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Träfflista för sökning "WFRF:(Svensson My) srt2:(2010-2014)"

Sökning: WFRF:(Svensson My) > (2010-2014)

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1.
  • Assenova, Daniela, et al. (författare)
  • Bibliography for 2008
  • 2010
  • Ingår i: Slovo. - 0348-744X .- 2001-7359. ; 50, s. 157-160
  • Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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2.
  • Assenova, Daniela, et al. (författare)
  • Bibliography for 2009
  • 2010
  • Ingår i: Slovo. - 0348-744X .- 2001-7359. ; 50, s. 161-165
  • Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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3.
  • Schjelderup, Patrick, et al. (författare)
  • Anemia is a predictor of graft loss but not cardiovascular events and all-cause mortality in renal transplant recipients : follow-up data from the ALERT study
  • 2013
  • Ingår i: Clinical Transplantation. - : Wiley. - 0902-0063 .- 1399-0012. ; 27:6, s. E636-E643
  • Tidskriftsartikel (refereegranskat)abstract
    • BackgroundIt is well established that post-transplantation anemia (PTA) in renal transplant recipients (RTRs) is associated with reduced graft survival. However, there is an uncertainty of the effect of PTA on cardiovascular events and all-cause mortality. We examined prospectively in a large cohort of erythropoietin-naive patients the effects of PTA on cardiovascular morbidity, patient survival, and graft survival. MethodsA prospective cohort study of RTRs (n=2102) included in the ALERT study. Cox regression models were used to evaluate the impact of PTA on study endpoints: first occurrence of a major adverse cardiac event, all-cause death, and the incidence of death-censored graft loss. Mean follow-up was 6.7yr. All endpoints were adjudicated by an independent endpoint committee. ResultsTwenty-nine percent of women and 30% of men were anemic. Hemoglobin levels were not associated with any effect on cardiovascular morbidity and mortality (HR 0.97 [0.90-1.05] per g/dL, p=0.48) or all-cause death (HR 0.96 [0.90-1.03] per g/dL, p=0.24) after extensive multivariate adjustments for clinical and demographic factors. Hemoglobin levels were negatively associated with graft loss (HR 0.86 [0.80-0.92] per g/dL, p<0.001). ConclusionsPTA was not associated with an increased incidence of cardiovascular morbidity and mortality or all-cause mortality.
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6.
  • Stenvinkel, Peter, et al. (författare)
  • Metabolic Changes in Summer Active and Anuric Hibernating Free-Ranging Brown Bears (Ursus arctos)
  • 2013
  • Ingår i: PloS one. - : Public Library of Science (PLoS). - 1932-6203. ; 8:9, s. e72934-
  • Tidskriftsartikel (refereegranskat)abstract
    • The brown bear (Ursus arctos) hibernates for 5 to 6 months each winter and during this time ingests no food or water and remains anuric and inactive. Despite these extreme conditions, bears do not develop azotemia and preserve their muscle and bone strength. To date most renal studies have been limited to small numbers of bears, often in captive environments. Sixteen free-ranging bears were darted and had blood drawn both during hibernation in winter and summer. Samples were collected for measurement of creatinine and urea, markers of inflammation, the calcium-phosphate axis, and nutritional parameters including amino acids. In winter the bear serum creatinine increased 2.5 fold despite a 2-fold decrease in urea, indicating a remarkable ability to recycle urea nitrogen during hibernation. During hibernation serum calcium remained constant despite a decrease in serum phosphate and a rise in FGF23 levels. Despite prolonged inactivity and reduced renal function, inflammation does not ensue and bears seem to have enhanced antioxidant defense mechanisms during hibernation. Nutrition parameters showed high fat stores, preserved amino acids and mild hyperglycemia during hibernation. While total, essential, non-essential and branched chain amino acids concentrations do not change during hibernation anorexia, changes in individual amino acids ornithine, citrulline and arginine indicate an active, although reduced urea cycle and nitrogen recycling to proteins. Serum uric acid and serum fructose levels were elevated in summer and changes between seasons were positively correlated. Further studies to understand how bears can prevent the development of uremia despite minimal renal function during hibernation could provide new therapeutic avenues for the treatment of human kidney disease.
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8.
  • Svensson, My (författare)
  • News from Uppsala
  • 2012
  • Ingår i: Slovo. - 0348-744X .- 2001-7359. ; :53, s. 127-133
  • Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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9.
  • Svensson, My, et al. (författare)
  • Osteoprotegerin as a predictor of renal and cardiovascular outcomes in renal transplant recipients : follow-up data from the ALERT study
  • 2012
  • Ingår i: Nephrology, Dialysis and Transplantation. - : Oxford University Press (OUP). - 0931-0509 .- 1460-2385. ; 27:6, s. 2571-2575
  • Tidskriftsartikel (refereegranskat)abstract
    • Background. In patients with chronic kidney disease, vascular calcification contributes to increased cardiovascular (CV) morbidity and mortality. CV risk remains high after successful renal transplantation. Osteoprotegerin (OPG) is a glycoprotein, involved in the regulation of the vascular calcification process. Previous studies have shown that elevated OPG is predictive of mortality in high-risk populations. The aim of this study was to investigate the prognostic value of OPG for graft function, CV events and all-cause death, in a large transplant cohort.Methods. OPG was measured at baseline in renal transplant recipients enrolled in the Assessment of Lescol in Renal Transplantation (ALERT) study, a randomized placebo-controlled intervention study comparing fluvastatin and placebo. Patients were followed for 6.7 years with evaluation of pre-specified end points, graft loss, graft function, CV events and death.Results. OPG was analysed in 1889 renal transplant recipients, with a mean value of 4.69 +/- 1.85 pg/L. The number of renal and CV events increased by quartiles of OPG. In the multivariate analysis, OPG in the fourth as compared to first quartile was an independent predictor of graft failure or doubling of serum creatinine [hazard ratio (HR) 2.20 (1.56-3.11), P < 0.001], major CV events [HR 2.40 (1.58-3.64), P < 0.001], cardiac mortality [HR 2.80 (1.32-5.94), P = 0.007] and all-cause mortality [HR 2.31 (1.53-3.49), P < 0.001].Conclusion. In a large cohort of kidney transplant patients with long-term follow-up, OPG was independently associated with renal events, CV events and mortality.
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10.
  • Svensson, My, et al. (författare)
  • Prevention of cardiovascular disease after renal transplantation
  • 2012
  • Ingår i: Current Opinion in Organ Transplantation. - 1087-2418 .- 1531-7013. ; 17:4, s. 393-400
  • Forskningsöversikt (refereegranskat)abstract
    • Purpose of review After renal transplantation, cardiovascular disease (CVD) is the leading cause of death with a functioning graft. Guidelines for prevention of CVD are mainly based on data from the general population. The purpose of this review is to give a practical approach on prevention of CVD in renal transplant recipients.Recent findings New epidemiological data have shown that in addition to traditional risk factors for CVD, other risk factors may influence cardiovascular risk in renal transplant recipients. Recently, a specific risk calculator for CVD in renal transplant recipients has been developed. Prevention of CVD in renal transplant recipients should include lifestyle modifications, such as prevention of overweight, smoking cessation and physical exercise. Optimal treatment of hypertension, lipid disturbances and posttransplant diabetes should be encouraged. Accumulating evidence indicates that declining graft function and graft loss are potentially modifiable risk factors in this population, which make strategies for preserving graft function important. This situation may include individual tailoring of immunosuppression and use of new immunosuppressive medications with a more favorable effect on cardiovascular risk factors and graft function.Summary To prevent CVD in renal transplant recipients, cardiovascular risk assessment should be performed regularly. Prevention should include both lifestyle modifications, optimal treatment of cardiovascular risk factors and strategies to preserve graft function.
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