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Data regarding the risk of various liver diseases among different hepatitis viruses in kidney transplantation have not yet been identified.We selected individuals with kidney transplantation (ICD-9-CM V420 or 996.81) from 2000–2009 from the catastrophic illness registry of National Health Insurance Research Database (NHIRD)as the study cohort. The two end-points in the study included overall death and post-transplant occurrence of hepatic disease. After adjustment for other risk factors, the risk of mortality was increased in patients with HBV infection (N = 352) and with HCV infection (N = 275) compared to those with neither HBV nor HCV infection (N = 3485). In addition,renal transplant recipients with HBV alone,HCV alone and both with HBV and HCVinfectionrespectively had an approximately 10-fold hazard ratio (HR) = 9.84, 95% confidence interval (CI): 4.61–21.0, 4-fold increased risk (HR = 4.40, 95% CI: 1.85–10.5)and 5-fold increased risk (HR = 4.63, 95% CI: 1.06–20.2)of hepatocellular carcinoma (HCC)compared to those with neither HBV nor HCV infection. Our findings showed a significant risk of de novo liver disease in recipients with hepatitis virus infection. Based on our findings, we reinforce the importance and impact of hepatitis virus in renal transplantation.

Postcardiac arrest acidosis can decrease survival. Effective medications without adverse side effects are still not well characterized. We aimed to analyze whether early administration of glutamine could improve survival and protect cardiomyocytes from postcardiac arrest acidosis using animal and cell models. Forty Wistar rats with postcardiac arrest acidosis (blood pH < 7.2) were included. They were divided into study (500 mg/kg L-alanyl-L-glutamine,n=20) and control (normal saline,n=20) groups. Each of the rats received resuscitation. The outcomes were compared between the two groups. In addition, cardiomyocytes derived from human induced pluripotent stem cells were exposed to HBSS with different pH levels (7.3 or 6.5) or to culture medium (control). Apoptosis-related markers and beating function were analyzed. We found that the duration of survival was significantly longer in the study group (p<0.05). In addition, in pH 6.5 or pH 7.3 HBSS buffer, the expression levels of cell stress (p53) and apoptosis (caspase-3, Bcl-xL) markers were significantly lower in cardiomyocytes treated with 50 mM L-glutamine than those without L-glutamine (RT-PCR). L-glutamine also increased the beating function of cardiomyocytes, especially at the lower pH level (6.5). More importantly, glutamine decreased cardiomyocyte apoptosis and increased these cells’ beating function at a low pH level.

Background. In chronic kidney failure, a hypoxic state, infiltrating inflammatory cells play a crucial role in the progression to end-stage renal disease. No studies have evaluated the influence of hypoxia and infiltrating inflammatory cells on chronic allograft dysfunction. Methods. Renal transplant recipients who underwent renal allograft biopsy with interstitial fibrosis/tubular atrophy (IF/ TA) were enrolled and renal allograft tissue sections were processed for immunohistochemical staining including hypoxia-inducible factor-1α (HIF-1α), nitrotyrosine, αsmooth muscle actin and e-cadherin. Patients with total renal tissue HIF score ≥1 were defined as positive for HIF-1α .T o assess the phenotype of the infiltrating cells, dual staining of HIF-1α with CD45, CD68 and CD3 was performed. The correlation between HIF-1α score and Banff’s score was analysed. Clinical parameters including renal survival among patients with or without an expression of HIF-1α were compared. Results. Out of 55 patients enrolled, 23 patients (41.8%) had an HIF-1α score ≥1 (Group B). Compared with Group A (total renal HIF score

Background: Peritoneal dialysis (PD) is a widely used renal replacement therapy for end-stage renal disease (ESRD) patients. Using laparoscopic guidance for PD catheter placement, we have designed a safe method that resulted in a reduction in catheter migration. Methods: We retrospectively reviewed 250 consecutive patients who underwent PD catheter placement from January 2005 to December 2009. The patients were divided into two groups: the conventional open surgery group and the laparoscopic group. All patients received Tenckhoff straight catheters. In the laparoscopic group, the catheter was additionally fixed to the ventral abdominal wall. Data were collected and a statistical analysis was performed to compare patient characteristics, surgical complications and catheter removal between the groups. Results: Overall surgical complications in the laparoscopic group were lower than those in the conventional group (3.8% vs. 19.4%, p

Induction therapy with interleukin-2 receptor antagonist (IL2RA) is widely used for renal transplant recipients and this study aimed to examine the impact of IL2RA among Chinese renal transplant recipients. Two hundred and thirty-eight Chinese renal transplant recipients aged 18-65 years at the Taichung Veterans General Hospital from January 2004 to July 2009 were retrospectively studied to assess the influence of IL2RA on biopsy-proven acute rejection (BPAR) within 1 year. Secondary outcomes included acute rejection rate in the first 3 months, delayed graft function, post-transplant diabetes mellitus, and malignancy. Cox proportional hazard analysis was used for multivariate analysis. Of all the patients, 116 received IL2RA (basiliximab, n = 44; daclizumab, n = 72) and 122 had no induction therapy. The mean follow-up duration was 43.3 months (range, 1-79 months). Overall, 227 (95.4%) patients completed the 12-month follow-up period with a functioning graft. No difference of BPAR was observed between the two groups and the secondary outcomes were also similar. After adjusting potential covariates with Cox regression, IL2RA use still provided no benefit on BPAR. In conclusion, there is no benefit of IL2RA in decreasing BPAR was observed in our study. Routine use of IL2RA for adult Chinese kidney transplant recipients may not be as effective as we thought before. More research is still needed to elucidate the effect of IL2RA among Chinese kidney transplant recipients.

Background Membranous glomerulonephritis (MGN) is one of common causes of idiopathic nephrotic syndrome in adults, and 25% of MGN patients proceed to end-stage renal disease. STAT4 gene polymorphisms have been reported to be associated with many inflammatory diseases. The objective of this study was to clarify the relationship between STAT4 gene polymorphisms and the pathogenesis of MGN. Methods We investigated the association of three STAT4 gene polymorphisms (rs3024912, rs3024908, and rs3024877) with the susceptibility to MGN in 403 Taiwanese populations (138 MGN patients and 265 controls). Results The results indicated that the statistically significant difference in genotype frequency distribution was found at rs3024908 SNP in MGN patients and control groups ( p = 0.014). In addition, the individuals with the GG genotype at rs3024912 SNP may have a higher risk in kidney failure of MGN patients (adjusted odds ratio [OR] = 3.255; 95% confidence interval [CI] = 1.155–9.176, p = 0.026). Conclusions Our data provide a new information that the STAT4 (rs3024912 and rs3024908) polymorphisms may be the underlying cause of MGN, and these polymorphisms revealed by this study warrant further investigation.

Objective: Interleukin-1 (IL-1) is involved in the disease process of peritonitis. We hypothesize that IL-1 gene polymorphism may have an impact on the occurrence of peritonitis in uremic patients undergoing peritoneal dialysis (PD). Methods: Uremic patients were recruited for the study of IL-1β (–511) C/T gene polymorphism in 2002. These patients were then prospectively followed up to monitor their peritoneal membrane characteristics, biochemical parameters, occurrence of peritonitis and patient as well as PD technique survival. Results: A total of 74 patients were enrolled in the study. During follow-up, at least one episode of peritonitis occurred in 36 patients. Compared with patients without peritonitis, the carriage of C allele in IL-1β gene polymorphism (C/C and C/T genotypes) was significantly associated with the occurrence of peritonitis (p = 0.013). This was further confirmed in the multivariate logistic regression analysis (odds ratio 8.18, p = 0.017). Conclusion: Carriers of C allele were associated with an increased risk of peritonitis.

Background: The objective of this study was to determine the risk of renal failure in patients with under-recognized chronic kidney disease (CKD) in the self-pay standard medical screening program of health management centers. Methods: The abbreviated Modification of Diet in Renal Disease equation was used to calculate the estimated glomerular filtration rate (eGFR) of study subjects. Study subjects with eGFR less than 60 mL/min/1.73 m 2 but with normal results of routine assessment, including serum creatinine, blood urea nitrogen, urinalysis and kidney ultrasound, were defined as having under-recognized CKD. Episodes of renal failure requiring dialysis within 2 years in subjects with stage 3 to stage 5 CKD were evaluated. Results: A total of 15,817 subjects were recruited and 28.4% of subjects were identified by routine assessments as having a kidney problem. The prevalences of CKD 3A, 3B, 4 and 5 were 8.3%, 1.9%, 0.3% and 0.2%, respectively. All subjects with stages 4 and 5 CKD had abnormal serum creatinine levels, but 48.7% of 1,507 subjects with stage 3 CKD (stage 3A, n = 713; stage 3B, n = 21) had normal routine assessments. Subjects with under-recognized stage 3B CKD had the highest risk (20%) of developing renal failure compared to subjects with stages 3–5 CKD and abnormal results of routine assessments. Conclusion: Identifying subjects with CKD stage 3 by the eGFR equation, especially in stage 3B, is advantageous in detecting the risk of renal failure over the routine clinical assessment that is currently carried out by health management institutions in Taiwan. [J Chin Med Assoc 2010;73(10):515–522]

Background Membranous glomerulonephritis (MGN) is one of the most common causes of nephrotic syndrome in adults. NPHS1 encoding nephrin is a transmembrane protein of the immunoglobulin family. We clarified the relationship between NPHS1 gene polymorphisms and the susceptibility or progression of MGN. Methods We recruited a cohort of 132 biopsy-diagnosed MGN patients and 257 healthy subjects. Genotyping of three SNPs (rs401824, rs437168 and rs3814995) at chromosome positions 41034749 (5′UTR), 41026259(exon17) and 41034052 (exon 3) was performed using a Taqman SNP genotyping assay. Results There was a significant difference in genotype frequency distribution of rs437168 polymorphism between MGN patients and controls. The results also showed that the frequency of the G allele was significantly higher in the patient group. Among the polymorphisms rs437168, rs401824 and rs3814995, no significant haplotype was shown in MGN patients. A stratified analysis revealed that a high disease progression in the AA genotype of rs401824 and GG genotype of rs437168 patients were associated with a low rate of remission. Conclusions The presence of the different genotypes of NPHS1 was associated with susceptibility of MGN and the remission of proteinuria during disease progression after the therapy.

Liver allografts seem to be immunologically privileged; they are the only solid transplant that can protect cotransplanted organs from rejection. The mechanisms of this "hepatic tolerance" are poorly understood. The aim of this study was to examine the immunomodulatory effect of hepatic stellate cells (HSCs) in mixed lymphocyte reactions in vitro and in graft-versus-host disease (GVHD) in vivo. Using a carboxyfluorescein diacetate succinimidyl ester-labeling method, we observed that the percentage of proliferative T cells was reduced when HSCs were present in a mixed lymphocyte culture. In addition, the degree of reduction was the same when HSCs were co-cultured in transwell inserts. Thus, soluble factors may participate in the immunomodulatory effect of HSCs. In GVHD experiments, irradiated BALB/c (H-2d) mice simultaneously received an intravenous mixture of bone marrow and splenic T cells from C57BL/6 (H-2b) mice. The HSCs prominently reduced symptoms and pathologic severity of GVHD in target organs. HSC cotransplanted mice survived for 57.5+/-30.6 days whereas the control hosts only survived for 15.3+/-5.2 days (P

Granulocyte colony-stimulating factor (G-CSF) demonstrates neuroprotective effects through different mechanisms, including mobilization of bone marrow cells. However, the influence of G-CSF-mediated mobilization of bone marrow-derived cells on injured sciatic nerves remains to be elucidated. The administration of G-CSF promoted a short-term functional recovery 7 days after crush injury in sciatic nerves. A double-immunofluorescence study using green fluorescent protein-chimeric mice revealed that bone marrow-derived CD34+ cells were predominantly mobilized and migrated into injured nerves after G-CSF treatment. G-CSF-mediated beneficial effects against sciatic nerve injury were associated with increased CD34+ cell deposition, vascular endothelial growth factor (VEGF) expression, and vascularization/angiogenesis as well as decreased CD68+ cell accumulation. However, cell differentiation and VEGF expression were not demonstrated in deposited cells. The results suggest that the promotion of short-term functional recovery in sciatic nerve crush injury by G-CSF involves a paracrine modulatory effect and a bone marrow-derived CD34+ cell mobilizing effect.

Background Pulmonary hypertension (PH) is an overlooked cardiovascular morbidity in patients undergoing haemodialysis. Inflammation has been demonstrated to play a significant role with certain types of PH in non-uraemic patients, but studies analysing the mechanisms in dialyzed patients with PH are rare. Hence, we investigated systemic and local inflammation biomarkers associated with PH in uraemia patients to elucidate the potential mechanism. Methods A cross-sectional study was conducted in which 97 haemodialysis patients were initially evaluated in our hospital. Twelve inflammatory cytokines were measured using a cytometric beads assay in patients with and without PH. FE(NO) (fractional exhaled nitric oxide) was checked by a chemiluminescence analyser in patients with and without PH as well as by normal controls. Results Thirty-nine eligible patients were enrolled. Compared to patients without PH (group A), patients with PH (group B) had significantly higher serum levels of hs-CRP, IL-1beta, TNF-alpha and IL-6. FE(NO) was also measured. Though the pre-dialysis FE(NO) levels were elevated in both groups; group B patients had significantly higher pre-dialysis FE(NO) levels than group A patients (39.9 +/- 16.7 versus 31.8 +/- 10.3, P = 0.045). The post-dialysis FE(NO) levels returned to normal in group A while the remaining were significantly higher in group B (30.3 +/- 10.3 versus 20.1 +/- 10.9, P = 0.003). Conclusions Our study revealed that dialyzed patients with PH had a significantly higher level of airway FE(NO) as well as serum levels of acute phase reactive protein and cytokines, including IL-1beta, TNF-alpha and IL-6. A chronic inflammation might play an important role in the pathogenesis of PH in patients undergoing haemodialysis.

OBJECTIVE We have previously demonstrated that hypokalaemia is a risk factor for enteric peritonitis in CAPD patients. The underlying mechanism is unclear, and there have been no similar reports. We hypothesized that hypokalaemia may result in dysmotility of the intestinal tract and in turn cause bacterial overgrowth and subclinical translocation of enteral bacteria. METHODS Uraemic patients undergoing CAPD in our hospital were enrolled in the study. Hypokalaemia was defined as a serum potassium (K) level < or = 3.5 mEq/L despite treatment for 1 month. A breath hydrogen test (BHT) was performed to detect if intestinal bacterial overgrowth was present. Blood samples were also collected for the study of inflammatory cytokines, including interleukin 1 (IL1), IL2, IL6, IL8, TNF-alpha and gamma-IFN. RESULTS A total of 68 patients were recruited. Hypokalaemia was present in 18 cases (26.5%, group 1), while 50 cases (group 2) had normal serum K levels. A higher prevalence of abnormal BHT was found in group 1 (27.8%), compared with group 2 (8.0%, P = 0.048). There was a trend towards a higher prevalence of abnormal BHT in diabetes mellitus (DM) patients with hypokalaemia (80.0%) compared with normal kalaemia (22.2%, P = 0.09), while no similar trends were found in non-DM hypokalaemic patients (7.7 versus 4.9%). When comparisons were made among different subgroups, patients with DM and hypokalaemia had a significantly higher prevalence of abnormal BHT compared to non-DM, normokalaemic patients (P < 0.0004) and non-DM, hypokalaemic patients (P = 0.008). Multivariate logistic regression analysis revealed that DM was an independent risk factor for abnormal BHT (odds ratio: 12.39, 95% CI: 2.25-68.20, P = 0.004). There was no significant difference in serum albumin, Kt/V, weekly creatinine clearance, pattern of peritoneal equilibrium test, C-reactive protein and various inflammatory cytokines between the two groups. CONCLUSION CAPD patients with hypokalaemia may have intestinal bacterial overgrowth. While both DM and hypokalaemia might contribute to this abnormality, only DM appeared to be the independent risk factor.

Tinea capitis rarely occurs in renal transplant recipients. We report this living-related renal transplant patient receiving cyclosporine-based therapy who initially presented with severe exfoliation of the scalp with yellowish-white scales and marked hair loss. The lesions extended to the frontal area and both cheeks, resulting in several skin ulcers with perifocal erythematous inflammatory changes, and palpable cervical lymph nodes. A biopsy of a skin lesion revealed fungal infection and culture yielded Microsporum canis. The patient mentioned an outbreak of ringworm in her breeding dogs during this period. After adequate treatment of the patient and her infected animals with griseofulvin and disinfection of the environment, her skin lesions resolved dramatically, with regrowth of hair.

SUMMARY: Background: While polyomavirus nephropathy (PVN) is recognized as an emerging cause of graft loss in renal transplants, the prevalence rate of PVN in renal grafts is unclear in Taiwan. Methods: Biopsies (n = 412) from 323 Taiwanese renal transplant patients were retrospectively analysed. PVN was diagnosed by the characteristic viropathic change in epithelial cells under light microscopic examination and a positive immunohistochemistry staining of anti-SV40 large T antigen. The viral cytopathic changes, interstitial inflammation, fibrosis and tubular atrophy were semiquantitatively assessed, based on the Banff 1997 classification and scoring for renal allograft. Results: Seventeen cases were identified with evidence of PVN; the prevalence rate is 5.26%. Compared with non-PVN patients, they were more likely to have had previous rejection episodes, higher graft loss and shorter graft survival. Conclusion: This retrospective study showed that we have similar findings to other reports with at least 5% prevalence of PVN and that patients diagnosed early do better, while those diagnosed with severe inflammation or damage do worse or are likely to lose their grafts.

Emphysematous pyelonephritis is a rare, severe gas-forming infection of the kidney. Herein we report a case of a 51-year-old man who had received a cadaveric renal transplant 12 years ago. Post-transplant diabetes mellitus occurred 8 years later. He experienced urinary tract infection with graft pain one week before admission and presented with septic shock at the emergency room. Plain X-ray of the abdomen showed retroperitoneal air. A computed tomography scan of the abdomen showed retroperitoneal and extraperitoneal air being released from the graft kidney. These findings were compatible with extensive emphysematous pyelonephritis. The patient underwent percutaneous drainage. Blood culture and urine culture yielded Escherichia coli. After repeated percutaneous drainage and strong antibiotics for a prolonged period, the patient finally recovered.

Background: Kidney transplantation using organs from executed prisoners is a subject of controversy from the viewpoint of ethics. However, few reports have addressed the clinical outcome beyond the ethical issue. Methods: Between January 1990 and September 2004, a total of 435 kidney transplant recipients (group M) who underwent transplantation in 26 different hospitals in China were followed up at our hospital. It is believed that all the organs came from executed prisoners. The clinical data were retrieved and compared to those of 200 kidney transplant recipients (group T) who underwent transplantation in our hospital during the same period. Results: There was no significant difference between these 2 groups (T vs. M) in terms of hepatitis B virus infection (10.5% vs. 12.1%) or surgical complication rate (6.5% vs. 5.6%). The 1 st -year acute rejection rate was significantly lower in group M (31.1% vs. 24.5%, p = 0.015). The 1-year, 5-year, and 10-year patient survival rates were 94.3%, 89.5%, and 85.2%, respectively, for group T and 92.6%, 83.6%, and 76.7%, respectively, for group M (p > 0.05); the corresponding graft survival rates were 91.4%, 82.6%, and 66.9%, respectively, for group T and 91.6%, 80.0%, and 61.4%, respectively, for group M (p > 0.05). When patients were stratified according to the year of transplantation, patients who underwent transplantation between 2000 and 2004 had significantly better graft survival rates in both groups. Conclusion: We conclude that kidney transplantation using organs from executed prisoners had a clinical outcome similar to that of transplantation performed in our hospital during the same period. [J Chin Med Assoc 2007;70(5):193–199]

BACKGROUND Chronic allograft nephropathy (CAN) is characterized by a progressive deterioration of renal function with various degrees ofproteinuria. Currently, there is no effective treatment despite the introduction of new generations of immunosuppressants. Pentoxifylline (PTX) is a phosphodiesterase inhibitor that possesses antiproteinuric effect and has been proved to be effective in treating several glomerular diseases. The purpose of the current study was to examine the effect of PTX on renal transplant patients with established CAN. MATERIALS AND METHODS Renal transplant recipients with biopsyproven CAN were recruited for the study. All the patients had been on angiotensin-converting enzyme inhibitor or angiotensin receptor blocker for more than 1 year and were on a triple immunosuppressive regimen including corticosteroid, calcineurine inhibitor and mycophenolate mofetil. PTX in a dose of 1,200 mg/day was administered for at least 6 months. The following parameters were assessed at baseline, the 3rd and the 6th month post treatment: systolic and diastolic blood pressure, number of anti-hypertension drugs, serum creatinine (sCr),estimated glomerular filtration rate (eGFR), 24-hour urinary protein excretion (U/P), urinary N-acetylglucosaminidase (NAG) and intracytoplasmic Thl/Th2 cytokines production of peripheral blood CD4+ cells. RESULTS A total of 17 (11 male and 6 female) patients were enrolled in the study. The mean duration of follow-up post transplant was 10.6+/- 4.4 years. The baseline data of sCr, eGFR and U/P were 1.83+/-0.46 mg/dl, 38+/-8 ml/min and 2.65+/-2.15 g/day, respectively. Corresponding values at the 3rd and 6th month post treatment were 1.90+/-0.43 mg/dl (p = NS), 33+/-7 ml/min (p=NS), 2.13 +/-1.13 g/day (p < 0.05) and 2.03+/-0.64 mg/dl (p < 0.05), 32+/-10 ml/min (p < 0.05), 2.74 +/-0.93 g/day (p = NS), respectively. When individual data were analyzed, five cases (29.4%) showed a U/P significant reduction of more than 50% of baseline value, while in 10 cases (58.8%) the graft function remained either stable (9 cases) or improved (1 case) at the end of treatment. Urinary NAG was elevated at the 3rd month, but stabilized thereafter. The Thl/Th2 intracytoplasmic cytokine pattern of peripheral blood CD4+ cells showed a significant decrease of cells bearing TNF-alpha (15.0+/-14.4% vs 14.2+/-17.0%, p < 0.05) and cells bearing IL-10 (1.60 +/-1.23% vs 0.90+/-0.66%, p < 0.05) at the 3rd month. CONCLUSION In this pilot study, PTX seemed to be temporarily effective in reducing proteinuria. The graft function was stabilized in more than half of patients at the end of follow-up.

Tuberculosis (TB) is one of the major causes of morbidity and mortality worldwide. Post-transplant (post-Tx) TB is a problem in successful long-term outcome of renal transplantation recipients. It is a life-threatening opportunistic infection that is frequently encountered but the diagnosis is often delayed. With the emergence of newer potent immunosuppressive regimens and an increased incidence of TB in the general population post-Tx TB among transplant recipients can be anticipated. Our objective was to describe the pattern and risk factors of TB infection and the prognosis in an endemic area. This study was a retrospective review of the records of 756 renal transplant recipients in our hospital during the period from January 1983 to December 2003. The demographic data transplant characteristics clinical manifestations diagnostic criteria treatment protocol and longterm outcome of this cohort of patients were analyzed. Thirty-one episodes developed into TB in 29 patients (3.8%) with a mean age of 45.5 (range: 24.2^66.2) years and a mean post-Tx period of 57.9 (range: 1.2^145.2) months. The forms of the diseases were pulmonary in 22/31 (71%) disseminated in 1/31 (3%) miliary in 1/31 (3%) and extrapulmonary in 7/31 (23%). All patients initially received 4-drug combination therapy and then dosage was adjusted based on clinical condition. Because of drug interaction a mean 2-fold increase in the dose of calcineurium inhibitor but no change in steroid was required. Twenty-two patients (71%) had an elevated creatinine (Cr) level and 6 (19%) patients did not recover owing to tissue-proof acute rejection (3 cases) and chronic allograft nephropathy (3 cases) respectively after treatment. The serum Cr level on diagnosis of TB was 1.9 ± 0.7mg/dL; it then deteriorated to 2.4 ± 1.5 mg/dL (P = 0.134). Hepatotoxicity developed in 11 patients (35.5%) during treatment. Twenty-five patients were successfully treated 2 patients remain under treatment and 4 (12.9%) died. Based on univariate analysis we found the post-Tx TB risk factors were diabetes and more than 3 episodes of rejection modalities for acute rejection (high-dose steroid and anti-lymphocyte globulin) and maintenance therapy with steroid. Post-Tx TB is a serious problem worldwide and a high index of suspicion is warranted to ensure early diagnosis and prompt initiation of treatment for TB among renal transplant patients. The use of optimal immunosuppressive agents to minimize acute rejection seems reasonable to prevent TB infection in endemic areas like Taiwan. More than 9 months of treatment may be necessary to prevent recurrence. (authors)

Background Administration of immature dendritic cells (DC) prolongs but does not result in indefinite allograft survival. We attempted to achieve this goal by adding a sub-therapeutic dose of immunosuppression. Methods DC propagated from B10 ( H-2 b ) mouse bone marrow (BM) were transfected with nuclear factor-kappaB (NF-κB)-binding-site-specific oligodeoxyribonucleotide (ODN). The allostimulatory activity of transfected and normal DC were examined in mixed-lymphocyte reaction (MLR) and cytotoxic T-lymphocyte (CTL) assays in vitro, and their influence on allograft survival by systemic administration of DC in vivo. Results Transfection of DC with NF-κB ODN resulted in complete abrogation of NF-κB activity and inhibition of co-stimulation. Allogeneic (C3H, H-2 k ) T cells stimulated by ODN DC demonstrated impairment in MLR and CTL activity. Administration of ODN DC significantly prolonged B10 allograft survival. In contrast to cyclosporine, which failed to enhance the effect of ODN DC, a combination of ODN DC with sirolimus at 6 mg/kg/day for 6 days achieved long-term survival in all allografts. This was associated with low CTL activity of either graft-infiltrating cells or splenic T cells and increased TUNEL-positive cells in T-cell areas of recipient mesenteric lymph nodes. Analysis of transcription factor nuclear translocation with Cellomics indicated that stimulation with ODN DC showed inhibited T-cell nuclear translocation of signal transducer and activator of transcription (Stat)1 and Stat3, extracellular signal–related kinase (ERK) and activating transcription factor (ATF)-2, but not NF-κB and P38, compared with mature DC. The selective inhibition was enhanced by sirolimus, but not cyclosporine. Conclusions Sirolimus enhances immature DC tolerogenicity by induction of T-cell apoptosis, and promotes immature DC-induced inhibition of Stat1, ERK and ATF-2 activation.

End-stage-renal disease (ESRD) is a final result of various etiologies. Prognostic indicators leading to ESRD in chronic kidney diseases have been studied extensively, of which, genetic factors remain a subject of great concern. Interleukin-1 (IL-1) and tumor necrosis factor-α (TNF-α) are potent proinflammatory cytokines that are involved in several chronic kidney diseases. Studies on cytokine gene polymorphism have revealed important information about the role of genetic factors in disease susceptibility and severity. Gene polymorphism of interleukin-1 receptor antagonist (IL-1ra) and TNF-α were determined in 297 ESRD patients and in 145 normal healthy controls. IL-1ra gene polymorphism was characterized as a variable number of tandem repeats of a 86 bp sequence within intron 2. Five alleles were identified and were designated as IL1RN*1, IL1RN*2, IL1RN*3, IL1RN*4, and IL1RN*5, corresponding to 4,2,5,3, and 6 repeats, respectively. A polymorphism in the promoter region of the TNF-α gene was also studied....

Constipation is a frequent health concern for long-term dialysis patients. The increased incidence of constipation in long-term dialysis patients is based mainly on self-reported data. Our aim is to investigate this problem objectively by using colonic transit time in long-term hemodialysis (HD) and continuous ambulatory peritoneal dialysis (CAPD) patients.Segmental and total colonic transit time studies measured by means of radiopaque markers were conducted in 56 HD patients, 63 CAPD patients, and 25 healthy control subjects. Segmental colonic transit times were calculated separately for 3 segments of the colon (right, left, and rectosigmoid) and total transit time, which was the sum of all 3 segment times.Colonic transit time was significantly prolonged in HD patients (43.0 +/- 22.2 versus 32.7 +/- 13.7 hours in CAPD patients and 24.3 +/- 11.9 hours in controls; P0.001). Increased colonic transit times in the right and rectosigmoid segments, but not the left segment, contributed to the prolongation in total colonic transit time. Age and interdialytic weight gain correlated well with prolongation of total and segmental colonic transit times in HD patients (P0.01). Diabetes and female sex in all groups were associated with longer total and segmental colonic transit times, but this trend was not statistically significant.Total, right segmental, and rectosigmoid segmental colonic transit times are prolonged in long-term HD patients compared with CAPD patients and healthy controls. We believe colonic transit time measurement is helpful to tailor therapy because it helps define the pathogenesis of constipation.

A renal allograft transplant patient with tubulointerstitial nephritis was examined for possible involvement of human polyomaviruses. Biopsy of the allograft kidney revealed inflammatory interstitial infiltration with tubulitis and typical inclusion bodies in the nucleus of the tubulo-epithelium. Glomeruli showed duplication and lamination of Bowman's capsule with enlargement of the parietal and visceral epithelia. Immunohistochemical analysis on the graft section using a JC virus (JCV) VP1 peptide-specific antibody showed positive staining. Paracrystalline arrays of naked viral particles with diameters of 40 nm were visualized in the nuclear inclusions under an electron microscope. Molecular examination using the polymerase chain reaction (PCR) and DNA sequencing revealed that the JCV was involved in the nephritis. The results indicated that JCV may be associated with tubulointerstitial nephritis.

In the injured liver, hepatic stellate cells (HSCs) secrete many different cytokines, recruit lymphocytes, and thus participate actively in the pathogenesis of liver disease. Little is known of the role of HSCs in immune responses. In this study, HSCs isolated from C57BL/10 (H2b) mice were found to express scant key surface molecules in the quiescent stage. Activated HSCs express major histocompatibility complex class I, costimulatory molecules, and produce a variety of cytokines. Stimulation by interferon gamma (IFN-gamma) or activated T cells enhanced expression of these molecules. Interestingly, addition of the activated (but not quiescent) HSCs suppressed thymidine uptake by T cells that were stimulated by alloantigens or by anti-CD3-mediated T-cell receptor ligation in a dose-dependent manner. High cytokine production by the T cells suggests that the inhibition was probably not a result of suppression of their activation. T-cell division was also found to be normal in a CFSE dilution assay. The HSC-induced T-cell hyporesponsiveness was associated with enhanced T-cell apoptosis. Activation of HSCs was associated with markedly enhanced expression of B7-H1. Blockade of B7-H1/PD-1 ligation significantly reduced HSC immunomodulatory activity, suggesting an important role of B7-H1. In conclusion, the bidirectional interactions between HSCs and immune cells may contribute to hepatic immune tolerance.

QT dispersion (the difference between maximum and minimum QT across the 12-lead electrocardiogram [ECG]), which reflects regional variations in ventricular repolarization, is a predictor of arrhythmia and cardiovascular mortality. The present study was undertaken to assess the difference in QT dispersion between uremic and nonuremic patients with acute myocardial infarction (AMI) and its relationship to post-AMI clinical outcome. Twelve-lead ECG recordings were obtained the first and third days after the onset of AMI in 21 uremic and 21 nonuremic patients. QT intervals were measured on 12-lead ECGs and corrected by heart rate (QTc). Our findings show that uremic patients with AMI had greater QTc dispersion (84 ± 35 versus 55 ± 15 milliseconds; P P = 0.003), and underwent fewer reperfusion therapies (5 of 21 versus 17 of 21 patients; P = 0.002) compared with nonuremic patients with AMI. Patients with AMI who died had greater QTc dispersion than those who survived (102 ± 40 versus 67 ± 40 milliseconds; P = 0.015). An optimal QTc dispersion cutoff value of 60 milliseconds had a sensitivity of 100% and specificity of 55% in predicting 1-year mortality in uremic patients with AMI. Uremic patients with AMI administered thrombolytic therapies (n = 5) had reduced 1-year mortality rates (0% versus 63%; P = 0.003) and shortened QTc dispersion from days 1 to 3 (changes in QTc dispersion between days 1 and 3, 29% ± 9% decrease versus 13% ± 5% increase; P = 0.001) compared with those without therapies (n = 16). Our findings suggest that greater QT dispersion is associated with greater total mortality, and thrombolytic therapies could reduce QTc dispersion and mortality in uremic patients with AMI. It is prudent to refine our current management regimen for uremic patients with AMI to improve the poor clinical outcome. © 2002 by the National Kidney Foundation, Inc.

Background/Purpose Retention of excess iron from transfused blood in organs in patients with renal anemia may lead to various systemic complications. Iron chelating agents such as deferasirox (DFX) decrease such iron overload. This study assessed the efficacy, safety, and tolerability of DFX in hemodialysis (HD) patients with iron overload. Methods We retrospectively (February 2008 to June 2012) reviewed data for eight HD patients with end-stage renal disease who were prescribed DFX (15 mg/kg/day) for transfusion-induced iron overload. Baseline and post-treatment levels of hematocrit, ferritin, erythropoietin (EPO), transferrin saturation (TSAT), total and unsaturated iron-binding capacity (TIBC and UIBC, respectively), and blood transfusion volumes were measured. Treatment efficacy was evaluated by observing changes in ferritin and TSAT during the study period; monthly EPO doses and blood transfusions were also recorded. Safety was evaluated in the form of adverse events. Results DFX administration caused statistically significant reductions in TSAT (68.2-49.2%; P = 0.036) and ferritin (3133.1-1215.6 ng/ml; P = 0.017). Significant post-treatment increases in UIBC (63.3-196.6 µg/dl; P = 0.018) and TIBC (210.0-422.4 µg/dl; P = 0.012) were also observed. While there were no significant differences in hematocrit values or EPO requirements after treatment, significant reductions in average monthly transfusion volumes (P = 0.026) were recorded. DFX was generally well tolerated; common adverse effects included nausea, vomiting, diarrhea, and abdominal pain. Conclusion DFX significantly improved iron metabolism in HD patients with iron overload and had an acceptable frequency of adverse effects.

Idiopathic membranous nephropathy (MN) is one common cause of idiopathic nephrotic syndrome in adults; 25% of MN patients proceed to end-stage renal disease. In adults, membranous nephropathy is a lead cause of nephrotic syndrome, with about 75% of the cases idiopathic. Secondary causes include autoimmune disease, infection, drugs and malignancy. Three hypotheses about pathogenesis have surfaced: preformed immune complex, in situ immune complex formation, and auto-antibody against podocyte membrane antigen. Pathogenesis does involve immune complex formation with later deposition in sub-epithelial sites, but definite mechanism is still unknown. Several genes were recently proven associated with primary membranous nephropathy in Taiwan: IL-6, NPHS1, TLR-4, TLR-9, STAT4, and MYH9 . These may provide a useful tool for diagnosis and prognosis. This article reviews epidemiology and lends new information on KIRREL2 (rs443186 and rs447707) polymorphisms as underlying causes of MN; polymorphisms revealed by this study warrant further investigation.

The CCN family of proteins is composed of six extracellular matrix-associated proteins that play crucial roles in skeletal development, wound healing, fibrosis, and cancer. Members of the CCN family share four conserved cysteine-rich modular domains that trigger signal transduction in cell adhesion, migration, proliferation, differentiation, and survival through direct binding to specific integrin receptors and heparan sulfate proteoglycans. In the present review, we discuss the roles of the CCN family proteins in regulating resident cells of the bone microenvironment. In vertebrate development, the CCN family plays a critical role in osteo/chondrogenesis and vasculo/angiogenesis. These effects are regulated through signaling via integrins, bone morphogenetic protein, vascular endothelial growth factor, Wnt, and Notch via direct binding to CCN family proteins. Due to the important roles of CCN family proteins in skeletal development, abnormal expression of CCN proteins is related to the tumorigenesis of primary bone tumors such as osteosarcoma, Ewing sarcoma, and chondrosarcoma. Additionally, emerging studies have suggested that CCN proteins may affect progression of secondary metastatic bone tumors by moderating the bone microenvironment. CCN proteins could therefore serve as potential therapeutic targets for drug development against primary and metastatic bone tumors.

Background Currently, the contribution of kidney function decline in renal and patient outcomes is unclear. There are few data on the associations of different etiologies of estimated glomerular filtration rate (eGFR) decline with outcomes in multidisciplinary care. The purpose of this investigation was to establish whether eGFR decline in patients with disease is an important risk factor for developing end-stage renal disease (ESRD) and death. Methods From December 1, 2001 to December 31, 2011, 5097 adults with chronic kidney disease (CKD) received biochemical tests, physical examinations, a pathological examination, and a comprehensive questionnaire. We used linear regression models and multivariate Cox proportional hazards model to examine the outcome of eGFR decline in renal diseases with different etiologies. Results Mean age was 68.1±16.1 (standard deviation, SD) years, and 63.3% patients were male. In the studied cohort, 58.2% of the patients had systemic disease-related nephropathy (SDRN), 29.4% had primary renal diseases (PRDs), and 12.4% had other etiologies. The eGFR decline in SDRN had a significant association with dialysis in the Cox proportional hazards model [crude hazard ratio (HR) = 1.07, 95% confidence interval (CI), 1.04 to 1.10; adjusted HR 1.05, 95% CI, 1.02 to 1.08]. Diabetic nephropathy (DN) had the most severe eGFR decline in CKD stages 3, 4, and 5, and all contributed to the initiation of dialysis and death regardless of whether DN with or without eGFR decline was considered to be the cause. Although hypertensive nephropathy (HN) was related to significant acceleration of eGFR decline, it did not lead to poor outcome. There were still discrepancies between eGFR decline and outcomes in PRDs, hypertensive nephropathy, and lupus nephritis. Conclusions eGFR decline and CKD staging provide an informative guide for physicians to make proper clinical judgments in the treatment of CKD, especially SDRN. Poor control of the underlying systemic disease will thus lead to more rapid progression of SDRN.

Chronic liver disease and its complications are major problems in renal transplant recipients. Our aim was to elucidate the influence of hepatitis B, C virus infection on the long-term outcome of renal transplantation. Four hundred and seventy-seven patients who received renal transplantation between January 1984 and December 1999, and who were followed up at our hospital were enrolled. HBsAg was detected by the RIA method and anti-HCV Ab was assayed by the second-generation RIA kit. SGOT/ SGPT were checked every 3 months. Hepatoma was diagnosed by dynamic CT scan, elevated α-fetoprotein, hypervascularity by angiography and confirmed by pathological examination. The prevalence of HBV, HCV, coinfected HBV/HCV was 9.9% (n = 47), 28.5% ( n = 136), 3.1% (n = 15), respectively. The incidences of hepatoma in the HBV–/HCV–, HBV–/HCV+, HBV+/HCV–, HBV+/HCV+ groups were 1.4% (n = 4), 4.4% (n = 6), 6.4% (n = 3), 6.7% (n = 1), respectively (p = 0.114). The incidences of liver cirrhosis/hepatic failure were 3.2% (n = 9) , 6.6% (n = 9) , 21.3% (n = 10) , 20% (n = 3), respectively (p < 0.001). The frequencies of chronic liver disease were 10.4% (n = 29) , 45.6% (n = 62) , 66% (n = 31) , 80% (n = 12), respectively (p < 0.001). Patient and graft survival rates were lower in the HBV-infected group than in the other groups. Cox regression analysis revealed that HBV infection is likely an independent risk factor for patient mortality although the statistical significance was only borderline. Patients with HBV as well as HCV infection were not at risk of graft loss according to this model of analysis. Patients with HBV infection showed higher incidences of hepatoma, hepatic failure, graft failure and death. Therefore, HBV-infected patients who are candidates for renal transplantation should be carefully evaluated. It seems that HCV infection has little influence on the outcome of renal transplant recipients. A longer period of follow-up is needed to clarify the impact of HCV on renal transplant recipients.

Background/Aim: The purpose of this study was to evaluate pusled-field gel electrophoresis (PFGE) for distinguishing between relapse and reinfection of Staphylococcus aureus infections in patients on continuous ambulatory peritoneal dialysis (CAPD). Methods: Between July 1993 and May 1997, 4 patients with recurrent CAPD-associated infections caused by S. aureus we enrolled in this study. There were nine episodes of peritonitis, one episode of temporary double lumen catheter infection, and one episode of Hickman catheter infection. A total of eleven S. aureus isolates were collected from peritoneal fluid (n = 9) and blood (n = 2). PFGE typing was applied. Results: In our study, from PFGE typing, the 11 S. aureus isolates were classified into seven patterns. Antibiogram profiling classified only four patterns. Patient A had a reinfection by another strain of S. aureus, and patient B had three episodes of peritonitis caused by the same strain of S. aureus due to exit site infections. Patient C had two episodes of CAPD peritonitis caused by two different strains, respectively. Patient D had four episodes of S. aureus infection (three CAPD peritonitis and one bacteremia); the first two episodes of peritonitis were caused by an identical strain of S. aureus, whereas the subsequent two infections were caused by other organisms. Conclusion: PFGE has a high discriminatory power and can be an assistant method to antibiogram profiling for distinguishing relapse from reinfection in CAPD-associated peritonitis.

Advances in immunosuppressants for solid organ transplantation (SOT) have improved prevention and treatment of acute rejection as well as reduced the risk of chronic graft damage. However, SOT recipients are prone to developing opportunistic infections because of their long-term immunosuppressed status. Tuberculosis (TB) is a serious opportunistic infection that is associated with increased morbidity and mortality in SOT recipients. However, nationwide population-based research specifically focused on the associations between kidney transplantation (KTx), liver transplantation (LTx), and heart transplantation (HTx), and subsequent TB infection is lacking. This study was conducted using Taiwan's National Health Insurance Research Database, which provided claims data for SOT recipients from 2000 to 2009. Clinical features, treatment, and outcomes were analyzed to determine the risk for TB after SOT. In total, 153 (3.2%) RTx, 19 (1.1%) LTx, and 26 (2.8%) HTx recipients became infected with TB. Compared with non-TB patients, HTx recipients with TB had significantly higher prevalence of older age (P = .037), hypertension (P < .001), and coronary artery disease (CAD) (P = .002). There were also greater percentages of male sex (P = .018), diabetes (P = .029), hyperlipidemia (P = .016), CAD (P < .001), and chronic obstructive pulmonary disease (COPD) (P < .001) in RTx recipients with TB than in those without. In conclusion, posttransplantation TB is a serious problem worldwide, and a high index of suspicion is warranted to ensure early diagnosis and prompt initiation of treatment for TB among SOT patients. In this preliminary study, KTx recipients had a higher risk of TB infection than LTx and HTx recipients, and the high-risk factors were male sex, diabetes, hyperlipidemia, CAD, and COPD. The use of optimal immunosuppressive agents to minimize acute rejection, monitoring of high-risk recipients, prompt diagnosis, and appropriate treatment are required for the management of TB infection in endemic areas such as Taiwan.

Earlier detection and intervention for chronic renal allograft injury (CRAI) remain major challenges for transplantation physicians. Endocan plays a key role in the regulation of cell adhesion, inflammatory disorders, and tumor progression. We conducted this cross-sectional study of 97 renal transplant (RT) recipients with mean RT duration of 7.0 ± 5.7 years to determine whether Endocan could be a diagnostic and prognostic marker. The patients' mean age was 43.6 ± 13.2 years, and 55.7% (54/97) were male. Higher Endocan levels were found in more advanced chronic kidney disease (CKD) stages in a dose-dependent manner. Interestingly, the Endocan ≥ 643.19 pg/mL group had higher creatinine (Cr; 1.2 ± 0.4 vs 1.6 ± 1.1 mg/dL; P = .029) and lower estimated glomerular filtration rate (eGFR; 67.8 ± 23.8 mL/min vs 54.4 ± 22.0; P = .006) than the Endocan643.19 pg/mL group after 3 months of follow-up, respectively. Linear regression analysis found tumor necrosis factor (TNF)-α correlated well with Endocan. To elucidate the response of endothelium activation, we stimulated human umbilical vein endothelial cells (HUVECs) with TNF-α in vitro, and found the levels of Endocan (P = .022) and transforming growth factor (TGF)-β1 (P = .034) increased with time, but interleukin (IL)-10 decreased (P = .013). In summary, Endocan may reflect the degree of endothelial cell injury in renal allografts, and showed a trend of elevation in late-stage CKD. An in vitro study demonstrated TNF-α-activated HUVECs secreted high levels of Endocan and TGF-β1, which could lead to a better understanding of the role of endothelium in immune balance. In conclusion, Endocan may have potential as a useful long-term indicator of CRAI in RT recipients, but further study is needed to verify our findings.

The risk of developing chronic kidney disease (CKD) among living kidney donors (LKDs) is seldom included in evaluations of patients' outcomes. Potential risk factors and new criteria for estimating the glomerular filtration rate (eGFR) indexed for body surface area (BSA) were investigated with a view to prevent the development of CKD in LKDs.We conducted a retrospective study of LKDs from May 1983 to March 2011. The Mann-Whitney U test and χ(2) test were used to analyze the male versus female groups. Survival analysis was plotted as CKD-free survival and analyzed separately by different eGFR index classifications. The Cox regression model was used to identify potential risk factors for development of CKD.A total of 105 LKDs with a mean age of 46.3 ± 12.5 years had a mean eGFR indexed for BSA of 88.9 ± 21.5 ml/min per 1.73 m(2). After a mean duration of 5.4 ± 4.9 years' follow-up, eGFR dropped to 61.4 ± 16.4 ml/min per 1.73 m(2) (p = 0.002). Median CKD-free survival was only 5.7 years. The difference between eGFR ≥ 80 ml/min per 1.73 m(2) and80 ml/min per 1.73 m(2) was not statistically significant (p = 0.980). Multivariate Cox regression analysis showed that higher eGFR at donation (HR = 0.952, p = 0.0199) could be a protective factor. The receiver operating characteristic (ROC) curve for initial eGFR with best sensitivity of 52.78 % and specificity of 81.40 % was obtained with a cutoff value of 90.2 ml/min per 1.73 m(2) for preoperative eGFR. An eGFR of 90 ml/min per 1.73 m(2) yielded a significant survival curve (p = 0.0199) after 21 years of follow-up. Further classifications of eGFR90 ml/min per 1.73 m(2) into 90-99 ml/min per 1.73 m(2), 100-109 ml/min per 1.73 m(2), and ≥110 ml/min per 1.73 m(2) were examined, but this survival curve was not statistically significant (p = 0.1247).Living kidney donors will develop CKD after a long duration of follow-up if there is insufficiently high eGFR at donation. An eGFR above 90 ml/min per 1.73 m(2) before donation is the only factor that predicts prevention of CKD. Larger studies with longer duration of follow-up are necessary to clarify the clinical outcome of this postoperative CKD group, especially for patients with eGFR between 80 and 90 ml/min per 1.73 m(2).

Upper gastrointestinal bleeding (UGIB) is a major cause of clinical bleeding among patients with end-stage renal disease (ESRD). This study aimed to investigate the association between mortality and UGIB in patients with uremia.From 2004 to 2010, a tertiary hospital-based retrospective cohort comprising 322 patients undergoing hemodialysis was investigated. All the patients were diagnosed with UGIB according to the International Classification of Diseases, 9th Revision (ICD-9) that included peptic ulcer bleeding, duodenal ulcer bleeding, and other symptoms. UGIB was required to be one of the first three discharge diagnoses. Rehospitalization within 3 days after discharge was regarded as the same course. Exclusion criteria were age20 years, previous gastric resection or vagotomy, esophageal and gastric variceal bleeding, or gastric cancer within the first 2 years of the index hospitalization.The all-cause in-hospital mortality rate of patients with UGIB undergoing hemodialysis was high, with the first-month mortality rate of 13.7%, sixth-month mortality rate of 26.7%, and first-year mortality rate of 27.0%. Using Cox regression models, we found that the high mortality rate of the UGIB group was significantly correlated with older age [adjusted hazard ratio (HR) = 1.02, 95% confidence interval (CI) = 1.01-1.04], female sex (adjusted HR = 1.62, 95% CI = 1.05-2.51), infection during hospitalization (adjusted HR = 1.85, 95% CI = 1.13-3.03), single episodic UGIB (adjusted HR = 2.00, 95% CI = 1.08-3.70), abnormal white blood cell (WBC) count (adjusted HR = 1.59, 95% CI = 1.03-2.45), and albumin level ≤3 g/dL (adjusted HR = 2.67, 95% CI = 1.51-4.72).In conclusion, patients with ESRD who are admitted with primary UGIB have a profoundly increased risk of all-cause in-hospital mortality during the follow-up period.

BACKGROUND:The neurotransmitter pathways in irritable bowel syndrome (IBS) and urinary stone attacks are both related to serotonin, and each disease may be influenced by viscero-visceral hyperalgesia. However, the relationship between urinary tract stone disease and IBS has never been addressed. We aimed to investigate the risk of suffering new-onset IBS after an initial urinary stone attack using a nationwide database. METHODS:A study group enrolled a total of 13,254 patients who were diagnosed with an initial urinary stone attack; a comparison group recruited 39,762 matched non-urinary stone participants during 2003 and 2007. We followed each patient for 3 years to determine new-onset IBS. We also used Cox proportional hazards models to analyze the risk of IBS between the study and comparison groups after modified by demographics, residence, patient characteristics and personal histories. RESULTS:The occurrence rates of IBS were 3.3% (n = 440) and 2.6% (n = 1,034) respectively in the study and comparison groups. A covariate-adjusted hazard ratio (HR) of IBS in the study group that was 1.28 times greater (HR = 1.29, 95% CI, 1.15-1.44) than that in the comparison group was showed in the stratified Cox proportional analysis. The adjusted HRs of IBS did not decrease after considering demographics and past histories. The majority of IBS (30.5%) occurred within the first 6 months after the stone attack. CONCLUSION:Patients with an initial urinary stone attack are at increased risk of developing new-onset IBS. The HRs of IBS did not decrease even after adjusting for patient demographics and past histories. Most importantly, 30.5% of IBS occurred within the first 6 months after the urinary stone attack.

Paraquat poisoning is very severe. Most victims, including those who have ingested a small amount, will die from Paraquat poisoning. The cause of death in the majority of such cases is lung fibrosis. Paraquat poisoning in patients with positive human immunodeficiency virus (HIV) infection status has seldom been reported. Herein, we report a case of an HIV patient with Paraquat poisoning who had an excellent outcome even without standard treatment. Currently, only 3 such cases have been reported in the literature and in each case there was a good outcome, which was not expected according to predictive models. A possible mechanism may involve the relative lack of functional macrophages in HIV patients, which would tend to result in much less severe lung injury. None of the available predictive models of Paraquat poisoning appear to be appropriate for HIV patients.Paraquat poisoning in HIV patients may have better survival due to less lung injury.

Renal biopsy remains the golden standard diagnosis of renal function deterioration. The safety in native kidney biopsy is well defined. However, it is a different story in allograft kidney biopsy. We conduct this retrospective study to clarify the safety of allograft kidney biopsy with indication.All variables were grouped by the year of biopsy and they were compared by Mann-Whitney U test (for continuous variables) or Chi-square test (for categorical variables). We collected possible factors associated with complications, including age, gender, body weight, renal function, cause of uremia, status of coagulation, hepatitis, size of needle, and immunosuppressants.We recruited all renal transplant recipients undergoing allograft biopsy between January of 2009 and December of 2014. This is the largest database for allograft kidney biopsy with indication. Of all the 269 biopsies, there was no difference in occurrence among the total 14 complications (5.2%) over these 6 years. There were only 3 cases of hematomas (1.11%), 6 gross hematuria (2.23%), 1 hydronephrosis (0.37%), and 2 hemoglobin decline (0.74%). The outcome of this cohort is the best compared to all other studies, and it is even better than the allograft protocol kidney biopsy. Among all possible factors, patients with pathological report containing "medullary tissue only" were susceptible to complications (P

Chronic kidney disease (CKD) and obesity are important public health concerns. Because obesity may initiate and/or accelerate kidney damage, weight control may benefit CKD patients.We examined the influence of dietary management and physical exercise in 38 obese CKD patients with or without target reduction of body weight 3% or more from baseline.After a 2-month lifestyle intervention program, those with target body weight control had significant improvement of blood pressure control, as well as reduced lipid profiles, serum creatinine level (1.1 ± 0.3 vs. 0.8 ± 0.3; P.001), estimated glomerular filtration rate (75.9 ± 21.2 vs. 104.9 ± 38.1; P.001), and proteinuria (76.3% vs. 50.0%; P = .02). They had greater improvement in cardiorespiratory endurance in an 800-m running test (375.1 ± 64.7 vs. 327.1 ± 84.0 seconds; P = .001), better abdominal muscle strength and endurance in a timed sit-up test (13.6 ± 9.1 vs. 19.9 ± 9.2 number/minute; P = .005), and greater flexibility in a sit-and-reach test (18.8 ± 10.9 vs. 27.8 ± 10.9 cm; P.001) comparing baseline and postintervention values.A combination of dietary management and exercise were associated with improvements in health-related physical fitness, cardiovascular risk factors (blood pressure and lipid control), and renal profiles in obese CKD patients. Supportive individualized programs for lifestyle change could exert beneficial effects, but long-term research with a larger patient population is needed to elucidate the optimal effective combination of dietary management and exercise.

Successful renal transplantation has been performed in patients with end-stage renal disease and has been routine in patients with end-stage renal failure for more than two decades. Despite advances in the use of immunosuppressants, there has been only modest improvement in long-term allograft survival. Accumulating data have demonstrated that chronic rejection and recurrent glomerulonephritis are major causes of long-term allograft loss. However, data regarding the long-term impact of posttransplantation glomerulonephritis (PTGN) on ethnic Chinese populations are still unavailable. From 1984 to 2010, a total of 268 patients who underwent renal allograft biopsies were reviewed retrospectively. Renal outcomes were compared by Kaplan–Meier analysis, and risk factors for renal survival and all-cause mortality were analyzed using the Cox proportional hazards model. In all, 85 patients (31.7 %) had PTGN, and the mean time of disease onset was 5.32 ± 5.18 years after transplantation. Among the 85 PTGN cases, 33 (39 %) were immunoglobulin A (IgA) nephropathy, 24 (28 %) were focal segmental glomerulosclerosis, and 8 (9.4 %) were membranous GN. Significant risk was associated with posttransplant IgA GN in hepatitis B virus carriers (odds ratio 5.371, 95 % confidence interval 1.68, 17.19; p = 0.0064). A total of 45 PTGN patients had allograft loss, of whom 49 % had IgA nephropathy. Patients with PTGN had inferior allograft survival rates compared to those with other pathologic findings (p