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BACKGROUND The process of vascular calcification has been associated with the canonical Wnt/β-catenin signalling pathway in cell cultures and animal studies. The relationship between circulating Wnt/β-catenin inhibitors and vascular calcification in dialysis patients is unknown. The aim of this study was to investigate the associations between serum dickkopf-1 (Dkk-1) and sclerostin, two circulating inhibitors of the Wnt/β-catenin signalling pathway, and the severity of aortic calcification (AoC) and cardiovascular outcomes in dialysis patients. METHODS This was a prospective observational cohort study. One hundred and twenty-five patients on maintenance haemodialysis participated in the study. Serum levels of Dkk-1 and sclerostin were measured. AoC scores were calculated from plain films of both posterior-anterior and lateral views. The patients were followed up for 2 years or until death or withdrawal. RESULTS The circulating sclerostin level was inversely associated with the severity of AoC (P = 0.035) and indicators of the bone turnover rate including serum alkaline phosphatase (ALP) (r = -0.235, P = 0.008) and intact parathyroid hormone (r = -0.523, P < 0.001). Furthermore, Cox regression analysis indicated that the patients with high circulating sclerostin levels were less likely to experience future cardiovascular events [1 pmol/L sclerostin increase, hazard ratio 0.982 (95% CI, 0.967-0.996), P = 0.015] after adjusting for a propensity score. In contrast, serum Dkk-1 was not associated with AoC and clinical outcomes. CONCLUSIONS In long-term haemodialysis patients, circulating sclerostin but not Dkk-1 is inversely associated with AoCs and future cardiovascular events. Our findings suggest that sclerostin, as a bone-related protein, might act as a communicator between uraemic bone and vasculature.

Background The pathological recognition of secondary membranous nephropathy (MN) is sometimes difficult, especially in those showing primary idiopathic MN-like histomorphology. The ultrastructural finding of tubuloreticular inclusions (TRIs) in MN always evokes suspicion of their association with underlying diseases such as viral infections and autoimmune diseases. However, it is not clear whether some other underlying diseases are associated with TRI expression in MN. Since treatment of the underlying diseases is the primary consideration for the management of secondary MN, it is important to make out the clinical significance of TRI expression in MN. Methods Excluding the patients fully qualified for systemic lupus erythematosus (SLE) diagnostic criteria, we recruited 36 cases having a renal biopsy featured with histopathology of primary idiopathic MN but ultrastructural appearance of TRIs in glomerular endothelial cells (GECs). We investigated their clinical and pathological profiles and focused on the potential connections with the underlying diseases and treatment outcomes. Results One-third of our cases showed no identifiable underlying aetiology. Other underlying disease groups included autoimmune disease (25%), hepatitis (14.7%), potential Helicobacter pylori infection (13%), diabetes (5.6%) and lymphoma (5.6%). Pathologically, patients in the autoimmune group tended to have more heterogeneous membranous deposits with frequent mesangial and subendothelial deposits. While all patients of the autoimmune group presented complement C1q in glomeruli, more than two-thirds of the patients in others groups were negative for C1q. Clinically, the patients in autoimmune and hepatitis groups were younger in age and had less remission of proteinuria following treatment, while the other groups of patients achieved partial or complete remission more frequently. Conclusion The underlying diseases of our patients were consistent with the major disease categories that have been frequently linked to secondary MN. The HP group was more akin to undefined groups regarding their pathological and clinical profiles. Since the MN in the undefined group might be the only renal manifestation antedating other clinical presentations of the corresponding underlying disease, a long-term follow-up and meticulous search for aetiological factors are required to validate this assumption.

Background Incident and prevalent (I&P) rates in dialysis end-stage renal disease (ESRD) patients in Taiwan increased rapidly following the launch of National Health Insurance (NHI) in 1995. Our aim was to explore the impact of NHI on the status and trends of ESRD epidemiology in Taiwan. Methods This study was conducted using retrospective cohort analysis of data collected from the Taiwan national dialysis registry. Results From 1990 to 2001, I&P rates of ESRD patients increased 2.6 times from 126 to 331 per million populations (pmp) and 3.46 times from 382 to 1322 pmp, respectively. Increasing ESRD was seen in patients who were middle-aged, elderly and who had diabetic nephropathy as their primary renal disease. The mean age of I&P patients increased by 7.2 years and 7.1 years, respectively. All of these parameters increased markedly in 1995, the year of NHI implementation. First-year mortality decreased to 7.8 per 1000 patient-months in 1994, and then increased to 18.0 in 2001. The cumulative survival rate of the elderly subgroup (age >65) in the incident 1990-1994 cohort was greater than in the 1995-1999 cohort. These data indicated that NHI implementation significantly influenced the inflow and the mortality of ESRD patients. Conclusion In addition to presenting ESRD epidemiology in Taiwan, this study demonstrated that NHI implementation stimulated the growth of treated ESRD populations. Preventive plans mounted against chronic kidney diseases will be essential to reduce the growth of ESRD patient numbers and consequent economic burdens.

Taiwan has the world's highest incidence and second highest prevalence of end-stage renal disease (ESRD), particularly in older age groups. However, the transition from chronic kidney disease (CKD) to death or ESRD remains unclear. This study aimed to investigate the impact of late-stage CKD on all-cause and cause-specific mortality by identifying the CKD population.This was an observational cohort study (n = 35 529), mean age 75.7 years (SD = 5.3), of participants in the Elderly Health Examination Program (EHEP) in Kaohsiung City, Taiwan, between 2002 and 2004. Estimated glomerular filtration rate (eGFR) was calculated by the simplified modified diet in renal disease equation. Proportional hazard ratios (HR) of mortality associated with late-stage CKD were assessed by Cox regression.The crude prevalence rate of CKD stages 3-5 was 39.4%; 1840 participants (5.18%) died within 2-year follow-up, a mortality rate of 20.3 per 1000 person-years overall and 16.4 per 1000 person-years in the reference group. Higher HR for all-cause and cause-specific mortality were found in the groups with decreased eGFR. Compared with the reference group (eGFR60 mL/min/1.73 m(2)), adjusted HR for all-cause mortality were 1.5, 2.1 and 2.6 for groups with eGFR 30-44, 15-29 and15 mL/min/ 1.73 m(2), respectively (P0.001). Higher HR of mortality due to cardiovascular or renal diseases were also significantly associated with decreased eGFR (P0.05).Late-stage CKD is a significant risk factor for mortality, especially due to cardiovascular and renal diseases, in elderly Taiwanese. Given the higher prevalence rate of late-stage CKD in the study area, CKD patient mortality was relatively lower, which might reflect underestimation of renal function for patients at early stages of CKD, or partly explain the high ESRD population.

Background. Hyperphosphataemia contributes to sec-ondary hyperparathyroidism and renal osteodystrophyin patients with end-stage renal disease (ESRD).Calcium salts are widely employed to bind dietaryphosphate (P) but they may promote positive netcalcium balance and metastatic calcification. Werecently reported that ferric compounds bind intestinalphosphate in studies of normal and azotemic rats.Methods. To extend this observation, we performed anopen-label, random order, crossover comparison studyof ferric citrate and calcium carbonate in haemodia-lysis patients from two teaching hospitals. The studysample consisted of 23 women and 22 men with anaverage age of 52.5"11.8 (SD) years and an averageweight of 54.5"10.7 kg. All forms of iron therapy werediscontinued. Two weeks before the study, patientswere instructed to discontinue all P-binding agents.The patients were randomly assigned to receive eithercalcium carbonate (3 guday) or ferric citrate (3 guday)for 4 weeks followed by a 2 week washout period, andthen crossed over to the other P-binding agent for4 weeks.Results. From a baseline concentration of 5.6"1.5 mgudl, the serum P increased during the washoutperiod to 7.2"1.9 mgudl prior to calcium carbonatetreatment, and to 6.7"1.9 mgudl prior to ferric citratetreatment. The serum P concentration fell signific-antly during treatment with both calcium carbonate(7.2"1.9 to 5.2"1.5 mgudl, P-0.0001) and ferriccitrate (6.7"1.9 to 5.7"1.6 mgudl, P-0.0001). Theresults were not influenced by order of treatment.Under the conditions of the study protocol, ferriccitrate was less effective than calcium carbonateat lowering the serum phosphate concentration.The serum Ca concentration increased during treat-ment with calcium carbonate but not ferric citrate.Ferric citrate treatment did not affect the serumconcentration of aluminium. Ferric citrate treatmentwas associated with mild and generally tolerablegastrointestinal symptoms.Conclusion. Ferric citrate shows promise as a meansof lowering the serum phosphate concentration inhaemodialysis patients. Further studies are needed tofind the optimal dose.Keywords: ferric citrate; haemodialysis; open-labelcrossover study; phosphate-binding agent

1996. He suVered from malar rashes and photosensitivity for 1 month. At that time, C 3 and C 4 were 95 mg/dl ible with bullous SLE (Figure 3A and B). Because of (normal, 80‐155 mg/dl ) and 39.7 mg/dl (normal, the persistent vesicobullous eruption, five plasma 13‐37 mg/dl ), respectively. Double-stranded DNA exchanges were made on alternative days following (dsDNA) was 10 IU/ml (normal, 300 mg/dl ) and microhaematuria (RBC eruptions ( Table 1), cyclosporin (125 mg per day) was 3+/HPF ) were noted on urinalysis. A renal fine- added to azathioprine (100 mg per day) and prednisoneedle biopsy was performed. Light microscopy (LM ) lone (60 mg per day) after completion of the MTP pulse therapy. Proteinuria and lupus activity indices

arteriovenous fistula; brachiocephalic vein

A 64-year-old post-menopausal woman presented with dysuria, weakness and poor appetite that had lasted 3 months. A bilateral percutaneous nephrostomy (PCN) catheter was placed for bilateral hydroureteronephrosis at a local hospital, but malfunctioned due to blood clot formation. Physical examination revealed peritoneal signs. Laboratory test revealed leucocytosis, azotaemia with blood urea nitrogen (BUN) 93mg/dl, creatimine (Cr) 16.3mg/dl, and severe metabolic acidosis. Haemodialysis was initiated for uraemia. Computed tomography of the abdomen demonstrated the presence of ascites with peritoneal thickening in the lower peritoneal cavity, obstruction of the uterine outlet with intra-uterine fluid retention, tissue plane blurring between the uterine cervix and urinary bladder, and obstructive uropathy with the obstruction level at the bilateral uretero-vesical junction (Figures 1 and 2). Cervical cancer with pyometra was suspected and treated with dilation and curettage surgery, during which 150 c.c. of pus was drained out. Empiric antibiotics were given and sepsis resolved thereafter. A bilateral PCN catheter functioned well after repeated revisions. Haemodialysis was discontinued 3 weeks later (BUN 33mg/dl, Cr 2.8mg/dl). A biopsy of the cervix revealed squamous cell carcinoma with stromal invasion and the staging was IVA because of urinary bladder spreading. The patient recalled that she had suffered from intermittent vaginal spotting for the last 4 years, but had ignored it.

A 42-year-old woman who was receiving long-term continuous ambulatory peritoneal dialysis (CAPD) for renal failure was admitted to the hospital because of high fever and chills. Five years earlier, she had been diagnosed to have tuberculous (TB) lymphadenitis based on neck lymph-node biopsy and had been treated with rifampicin, isoniazid and ethambutol for 9 months. She remained well until 1 month before admission, when she began to develop fatigue and body-weight loss. On physical examination, the patient’s abdomen was generally tender, with guarding and rebound tenderness. Initial peritoneal fluid cell count was 18uml and then became 300uml with neutrophil predominance on day 3. Peritoneal fluid for Gram stain and acid-fast bacilli smear were negative. Specimens of blood and peritoneal fluid were obtained for culture and empirical antibiotic therapy was started. However, daily fever spikes persisted, with nightly shaking chills and sweats despite changing antibiotics to a combination of vancomycin, ceftazidime and metronidazole for possible septic syndrome. A computed tomographic scan of the abdomen and pelvis showed ascitic fluid, thickening and oedema of the mesentery and omentum, and multiple enlarged lymph nodes. Repeated peritoneal fluid cultures were sterile. The peritoneal catheter was removed and the patient was transferred to haemodialysis. Six weeks after admission, the peritoneal fluid culture grew Mycobacterium tuberculosis, which was found to be sensitive to isoniazid, rifampicin, ethambutol, pyrazinamide and streptomycin on susceptibility testing. The patient was placed on anti-TB medications consisting of isoniazid, rifampicin and pyrazinamide. The patient was readmitted 3 months later, however, with recurrence of fever and pus discharge from the umbilicus. The pus smear was positive with a moderate (2q) amount of acid-fast bacilli present. A fistulogram (Figure 1), performed under fluoroscopy with contrast injection into the umbilical orifice through an 8 Fr. Foley’s catheter, revealed even dispersion of the contrast medium into the peritoneal cavity, suggesting a direct communication. To our knowledge, umbilical fistula formation has never been observed in association with TB peritonitis during CAPD [1]. The umbilicus is the thinnest part of the lower abdomen. As the peritoneal granulomatous inflammation expands due to non-compliance or development of