Pieter Evenepoel

Universitair Ziekenhuis Leuven, Louvain, Flemish, Belgium

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Publications (215)1200.84 Total impact

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    ABSTRACT: There is increasing interest in the colonic microbiota as a relevant source of uremic retention solutes accumulating in CKD. Renal disease can also profoundly affect the colonic microenvironment and has been associated with a distinct colonic microbial composition. However, the influence of CKD on the colonic microbial metabolism is largely unknown. Therefore, we studied fecal metabolite profiles of hemodialysis patients and healthy controls using a gas chromatography-mass spectrometry method. We observed a clear discrimination between both groups, with 81 fecal volatile organic compounds detected at significantly different levels in hemodialysis patients and healthy controls. To further explore the differential impact of renal function loss per se versus the effect of dietary and other CKD-related factors, we also compared fecal metabolite profiles between patients on hemodialysis and household contacts on the same diet, which revealed a close resemblance. In contrast, significant differences were noted between the fecal samples of rats 6 weeks after 5/6th nephrectomy and those of sham-operated rats, still suggesting an independent influence of renal function loss. Thus, CKD associates with a distinct colonic microbial metabolism, although the effect of renal function loss per se in humans may be inferior to the effects of dietary and other CKD-related factors. The potential beneficial effect of therapeutics targeting colonic microbiota in patients with CKD remains to be examined.
    Journal of the American Society of Nephrology 09/2015; DOI:10.1681/ASN.2015030279 · 9.34 Impact Factor
  • L Viaene · G J Behets · S Heye · K Claes · D Monbaliu · J Pirenne · P C D'Haese · P Evenepoel
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    ABSTRACT: Bone loss and vascular calcification coincide in patients with end-stage renal disease, similar as to what is observed in the general population. In the present bone biopsy study, we provide further evidence that (micro-)inflammation may represent a common soil for both diseases. Vascular calcification is a common complication of end-stage renal disease (ESRD) and is predictive of subsequent cardiovascular disease and mortality. Mounting evidence linking bone disorders with vascular calcification has contributed to the development of the concept of the bone-vascular axis. Inflammation is involved in the pathogenesis of both disorders. The aim of the present study was to evaluate the relationship between aortic calcification, inflammation, and bone histomorphometry in patients with ESRD. Parameters of inflammation and mineral metabolism were assessed in 81 ESRD patients (55 ± 13 year, 68 % male) referred for renal transplantation. Static bone histomorphometry parameters were determined on transiliac bone biopsies performed during the transplant procedure. Aortic calcification was quantified on lateral lumbar X-rays using the Kauppila method. Aortic calcification, low bone turnover, and low bone area were observed in 53, 37, and 21 % of patients respectively. Inflammatory markers were found to be independently associated with aortic calcification (hsIL-6) and low bone area (TNF-α). Low bone area associated with aortic calcification, independent of age, diabetes, and inflammation. Low bone area and inflammation associates with aortic calcification, independent of each other and traditional risk factors. Our data emphasize the role of (micro-)inflammation in the bone-vascular axis in CKD.
    Osteoporosis International 08/2015; DOI:10.1007/s00198-015-3233-8 · 4.17 Impact Factor
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    ABSTRACT: Proteinuria is routinely measured to assess renal allograft status, but the diagnostic and prognostic values of this measurement for renal transplant pathology and outcome remain unclear. We included 1518 renal allograft recipients in this prospective, observational cohort study. All renal allograft biopsy samples with concomitant data on 24-hour proteinuria were included in the analyses (n=2274). Patients were followed for ≥7 years post-transplantation. Compared with proteinuria <0.3 g/24 h, the hazard ratios for graft failure were 1.14 (95% confidence interval [95% CI], 0.81 to 1.60; P=0.50), for proteinuria 0.3-1.0 g/24 h, 2.17 (95% CI, 1.49 to 3.18; P<0.001), for proteinuria 1.0-3.0 g/24 h, and 3.01 (95% CI, 1.75 to 5.18; P<0.001), for proteinuria >3.0 g/24 h, independent of GFR and allograft histology. The predictive performance of proteinuria for graft failure was lower at 3 months after transplant (area under the receiver-operating characteristic curve [AUC] 0.64, P<0.001) than at 1, 2, and 5 years after transplant (AUC 0.73, 0.71, and 0.77, respectively, all P<0.001). Independent determinants of proteinuria were repeat transplantation, mean arterial pressure, transplant glomerulopathy, microcirculation inflammation, and de novo/recurrent glomerular disease. The discriminatory power of proteinuria for these intragraft injury processes was better in biopsy samples obtained >3 months after transplant (AUC 0.73, P<0.001) than in those obtained earlier (AUC 0.56, P<0.01), with 85% specificity but lower sensitivity (47.8%) for proteinuria >1.0 g/24 h. These data support current clinical guidelines to routinely measure proteinuria after transplant, but illustrate the need for more sensitive biomarkers of allograft injury and prognosis. Copyright © 2015 by the American Society of Nephrology.
    Journal of the American Society of Nephrology 07/2015; DOI:10.1681/ASN.2015010062 · 9.34 Impact Factor
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    ABSTRACT: CD14 plays a key role in the innate immunity as pattern-recognition receptor of endotoxin. Higher levels of soluble CD14 (sCD14) are associated with overall mortality in hemodialysis patients. The influence of kidney function on plasma sCD14 levels and its relationship with adverse outcomes in patients with CKD not yet on dialysis is unknown. This study examines the associations between plasma levels of sCD14 and endotoxin with adverse outcomes in patients with CKD. We measured plasma levels of sCD14 and endotoxin in 495 Leuven Mild-to-Moderate CKD Study participants. Mild-to-moderate CKD was defined as presence of kidney damage or eGFR<60 ml/min per 1.73 m(2) for ≥3 months, with exclusion of patients on RRT. Study participants were enrolled between November 2005 and September 2006. Plasma sCD14 was negatively associated with eGFR (ρ=-0.34, P<0.001). During a median follow-up of 54 (interquartile range, 23-58) months, 53 patients died. Plasma sCD14 was predictive of mortality, even after adjustment for renal function, Framingham risk factors, markers of mineral bone metabolism, and nutritional and inflammatory parameters (hazard ratio [HR] per SD higher of 1.90; 95% confidence interval [95% CI],1.32 to 2.74; P<0.001). After adjustment for the same risk factors, plasma sCD14 was also a predictor of cardiovascular disease (HR, 1.30; 95% CI, 1.00 to 1.69; P=0.05). Although plasma sCD14 was associated with progression of CKD, defined as reaching ESRD or doubling of serum creatinine in models adjusted for CKD-specific risk factors (HR, 1.24; 95% CI, 1.01 to 1.52; P=0.04), significance was lost when adjusted for proteinuria (HR, 1.19; 95% CI, 0.96 to 1.48; P=0.11). There was neither correlation between plasma endotoxin and sCD14 (ρ=-0.06, P=0.20) nor was endotoxin independently associated with adverse outcome during follow-up. Plasma sCD14 is elevated in patients with decreased kidney function and associated with mortality and cardiovascular disease in patients with CKD not yet on dialysis. Copyright © 2015 by the American Society of Nephrology.
    Clinical Journal of the American Society of Nephrology 07/2015; 10(9). DOI:10.2215/CJN.03100315 · 4.61 Impact Factor
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    ABSTRACT: Calcific uraemic arteriolopathy (CUA) is a rare disease and continues to be a clinical challenge. The typical course of CUA is characterized by painful skin discolouration and induration evolving to necrotic ulcerations. Medial calcification of cutaneous arterioles and extensive extracellular matrix remodelling are the hallmarks of CUA. The epidemiology and risk factors associated with this disease are still not fully understood. Moreover, CUA treatment strategies vary significantly among centres and expert recommendations are heterogeneous. Registries may provide important insights and information to increase our knowledge about epidemiology and clinical aspects of CUA and may help to optimize its therapeutic management. In 2006, we established an internet-based registry in Germany (www.calciphylaxie.de) to allow online notification of patients with established or suspected CUA. The registry includes a comprehensive database with questions covering >70 parameters and items regarding patient-related and laboratory data, clinical background and presentation as well as therapeutic strategies. The next phase will be to allow international patient registration via www.calciphylaxis.net as part of the multinational EuCalNet (European Calciphylaxis Network) initiative, which is supported by the ERA-EDTA scientific working group ‘CKD-MBD’. Based on the valuable experience with the previous German CUA registry, EuCalNet will be a useful tool to collect data on the rare disease CUA and may become a basis for prospective controlled trials in the near future.
    CKJ: Clinical Kidney Journal 07/2015; 8(5):sfv056. DOI:10.1093/ckj/sfv056
  • Pieter Evenepoel · Patrick D'Haese · Vincent Brandenburg
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    ABSTRACT: For more than a decade, the Wnt-β-catenin pathway has been the focus of intense basic and clinical research in the bone field because of its importance in skeletal development and maintenance of bone mass. Wnt activation increases bone formation and decreases bone resorption. The Wnt-β-catenin signaling pathway is tightly regulated by several inhibitors, among which Dickkopf-related protein 1 (DKK1) and sclerostin have been most comprehensively studied. Mounting evidence indicates that a disturbed Wnt-β-catenin signaling is also implicated in the pathogenesis of the chronic kidney disease-associated bone and mineral disorder (CKD-MBD) and affects its various components. DKK1 and sclerostin, more specifically, may be involved in the intense cross-talk between the kidneys, vasculature, and bone. Studies exploring clinical correlates of circulating sclerostin and DKK1 levels so far yielded conflicting results. Biological variability and analytical issues account at least partly for this inconsistency. Antibodies neutralizing Wnt inhibitors may be an appealing strategy to prevent or treat CKD-MBD. Caution is however warranted as sclerostin not only opposes mineralization in the bone but possibly also in the vasculature. Additional studies are required to define determinants of Wnt inhibitors in CKD and to evaluate the efficacy and safety of recently introduced pharmaceuticals targeting these inhibitors.Kidney International advance online publication, 17 June 2015; doi:10.1038/ki.2015.156.
    Kidney International 06/2015; 88(2). DOI:10.1038/ki.2015.156 · 8.56 Impact Factor
  • 06/2015; DOI:10.1530/boneabs.4.P31
  • Ruben Poesen · Pieter Evenepoel · Björn Meijers
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    ABSTRACT: Kidney International aims to inform the renal researcher and practicing nephrologists on all aspects of renal research. Clinical and basic renal research, commentaries, The Renal Consult, Nephrology sans Frontieres, minireviews, reviews, Nephrology Images, Journal Club. Published weekly online and twice a month in print.
    Kidney International 04/2015; 87(4):864. DOI:10.1038/ki.2014.396 · 8.56 Impact Factor
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    ABSTRACT: Canonical Wnt signaling activity contributes to physiological and adaptive bone mineralization and is an essential player in bone remodeling. Sclerostin is a prototypic soluble canonical Wnt signaling pathway inhibitor that is produced in osteocytes and blocks osteoblast differentiation and function. Therefore, sclerostin is a potent inhibitor of bone formation and mineralization. Accordingly, rodent sclerostin-deficiency models exhibit a strong bone phenotype. Moreover, blocking sclerostin represents a promising treatment perspective against osteoporosis. Beyond the bone field novel data definitely associate Wnt signaling in general and sclerostin in particular with ectopic extraosseous mineralization processes, as is evident in cardiovascular calcification or calciphylaxis. Uremia is characterized by parallel occurrence of disordered bone mineralization and accelerated cardiovascular calcification (chronic kidney disease - mineral and bone disorder, CKD-MBD), linking skeletal and cardiovascular disease-the so-called bone-vascular calcification paradox. In consequence, sclerostin may qualify as an emerging player in CKD-MBD. We present a stepwise review approach regarding the rapidly evolving field sclerostin participation in CKD-MBD. Starting from data originating in the classical bone field we look separately at three major areas of CKD-MBD: disturbed mineral metabolism, renal osteodystrophy, and uremic cardiovascular disease. Our review is intended to help the nephrologist revise the potential importance of sclerostin in CKD by focusing on how sclerostin research is gradually evolving from the classical osteoporosis niche into the area of CKD-MBD. In particular, we integrate the limited amount of available data in the context of pediatric nephrology.
    Pediatric Nephrology 03/2015; DOI:10.1007/s00467-015-3069-7 · 2.86 Impact Factor
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    Nephrology Dialysis Transplantation 03/2015; 30(3):357. DOI:10.1093/ndt/gfv021a · 3.58 Impact Factor
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    ABSTRACT: Background: Transplant recipients are at risk for invasive aspergillosis (IA), associated with a significant mortality rate. Renal transplant-specific risk factors have not been established. Methods: Forty-one adult kidney transplant recipients diagnosed with proven or probable IA from 1995 through 2013 were identified by search of the computerized patient files in the University Hospitals Leuven. The control population in this 1:2 case-control study consisted of the 2 patients who received a kidney transplant immediately before and after each identified patient and did not develop IA (n = 82). Results: Leukopenia after kidney transplant increased the risk of IA among all patients (odds ratio [OR], 2.345 [95% confidence interval {CI}, 1.084-5.071]). For early-onset infection (ie, occurred during the first 3 months after transplant), a longer duration of renal replacement therapy pretransplant and the occurrence of leukopenia were risk factors (OR per year, 1.192 [95% CI, 1.006-1.413] and OR, 3.346 [95% CI, 1.063-10.527], respectively), whereas donor cytomegalovirus seropositivity increased the risk for late-onset IA (ie, occurred >3 months after transplant) (OR, 3.677 [95% CI, 1.388-9.743]). Twelve-week mortality rate was 39%. Disseminated infection, leukopenia, and the height of the serum galactomannan index were associated with an increased risk of death (hazard ratio [HR], 5.080 [95% CI, 1.740-14.830]; HR, 3.198 [95% CI, 1.183-8.649]; and HR, 1.371 [95% CI, 1.123-1.674], respectively). Conclusions: Prolonged renal replacement therapy before kidney transplant increases the risk of IA early after transplant. The height of the serum galactomannan index predicts mortality.
    Clinical Infectious Diseases 02/2015; 60(10). DOI:10.1093/cid/civ103 · 8.89 Impact Factor
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    ABSTRACT: A new definition and classification of chronic kidney disease-mineral and bone disorder (CKD-MBD) was proposed in 2005 and it was later followed by a guideline publication on this topic from Kidney Disease: Improving Global Outcomes (KDIGO) in 2009. This work recognized that CKD-MBD is a syndrome of bone abnormalities, laboratory abnormalities, and vascular calcification linked to fractures, cardiovascular disease, and mortality. Because of limited data at the time of the original guideline systematic review, many of the recommendations were cautiously vague. KDIGO convened a Controversies Conference in October 2013 to review the CKD-MBD literature published since the 2009 guideline. Specifically, the objective of this conference was to determine whether sufficient new data had emerged to support a reassessment of the CKD-MBD guideline and if so to determine the scope of these potential revisions. This report summarizes the results of these proceedings, highlighting important new studies conducted in the interval since the original KDIGO CKD-MBD guideline.Kidney International advance online publication, 4 February 2015; doi:10.1038/ki.2014.425.
    Kidney International 02/2015; 87(3). DOI:10.1038/ki.2014.425 · 8.56 Impact Factor
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    ABSTRACT: Experimental data indicate that microscopic calcium phosphate deposition in the kidney (nephrocalcinosis) may accelerate progression of chronic kidney disease (CKD). Data on the prevalence, risk factors and implications of nephrocalcinosis in CKD patients are scarce. A mineral metabolism disorder could play an important pathogenetic role, as suggested by recent protocol biopsy findings in incident renal transplant recipients. Kidney biopsy cylinders of CKD patients, collected between January 1989 and December 2007, were screened for the presence of nephrocalcinosis. Only patients with ≥1 parathyroid hormone (PTH) level available within 180 days of the biopsy were eligible for inclusion (n = 211). Demographics and mineral metabolism parameters were retrieved from medical files. Data on renal death (up to December 2012) were obtained from the Flemish ESRD registry. Baseline biopsies from 110 deceased kidney transplant donors served as controls. The prevalence of nephrocalcinosis in kidney donors and patients with CKD 1-2, CKD 3-4 and CKD 5-5D was 4.6, 14.3, 20.2 and 54.0%, respectively (P < 0.0001). Among CKD patients, patients with nephrocalcinosis were characterized by lower estimated GFR, lower serum bicarbonate level and higher serum PTH and calcium level. In multivariate regression analysis, high serum PTH, calcium and creatinine level, and low serum bicarbonate level were all significantly and independently associated with nephrocalcinosis. Serum phosphorus level, but not nephrocalcinosis predicted renal death, independent of renal function. Our data demonstrate that prevalence rates of nephrocalcinosis increase with increasing CKD stage to reach more than 50% in end-stage renal disease patients and suggest that acid-base and mineral metabolism disturbances are implicated in its pathogenesis. © The Author 2015. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.
    Nephrology Dialysis Transplantation 01/2015; 30(5). DOI:10.1093/ndt/gfu400 · 3.58 Impact Factor
  • Björn K I Meijers · Ruben Poesen · Pieter Evenepoel
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    ABSTRACT: Evidence on the optimal anticoagulation regimen for hemodialysis in patients at high bleeding risk is scarce. The HepZero study is the first large multinational study comparing two different anticoagulation strategies to avoid systemic heparinization. The use of a heparin-coated dialysis membrane proved to be non-inferior to saline infusion. Superiority of either treatment, however, could not be demonstrated. These findings challenge current guidelines but equally raise questions on the choice of either strategy as compared with regional citrate anticoagulation.
    Kidney International 12/2014; 86(6):1084-6. DOI:10.1038/ki.2014.315 · 8.56 Impact Factor
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    Mario Cozzolino · Pieter Evenepoel · Adrian Covic
    Seminars in Nephrology 11/2014; 34(6):577. DOI:10.1016/j.semnephrol.2014.09.002 · 3.48 Impact Factor
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    ABSTRACT: Background Sclerostin is a Wnt pathway antagonist regulating osteoblast activity and bone turnover, and it plays a role in cardiovascular calcification processes. Previous findings indicate that sclerostin regulation is disturbed in chronic kidney disease (CKD). The aim of this study was to assess the association of circulating sclerostin levels with mortality in dialysis patients. Methods From a prospective cohort study of incident dialysis patients in the Netherlands, all patients with measured circulating sclerostin at 3 months after the start of dialysis (baseline) were included in the present analysis: n = 673, age 63 ± 14 years, mean serum sclerostin (ELISA) 1.24 ± 0.57 ng/mL. By Cox regression analyses, we assessed the association of sclerostin levels with cardiovascular and non-cardiovascular mortality both in the short (18 months) and long term (4-year follow-up). ResultsSerum sclerostin levels in the entire cohort correlated with intact parathyroid hormone levels (r = -0.25, P < 0.001), age (r = 0.16, P < 0.001) and serum alkaline phosphatase (r = -0.13, P = 0.001). After adjustment for various clinical and biochemical parameters, patients in the highest sclerostin tertile had a significantly lower risk of cardiovascular death [hazard ratio 0.29, 95% confidence interval (CI) 0.13-0.62] and for all-cause mortality (0.39, 95% CI 0.22-0.68) within 18 months compared with patients of the lowest tertile. The association of sclerostin levels with outcome was less pronounced for long-term cardiovascular mortality and absent for non-cardiovascular mortality. Conclusions High levels of serum sclerostin are associated with lower short-term cardiovascular mortality in dialysis patients. The exact mechanisms of this association, e.g. how sclerostin influences or reflects uraemic vascular calcification, need to be investigated in further studies. © The Author 2014. Published by Oxford University Press on behalf of ERA-EDTA.
    Nephrology Dialysis Transplantation 09/2014; 30(2). DOI:10.1093/ndt/gfu301 · 3.58 Impact Factor
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    ABSTRACT: Persistent hyperparathyroidism (HPT) after kidney transplantation (KTx) is associated with hypercalcemia, hypophosphatemia and abnormally high levels of parathyroid hormone (PTH). In this randomized trial, cinacalcet was compared to placebo for the treatment of hypercalcemia in adult patients with persistent HPT after KTx. Subjects were randomized 1:1 to cinacalcet or placebo with randomization stratified by baseline corrected total serum calcium levels (≤11.2 mg/dL [2.80 mmol/L] or >11.2 mg/dL [2.80 mmol/L]). The primary end point was achievement of a mean corrected total serum calcium value <10.2 mg/dL (2.55 mmol/L) during the efficacy period. The two key secondary end points were percent change in bone mineral density (BMD) at the femoral neck and absolute change in phosphorus; 78.9% cinacalcet- versus 3.5% placebo-treated subjects achieved the primary end point with a difference of 75.4% (95% confidence interval [CI]: 63.8, 87.1), p < 0.001. There was no statistical difference in the percent change in BMD at the femoral neck between cinacalcet and placebo groups, p = 0.266. The difference in the change in phosphorus between the two arms was 0.45 mg/dL (95% CI: 0.26, 0.64), p < 0.001 (nominal). No new safety signals were detected. In conclusion, hypercalcemia and hypophosphatemia were effectively corrected after treatment with cinacalcet in patients with persistent HPT after KTx.
    American Journal of Transplantation 09/2014; 14(11). DOI:10.1111/ajt.12911 · 5.68 Impact Factor
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    ABSTRACT: Background: The relative impact on renal allograft outcome of specific histological diagnoses versus nonspecific chronic histological damage remains unclear. Methods: All 1,197 renal allograft recipients who were transplanted at a single center between 1991 and 2001 were included. All posttransplant renal allograft indication biopsies performed in this cohort during follow-up (mean, 14.5±2.80 years after transplantation) were rescored according to the current histological criteria and associated with death-censored graft outcome. Results: In this cohort, 1,365 allograft indication biopsies were performed. Specific diagnoses were present in 69.4% of graft biopsies before graft loss, but 30.6% of grafts did not have specific diagnoses in the last biopsy before graft loss. Only 14.6% of the patients did never have any specific disease diagnosed before graft loss. Extensive interstitial fibrosis and tubular atrophy without a clear cause was identified as the single cause of graft loss in only 6.9% of the cases. Acute T-cell-mediated rejection and changes suggestive of acute antibody-mediated rejection, diagnosed after the first year posttransplant, associated independently with graft survival. Transplant glomerulopathy increased over time after transplantation and represented a major risk for graft loss, as well as de novo or recurrent glomerular pathologies and polyomavirus nephropathy. Chronic histological injury associated with graft outcome, independent of specific diagnoses. Conclusion: Renal allograft loss is multifactorial. Chronic histological damage and specific diseases had additive and independent impact on graft outcome. Chronic damage should be taken into account in prognostication of renal allograft outcome and could be implemented in treatment algorithms for specific diseases of kidney allografts.
    Transplantation 08/2014; 98(4):427-435. DOI:10.1097/TP.0000000000000183 · 3.83 Impact Factor
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    ABSTRACT: Background Although renal transplantation (Tx) improves the outcome of patients with renal disease, cardiovascular (CV) risk remains high. Recently, it was demonstrated that asymmetric dimethylarginine (ADMA) levels predict CV events and graft survival in renal transplant recipients (RTRs). Little is known about the impact of renal Tx on the plasma levels of ADMA and symmetric dimethylarginine (SDMA). The present study aimed to define the time course of ADMA and SDMA after Tx.
    Nephrology Dialysis Transplantation 06/2014; 29(10). DOI:10.1093/ndt/gfu219 · 3.58 Impact Factor
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    ABSTRACT: Functional catheter problems are a major challenge for peritoneal dialysis (PD) programs. Here we performed a retrospective single-center study of 110 consecutive patients receiving a first PD catheter (swan neck double-cuff Missouri curled catheters, open surgical technique). Using postimplantation X-ray, the following categories were defined: swan neck angle (posterioanterio view (PA): under 45°, 45-90°, over 90°), inclination (angle between intramural part of catheter and horizontal line; lateral view: greater than/equal to 30°, under 30°), and the position of silicone bead relative to spine (PA view: L1-2, L3-4, lower) and catheter tip (PA view: hypogastric, umbilical, subcostal). Covariates included demographics, body size, previous abdominal surgery, and abdominal wall hernias. During a mean follow-up of 36 months, the time to first functional catheter problem was significantly associated with both the swan neck angle and inclination. The need for surgical intervention was significantly associated with inclination only. Technique failure was not associated with any parameter. In multivariate analysis, inclination was the sole variable significantly associated with functional catheter problems (hazard ratio 3.65 [1.98-6.72]) and the need for surgical intervention (hazard ratio 2.86 [1.19-6.88]). Thus, our study defines a set of X-ray variables that predict functional PD catheter problems and can be used for troubleshooting in individual cases as well as for education and internal audit purposes.Kidney International advance online publication, 18 June 2014; doi:10.1038/ki.2014.203.
    Kidney International 06/2014; 86(5). DOI:10.1038/ki.2014.203 · 8.56 Impact Factor

Publication Stats

5k Citations
1,200.84 Total Impact Points


  • 1997–2015
    • Universitair Ziekenhuis Leuven
      • • Department of Nephrology
      • • Department of Gastroenterology
      Louvain, Flemish, Belgium
  • 1997–2014
    • University of Leuven
      • Department of Microbiology and Immunology
      Louvain, Flemish, Belgium
  • 2013
    • University of Antwerp
      • Laboratory of Pathophysiology
      Antwerpen, Flemish, Belgium
  • 2010
    • University of Geneva
      Genève, Geneva, Switzerland
  • 1998
    • Catholic University of Louvain
      Лувен-ла-Нев, Walloon, Belgium