein excretion in IgA nephropathy patients, but showed a tendency to increase the time-dependent anti-proteinuric effect. Therefore, long-term clinical trials on a larger scale are warranted to elucidate the hypothesis that sulodexide affords renal protection in IgA nephropathy patients.
Adult ; Anticoagulants/*therapeutic use ; Double-Blind Method ; Female ; Glomerulonephritis, IGA/complications/*drug therapy ; Glycosaminoglycans/*therapeutic use ; Humans ; Male ; Middle Aged ; Proteinuria/complications/*drug therapy

BACKGROUND: Cytokine gene polymorphisms regulate cytokine production. Conflicting results about the impact of several cytokines gene polymorphism on the development or progression of IgAN have been reported. We evaluated the influence of polymorphism of several Th1 and proinflammatory cytokine genes on development and progression of IgAN. METHODS: Two hundred forty patients with biopsy-proven IgAN who had a minimal follow-up of 4 years, were recruited. Patients were classified according to the slope of reciprocal serum creatinine into slow progressors (> or =-0.05 dLxmg(-1) x year(-1), N=170) and fast progressors (<-0.05 dL x mg(-1) x year(-1), N=70). Three hundred fifteen healthy subjects with normal renal function and normotension were analyzed as controls. The polymorphisms of tumor necrosis factor-alpha (TNF-alpha, G-308A), interleukin-6 (IL-6, C-634G), interferon-gamma (IFN-gamma, A874T) and interleukin-2 (IL-2, T-330G) were determined by the 5' nuclease allelic discrimination assay. RESULTS: The genotype and allele frequencies of TNF-alpha, IL-6, IFN-gamma and IL-2 were not different significantly between IgAN patients and controls. Initial renal function, amount of daily proteinuria, and frequency of hypertension did not differ significantly between IgAN patients with different genotypes of all the studied cytokines. The frequencies of genotypes of the studied cytokines did not differ according to the rate of disease progression. In Kaplan-Meier analyses, the renal survival rate did not differ significantly between IgAN patients with different genotypes of the Th1 and proinflammatory cytokines. The polymorphism of the cytokines were not an independent risk factor for the progression of IgAN in Cox regression analysis. CONCLUSIONS: Our results suggest that the polymorphism of Th1 and proinflammatory cytokines are not associated with development and progression of IgAN in Korean patients.
Creatinine ; Cytokines ; Discrimination (Psychology) ; Disease Progression ; Follow-Up Studies ; Gene Frequency ; Genotype ; Glomerulonephritis, IGA* ; Humans ; Hypertension ; Immunoglobulin A* ; Interferon-gamma ; Interleukin-2 ; Interleukin-6 ; Polymorphism, Genetic ; Proteinuria ; Risk Factors ; Survival Rate ; Tumor Necrosis Factor-alpha

The roles of interleukin-10 (IL-10) have been emphasized in several models of glomerulonephritis (GN). Three biallelic polymorphisms within the IL-10 promoter region, at positions -1,082, -819, and -592 from the transcription initiation site, were shown to affect the level of IL-10 production. To investigate the effect of IL-10 promoter polymorphisms on the predisposition to development of GN in Korea, IL-10 promoter polymorphisms were assayed by polymerase chain reaction followed by restriction fragment length polymorphism in 108 patients with IgA nephropathy (IgAN), 49 focal segmental glomerulosclerosis (FSGS), and 100 healthy controls. In comparison with the control, the frequency of -1,082*G alleles were lower in IgAN and the frequencies of -592*C and -819*C were lower in FSGS, respectively. As for the haplotype, GCC haplotype was less frequent among IgAN than the control and ATA haplotype was more frequent among FSGS than the control (p<0.05). The frequency of intermediate producer genotypes (GCC/ACC and GCC/ATA) were lower among IgAN or FSGS than the control. Our findings suggested that IL-10 promoter polymorphism predisposed to the development of IgAN and FSGS in Korean patients.
Alleles ; Base Sequence ; Case-Control Studies ; DNA/genetics ; Gene Frequency ; Glomerulonephritis, IGA/*genetics/*immunology ; Glomerulosclerosis, Focal/*genetics/*immunology ; Haplotypes ; Humans ; Interleukin-10/*genetics ; Korea ; Polymerase Chain Reaction ; *Polymorphism, Genetic ; Polymorphism, Restriction Fragment Length ; *Promoter Regions (Genetics) ; Research Support, Non-U.S. Gov't

Purpose: Development of malignancy is one of the key issues in the renal transplant recipients after long term follow up. Methods: We reviewed our renal transplant registry for the incidence of de novo malignancy after renal transplantation. Results: Among the 1006 renal transplant recipients from July 1969 until January 2006, 47 cases of de novo malignancy developed in 43 patients: stomach cancer (7 cases), Kaposi's sarcoma (6), post-transplantation lymphoproliferative disorder (PTLD, 7), primary liver cancer (4), thyroid cancer (3), skin cancer (4), colon cancer (3),), renal cell carcinoma (2), bladder cancer (2), anal cancer (2), sarcoma (3) and one malignancy case from conjunctiva, pancreas, uterine cervix, and tongue, respectively. Mean age at the time of diagnosis of cancer was 45.8+/-12.0 years (mean+/-standard deviation). The cancer diagnosis was made at 97.1+/-73.6 months after the renal transplantation. We have high prevalence of cancers with suspected viral etiology - i.e., Kaposi's sarcoma, PTLD, primary liver cancer and uterine cervix cancer. Conclusion: Careful surveillance of malignancy in renal allograft recipients is highly recommended.
Allografts ; Anus Neoplasms ; Carcinoma, Renal Cell ; Cervix Uteri ; Colonic Neoplasms ; Conjunctiva ; Diagnosis ; Female ; Follow-Up Studies ; Humans ; Incidence ; Kidney Transplantation* ; Kidney* ; Liver Neoplasms ; Lymphoproliferative Disorders ; Pancreas ; Prevalence ; Sarcoma ; Sarcoma, Kaposi ; Skin Neoplasms ; Stomach Neoplasms ; Thyroid Neoplasms ; Tongue ; Transplantation ; Urinary Bladder Neoplasms

BACKGROUND: Bcl-xL and bax act as checkpoints of the apoptotic cell death. Although apoptosis is one of major mechanism of cell death in renal allografts inflicted by various events, the role of bcl-xL and bax in kidney transplantation has not been characterized yet. We therefore studied intragraft expression of bcl-x and bax and its clinical significance in renal transplantation. METHODS: We localized the expression of bcl-x, bcl-xS and bax proteins by immunohistochemistry, and measured the magnitude of the gene transcription of bax and bcl-xL by semi-quantitative RT-PCR in 37 implantation allograft biopsies(18 from 9 cadaveric donors, 19 from living donors), and 17 biopsies from patients undergoing acute rejection(AR). RESULTS: Immunoreactivities for bax, bcl-x, and bcl-xS were observed in tubular epithelial cells but not in glomeruli and vessels in implantation and AR biopsies. The infiltrating lymphocytes in AR expressed bax and bcl-xS but not for bcl-x. Comparing the intragraft gene transcript level of each allograft of a pair of recipients, who received graft from the same cadaveric donor, showed a higher bcl-xL in the patients with a higher concentration of postoperative 7th day serum creatinine. The transcript level of bcl-xL was higher in the Banff grade II and III AR biopsies than in the borderline or grade I AR, and also higher in steroid-resistant AR than in steroid-responsive patients. CONCLUSION: These results implicated the apoptotic death of infiltrating lymphocytes during rejection, and the compensatory up-regulation of bcl-xL in response to various apoptotic stimuli occurring in renal allografts.
Allografts* ; Apoptosis ; bcl-2-Associated X Protein ; Biopsy ; Cadaver ; Cell Death ; Creatinine ; Epithelial Cells ; Gene Expression* ; Humans ; Immunohistochemistry ; Kidney Transplantation ; Lymphocytes ; Tissue Donors ; Transplantation ; Transplants ; Up-Regulation*

BACKGROUND: Bcl-xL and bax act as checkpoints of the apoptotic cell death. Although apoptosis is one of major mechanism of cell death in renal allografts inflicted by various events, the role of bcl-xL and bax in kidney transplantation has not been characterized yet. We therefore studied intragraft expression of bcl-x and bax and its clinical significance in renal transplantation. METHODS: We localized the expression of bcl-x, bcl-xS and bax proteins by immunohistochemistry, and measured the magnitude of the gene transcription of bax and bcl-xL by semi-quantitative RT-PCR in 37 implantation allograft biopsies(18 from 9 cadaveric donors, 19 from living donors), and 17 biopsies from patients undergoing acute rejection(AR). RESULTS: Immunoreactivities for bax, bcl-x, and bcl-xS were observed in tubular epithelial cells but not in glomeruli and vessels in implantation and AR biopsies. The infiltrating lymphocytes in AR expressed bax and bcl-xS but not for bcl-x. Comparing the intragraft gene transcript level of each allograft of a pair of recipients, who received graft from the same cadaveric donor, showed a higher bcl-xL in the patients with a higher concentration of postoperative 7th day serum creatinine. The transcript level of bcl-xL was higher in the Banff grade II and III AR biopsies than in the borderline or grade I AR, and also higher in steroid-resistant AR than in steroid-responsive patients. CONCLUSION: These results implicated the apoptotic death of infiltrating lymphocytes during rejection, and the compensatory up-regulation of bcl-xL in response to various apoptotic stimuli occurring in renal allografts.
Allografts* ; Apoptosis ; bcl-2-Associated X Protein ; Biopsy ; Cadaver ; Cell Death ; Creatinine ; Epithelial Cells ; Gene Expression* ; Humans ; Immunohistochemistry ; Kidney Transplantation ; Lymphocytes ; Tissue Donors ; Transplantation ; Transplants ; Up-Regulation*

BACKGROUND:Staphylococcu S. aureus (S. aureus) is one of the most important etiologic agents of CAPD-associated infection and the nasal carriage of S. aureus increases the risk of CAPD-associated infection. We evaluated the nasal carriage status of S. aureus in CAPD patients and the association between nasal carriage of S. aureus and CAPD-associated infection. METHODS:We did a retrospective study about 167 patients on CAPD who regularly visited outpatient department at Seoul National University Hospital, Seoul National University Boramae Hospital, Seoul National University Bundang Hospital. Nasal swab cultures for S. aureus were taken once between September of 2005 and February of 2006. RESULTS:Nasal swab culture showed that S. aureus nasal carriage rate was 22.2%. S. aureus nasal carrier group showed that increased incidence of exit site infection and peritonitis caused by S. aureus and all other causes of exit site infection, but these were statistically insignificant. In diabetic patients, S. aureus nasal carriage rate was 21.6%. The observation of these patients also showed that S. aureus nasal carriage insignificantly increased the incidence of exit site infection and peritonitis caused by S. aureus and all oth er causes of exit site infection. CONCLUSION:In our study, the S. aureus nasal carriers did not show significantly higher risk for development of exit site infection and peritonitis by S. aureus or all other causes of exit site infection.
Humans ; Incidence ; Outpatients ; Peritoneal Dialysis, Continuous Ambulatory ; Peritonitis ; Prevalence* ; Retrospective Studies ; Seoul ; Staphylococcus aureus* ; Staphylococcus*

BACKGROUND: Ischemic heart disease has become more important in regard to mortality in hemodialysis patients. Although PTCA has been used for the treatment of ischemic heart disease, its result has little been reported in chronic renal failure(CRF) patients not in maintenance dialysis. We examined the therapeutic outcome of PTCA in CRF group in comparison with that in control group with normal renal function. METHODS: In a retrospective case-control study, 15 patients with CRF(Scr >or=1.4 mg/dL) were compared with 29 sex, age and diabetes mellitus matched controls without renal disease who had been randomly selected from the PTCA registry of our institution. Restenosis was evaluated by follow-up angiography or recurrent angina. Twenty-two PTCAs were performed over 26 stenotic lesions in CRF group, and thirty-nine PTCAs undergone over 56 lesions in control group. RESULTS: CRF group consisted of 11 men and 4 women with a mean age of 59.2+/-9.2(mean+/-SD) years and a mean serum creatinine of 3.8+/-2.4 mg/ dL. Cause of renal failure was diabetes mellitus in 11 cases(73%). Angiographic lesion success was confirmed in 17(65%) out of the 26 stenotic sites and stents were inserted successfully in the other nine lesions. Restenosis was confirmed by angiography in 10 lesions(38.5%) over a mean of seven months and suspected by recurrent angina in 6 lesions(23.1%), so overall restenosis rate was 61.6% in CRF group. Risk of restenosis was little different compared with control group in single- and double vessel disease, but increased up to 89% in triple vessel disease in CRF in contrast with control group. Among CRF group patients with serum creatinine >or=2.5 mg/dL showed much increased restenosis rate(77%) compared with those with serum creatinine <2.5 mg/dL (46%). CONCLUSION: Restenosis rate significantly increased in CRF patients who have multivessel disease or advanced renal failure, so other reperfusion therapy should be considered for them.
Angiography ; Angioplasty, Balloon, Coronary* ; Case-Control Studies ; Creatinine ; Diabetes Mellitus ; Dialysis ; Female ; Follow-Up Studies ; Humans ; Kidney Failure, Chronic* ; Male ; Mortality ; Myocardial Ischemia ; Renal Dialysis ; Renal Insufficiency ; Reperfusion ; Retrospective Studies ; Stents

PURPOSE: Hypertension (HT) has been known to play an important role in progression of chronic kidney disease (CKD). However, limited data are available in Korean HT patients. We evaluated the prevalence of CKD and the predictors of decrease in kidney function (DKF) in HT patients. METHODS: We retrospectively analyzed the medical records of outpatients with HT in Bundang Seoul National University hospital. DKF was defined as annual loss of estimated glomerular filtration rate (eGFR) more than 7% of baseline eGFR. RESULTS: The prevalence of CKD was 51% in 981 total participants. In HT patients without CKD (NCKD-HT), the incidence of DKF was 46.2%. The incidence of DKF in HT patients with CKD (CKD- HT) was 40.8%. Age was only baseline risk factor of DKF in NCKD-HT group. In multifactorial analysis, history of diabetes mellitus (odds ratio [OR], 2.99; 95% Confidence Interval [CI], 1.88+/-4.78), hemoglobin levels (OR, 0.86; 95% CI, 0.76+/-0.98), proteinuria (OR, 1.86; 95% CI, 1.16+/-2.98), and hematuria (OR, 1.62; 95% CI, 1.02+/-2.58) were related to DKF in CKD-HT group. CONCLUSION: We suggest that the prevalence of CKD in HT patients is high and DKF is frequent in both NCKD-HT and CKD-HT groups. The pattern of the predictors of DKF shows the difference between the two groups. Especially diabetes, abnormal urinalysis, and anemia are strongly associated with DKF in CKD-HT group.
Anemia ; Diabetes Mellitus ; Glomerular Filtration Rate ; Hematuria ; Hemoglobins ; Humans ; Hypertension ; Incidence ; Kidney ; Medical Records ; Outpatients ; Prevalence ; Proteinuria ; Renal Insufficiency, Chronic ; Retrospective Studies ; Risk Factors ; Urinalysis