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  • 1.
    Arora, Satish
    et al.
    Oslo University Hospital.
    Ueland, Thor
    Oslo University Hospital.
    Wennerblom, Bertil
    Sahlgrens University Hospital.
    Sigurdadottir, Vilborg
    Sahlgrens University Hospital.
    Eiskjaer, Hans
    Skejby University Hospital.
    E. Botker, Hans
    Skejby University Hospital.
    Ekmehag, Bjorn
    Skane University Hospital.
    Jansson, Kjell
    Linköping University, Department of Medical and Health Sciences, Cardiology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Heart and Medicine Centre, Department of Cardiology UHL.
    Mortensen, Svend-Aage
    Rigshosp, Copenhagen.
    Saunamaki, Kari
    Rigshosp, Copenhagen.
    Simonsen, Svein
    Oslo University Hospital.
    Gude, Einar
    Oslo University Hospital.
    Bendz, Bjorn
    Oslo University Hospital.
    Solbu, Dag
    Novartis, Oslo.
    Aukrust, Pal
    Oslo University Hospital.
    Gullestad, Lars
    Oslo University Hospital.
    Effect of Everolimus Introduction on Cardiac Allograft Vasculopathy-Results of a Randomized, Multicenter Trial2011In: Transplantation, ISSN 0041-1337, E-ISSN 1534-6080, Vol. 92, no 2, p. 235-243Article in journal (Refereed)
    Abstract [en]

    Background. Everolimus reduces the progression of cardiac allograft vasculopathy (CAV) in de novo heart transplant (HTx) recipients, but the influence on established CAV is unknown. Methods. In this Nordic Certican Trial in Heart and lung Transplantation substudy, 111 maintenance HTx recipients (time post-HTx 5.8 +/- 4.3 years) randomized to everolimus+reduced calcineurin inhibitor (CNI) or standard CNI had matching (intravascular ultrasound) examinations at baseline and 12 months allowing accurate assessment of CAV progression. Results. No significant difference in CAV progression was evident between the treatment groups (P=0.30). When considering patients receiving concomitant azathioprine (AZA) therapy (n=39), CAV progression was attenuated with everolimus versus standard CNI (Delta maximal intimal thickness 0.00 +/- 0.04 and 0.04 +/- 0.04 mm, Delta percent atheroma volume 0.2%+/- 3.0% and 2.6%+/- 2.5%, and Delta total atheroma volume 0.25 +/- 14.1 and 19.8 +/- 20.4 mm(3), respectively [Pless than0.05]). When considering patients receiving mycophenolate mofetil (MMF), accelerated CAV progression occurred with everolimus versus standard CNI (Delta maximal intimal thickness 0.06 +/- 0.12 vs. 0.02 +/- 0.06 mm and Delta percent atheroma volume 4.0%+/- 6.3% vs. 1.4%+/- 3.1%, respectively; Pless than0.05). The levels of C-reactive protein and vascular cell adhesion molecule-1 declined significantly with AZA+everolimus, whereas MMF+everolimus patients demonstrated a significant increase in levels of C-reactive protein, vascular cell adhesion molecule-1, and von Willebrand factor. Conclusions. Conversion to everolimus and reduced CNI does not influence CAV progression among maintenance HTx recipients. However, background immunosuppressive therapy is important as AZA+everolimus patients demonstrated attenuated CAV progression and a decline in inflammatory markers, whereas the opposite pattern was seen with everolimus +MMF. The different effect of everolimus when combined with AZA versus MMF could potentially reflect hitherto unknown interactions.

  • 2.
    Fellstrom, B.
    et al.
    Fellström, B., University Hospital, Uppsala, Sweden, Department of Medical Science, Renal Unit, University Hospital, Uppsala, Sweden.
    Holdaas, H.
    Rikshospitalet, Oslo, Norway.
    Jardine, A.G.
    University of Glasgow, Glasgow, United Kingdom.
    Nyberg, G.
    Sahlgrenska University Hospital, Göteborg, Sweden.
    Gronhagen-Riska, C.
    Grönhagen-Riska, C., University Hospital, Helsinki, Finland.
    Madsen, S.
    Skejby Hospital, Aarhus, Denmark.
    Neumayer, H.-H.
    Univ. Klin. Charité, Berlin, Germany.
    Cole, E.
    Toronto General Hospital, Toronto, Ont., Canada.
    Maes, B.
    University Hospital, Leuven, Belgium.
    Ambuhl, P.
    Ambühl, P., University Hospital, Zürich, Switzerland.
    Olsson, Anders
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Health Sciences, Internal Medicine . Östergötlands Läns Landsting, Centre for Medicine, Department of Endocrinology and Gastroenterology UHL.
    Staffler, B.
    Novartis, Basel, Switzerland.
    Pedersen, T.R.
    Preventive Medicine Clinic, Ullevaal University Hospital, Oslo, Norway.
    Risk factors for reaching renal endpoints in the Assessment of Lescol in Renal Transplantation (ALERT) trial2005In: Transplantation, ISSN 0041-1337, E-ISSN 1534-6080, Vol. 79, no 2, p. 205-212Article in journal (Refereed)
    Abstract [en]

    Background. The aim of the study was to identity risk factors for long-term renal transplant function and development of chronic allograft nephropathy (CAN) in renal transplant recipients included in the Assessment of Lescol in Renal Transplantation (ALERT) trial. Methods. The ALERT trial was a randomized, double-blind, placebo-controlled study of the effect of fluvastatin, 40 and 80 mg/day, in renal transplant recipients who were randomized to receive fluvastatin (Lescol) (n=1,050) or placebo (n=1,052) over 5 to 6 years of follow-up. Renal endpoints including graft loss or doubling of serum creatinine or death were analyzed by univariate and multivariate regression analysis in the placebo group. Results. There were 137 graft losses (13.5%) in the placebo group, mainly caused by CAN (82%). Univariate risk factors for graft loss or doubling of serum creatinine were as follows: serum creatinine, proteinuria, hypertension, pulse pressure, time since transplantation, donor age, human leukocyte antigen-DR mismatches, treatment for rejection, low high-density lipoprotein cholesterol, and smoking. Multivariate analysis revealed independent risk factors for graft loss as follows: serum creatinine (relative risk [RR], 3.12 per 100-µM increase), proteinuria (RR, 1.64 per 1-g/24 hr increase), and pulse pressure (RR, 1.12 per 10 mm Hg), whereas age was a protective factor. With patient death in the composite endpoint, diabetes mellitus, smoking, age, and number of transplantations were also risk factors. Conclusions. Independent risk factors for graft loss or doubling of serum creatinine or patient death are mainly related to renal transplant function, proteinuria, and blood pressure, which emphasizes the importance of renoprotective treatment regimens in this population.

  • 3.
    Gullestad, Lars
    et al.
    University of Oslo.
    Iversen, Martin
    Rigshospital, Copenhagen.
    Mortensen, Svend-Aage
    University of Oslo.
    Eiskjaer, Hans
    Aarhus University Hospital.
    C. Riise, Gerdt
    Sahlgrens University Hospital.
    Mared, Lena
    Lund University Hospital.
    Bjortuft, Oystein
    University of Oslo.
    Ekmehag, Bjorn
    Lund University Hospital.
    Jansson, Kjell
    Linköping University, Department of Medicine and Health Sciences, Cardiology . Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Heart Centre, Department of Cardiology.
    Simonsen, Svein
    University of Oslo.
    Gude, Einar
    University of Oslo.
    Rundqvist, Bengt
    University of Gothenburg.
    E. Fagertun, Hans
    Capturo AS Stat Kjeller.
    Solbu, Dag
    Novartis Norge AS.
    Bergh, Claes-Hakan
    University of Gothenburg.
    Everolimus With Reduced Calcineurin Inhibitor in Thoracic Transplant Recipients With Renal Dysfunction: A Multicenter, Randomized Trial2010In: Transplantation, ISSN 0041-1337, E-ISSN 1534-6080, Vol. 89, no 7, p. 864-872Article in journal (Refereed)
    Abstract [en]

    Background. The proliferation signal inhibitor everolimus offers the potential to reduce calcineurin inhibitor (CNI) exposure and alleviate CNI-related nephrotoxicity. Randomized trials in maintenance thoracic transplant patients are lacking. Methods. In a 12-month, open-labeled, multicenter study, maintenance thoracic transplant patients (glomerular filtration rate greater than= 20 mL/min/1.73m(2) and less than90 mL/min/1.73 m(2)) greater than1 year posttransplant were randomized to continue their current CNI-based immunosuppression or start everolimus with predefined CNI exposure reduction. Results. Two hundred eighty-two patients were randomized (140 everolimus, 142 controls; 190 heart, 92 lung transplants). From baseline to month 12, mean cyclosporine and tacrolimus trough levels in the everolimus cohort decreased by 57% and 56%, respectively. The primary endpoint, mean change in measured glomerular filtration rate from baseline to month 12, was 4.6 mL/min with everolimus and -0.5 mL/min in controls (Pless than0.0001). Everolimus-treated heart and lung transplant patients in the lowest tertile for time posttransplant exhibited mean increases of 7.8 mL/min and 4.9 mL/min, respectively. Biopsy-proven treated acute rejection occurred in six everolimus and four control heart transplant patients (P=0.54). In total, 138 everolimus patients (98.6%) and 127 control patients (89.4%) experienced one or more adverse event (P=0.002). Serious adverse events occurred in 66 everolimus patients (46.8%) and 44 controls (31.0%) (P=0.02). Conclusion. Introduction of everolimus with CNI reduction offers a significant improvement in renal function in maintenance heart and lung transplant recipients. The greatest benefit is observed in patients with a shorter time since transplantation.

  • 4.
    Olsson, Anders
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Internal Medicine. Östergötlands Läns Landsting, Centre for Medicine, Department of Endocrinology and Gastroenterology UHL.
    Risk factors for reaching renal endpoints in the assessment of lescol in renal transplantation (ALERT) trial2005In: Transplantation, ISSN 0041-1337, E-ISSN 1534-6080, Vol. 792, p. 205-212Article in journal (Refereed)
  • 5.
    Pippias, Maria
    et al.
    University of Amsterdam, Netherlands.
    Stel, Vianda S.
    University of Amsterdam, Netherlands.
    Areste-Fosalba, Nuria
    University Hospital Virgen Macarena, Spain.
    Couchoud, Cecile
    Agence Biomed, France.
    Fernandez-Fresnedo, Gema
    University Hospital Marques de Valdecilla, Spain.
    Finne, Patrik
    University of Helsinki, Finland; Finnish Registry Kidney Disease, Finland.
    Heaf, James G.
    University of Copenhagen, Denmark.
    Hoitsma, Andries
    Radboud University of Nijmegen, Netherlands.
    De Meester, Johan
    Dutch Speaking Belgian Renal Registry NBVN, Belgium.
    Palsson, Runolfur
    Landspitali, Iceland; Fac Med, Iceland; University of Iceland, Iceland.
    Ravani, Pietro
    University of Calgary, Canada; University of Calgary, Canada.
    Segelmark, Mårten
    Linköping University, Department of Medical and Health Sciences, Division of Drug Research. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Heart and Medicine Center, Department of Nephrology.
    Traynor, Jamie P.
    Meridian Court, Scotland.
    Reisaeter, Anna V.
    National Hospital Norway, Norway.
    Caskey, Fergus J.
    Southmead Hospital, England; University of Bristol, England.
    Jager, Kitty J.
    University of Amsterdam, Netherlands.
    Long-term Kidney Transplant Outcomes in Primary Glomerulonephritis: Analysis From the ERA-EDTA Registry2016In: Transplantation, ISSN 0041-1337, E-ISSN 1534-6080, Vol. 100, no 9, p. 1955-1962Article in journal (Refereed)
    Abstract [en]

    Background We evaluated the 15-year kidney allograft survival in patients with primary glomerulonephritis and determined if the risk of graft loss varied with donor source within each glomerulonephritis group. Methods Using data from the European Renal Association-European Dialysis and Transplant Association Registry, Kaplan-Meier, competing risk, and Cox regression analyses were performed on adult, first kidney transplant recipients during 1991 to 2010 (n = 14 383). Follow-up was set to December 31, 2011. Adjustments for pretransplant dialysis duration, sex, country, and transplant era were made. Death-adjusted graft survival was assessed in patients with glomerulonephritis and compared with those with autosomal dominant polycystic kidney disease (ADPKD), in which the native kidney disease cannot recur. Additionally, death-adjusted graft survival was compared between living and deceased donor transplants within each glomerulonephritis group. Results All glomerulonephritides had a 15-year death-adjusted graft survival probability above 55%. The 15-year risk of death-adjusted graft failure compared to ADPKD ranged from 1.17 (95% confidence interval [95% CI], 1.05-1.31) for immunoglobulin A nephropathy to 2.09 (95% CI, 1.56-2.78) for membranoproliferative glomerulonephritis type II. The expected survival benefits of living over deceased donor transplants were not present in membranoproliferative glomerulonephritis type I (adjusted hazard ratios [HRa], 1.08; 95% CI, 0.73-1.60) or type II (HRa, 0.90; 95% CI, 0.32-2.52) but present in immunoglobulin A nephropathy (HRa, 0.74; 95% CI, 0.59-0.92), membranous nephropathy (HRa, 0.47; 95% CI, 0.29-0.75), and focal segmental glomerulosclerosis (HRa, 0.69; 95% CI, 0.45-1.06). Conclusions This large European study shows favorable long-term kidney graft survival in all primary glomerulonephritides, although this remains lower than graft survival in ADPKD, and confirms that the reluctance to use living donors in some primary glomerulonephritides remains unfounded. These data will further inform prospective renal transplant recipients and donors during pretransplant counselling.

  • 6.
    Wahlberg Topp, Jeanette
    et al.
    Department of Medical Cell Biology, Uppsala University, Sweden.
    Korsgren, Olle
    Department of Medical Cell Biology, Uppsala University, Sweden..
    Welsh, Nils
    Department of Medical Cell Biology, Uppsala University, Sweden..
    Jansson, Leif
    Department of Medical Cell Biology, Uppsala University, Sweden..
    Evidence of a negative feedback system regulating the total beta-cell volume in nondiabetic rats that received pancreas transplants.1998In: Transplantation, ISSN 0041-1337, E-ISSN 1534-6080, Vol. 66, no 10, p. 1392-1394Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: The aim of the present study was to investigate the long-term regulation of pancreatic beta-cell volume after pancreas transplantation into adult rats.

    METHODS: A syngeneic pancreaticoduodenal transplantation was made in normoglycemic Wistar-Furth rats. By this means, the recipients doubled their pancreatic islet volume. Nine months after transplantation, the total beta-cell volume was measured in serial pancreatic sections immunostained for insulin from both the native and transplanted pancreata, and in the native pancreas of age-matched Wistar-Furth rats that did not receive transplants.

    RESULTS: No changes in the volume of individual beta-cells were seen. A 50% decrease in total beta-cell volume was observed in both the native and transplanted pancreas when compared with that of age-matched controls. However, the combined beta-cell volumes of the native and transplanted pancreas in the rats that received transplants were similar to those of the native pancreas in control animals. No signs of increased apoptosis in any of the glands could be seen during the first postoperative week or after 9 months.

    CONCLUSIONS: These findings provide evidence of a negative feedback system, which regulates the total beta-cell volume to the levels seen in age-matched rats that did not receive transplants. The underlying mechanisms for the decreased beta-cell volume are unknown, but may involve a diminished replicatory rate of the beta-cells.

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