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Träfflista för sökning "WFRF:(Nordin Anders) "

Sökning: WFRF:(Nordin Anders)

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1.
  • Grubb, Anders, et al. (författare)
  • Generation of a new cystatin C-based estimating equation for glomerular filtration rate by use of 7 assays standardized to the international calibrator
  • 2014
  • Ingår i: Clinical Chemistry. - : Oxford University Press (OUP). - 0009-9147 .- 1530-8561. ; 60:7, s. 974-986
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND:Many different cystatin C-based equations exist for estimating glomerular filtration rate. Major reasons for this are the previous lack of an international cystatin C calibrator and the nonequivalence of results from different cystatin C assays.METHODS:Use of the recently introduced certified reference material, ERM-DA471/IFCC, and further work to achieve high agreement and equivalence of 7 commercially available cystatin C assays allowed a substantial decrease of the CV of the assays, as defined by their performance in an external quality assessment for clinical laboratory investigations. By use of 2 of these assays and a population of 4690 subjects, with large subpopulations of children and Asian and Caucasian adults, with their GFR determined by either renal or plasma inulin clearance or plasma iohexol clearance, we attempted to produce a virtually assay-independent simple cystatin C-based equation for estimation of GFR.RESULTS:We developed a simple cystatin C-based equation for estimation of GFR comprising only 2 variables, cystatin C concentration and age. No terms for race and sex are required for optimal diagnostic performance. The equation, [Formula: see text] is also biologically oriented, with 1 term for the theoretical renal clearance of small molecules and 1 constant for extrarenal clearance of cystatin C.CONCLUSIONS:A virtually assay-independent simple cystatin C-based and biologically oriented equation for estimation of GFR, without terms for sex and race, was produced.
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2.
  • Malmgren, Linnea, et al. (författare)
  • The complexity of kidney disease and diagnosing it - Cystatin C, selective glomerular hypofiltration syndromes and proteome regulation.
  • 2023
  • Ingår i: Journal of Internal Medicine. - : John Wiley & Sons. - 0954-6820 .- 1365-2796. ; 293:3, s. 293-308
  • Tidskriftsartikel (refereegranskat)abstract
    • Estimation of kidney function is often part of daily clinical practice, mostly done by using the endogenous GFR-markers creatinine or cystatin C. A recommendation to use both markers in parallel in 2010 has resulted in new knowledge concerning the pathophysiology of kidney disorders by identification of a new set of kidney disorders, selective glomerular hypofiltration syndromes. These syndromes, connected to strong increases in mortality and morbidity, are characterised by a selective reduction in the glomerular filtration of 5-30 kDa molecules, such as cystatin C, compared to the filtration of small molecules < 1kDa dominating the glomerular filtrate e.g., water, urea, creatinine. At least two types of such disorders, shrunken or elongated pore syndrome, are possible according to the pore model for glomerular filtration. Selective glomerular hypofiltration syndromes are prevalent in investigated populations, and patients with these syndromes often display normal measured GFR or creatinine-based GFR-estimates. The syndromes are characterised by proteomic changes promoting the development of atherosclerosis, indicating antibodies and specific receptor-blocking substances as possible new treatment modalities. Presently, the KDIGO guidelines for diagnosing kidney disorders do not recommend cystatin C as a general marker of kidney function and will therefore not allow the identification of a considerable number of patients with selective glomerular hypofiltration syndromes. Furthermore, as cystatin C is uninfluenced by muscle mass, diet or variations in tubular secretion and cystatin C-based GFR-estimation equations do not require controversial race or sex terms, it is obvious that cystatin C should be a part of future KDIGO guidelines.
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3.
  • Akerstrom, Finn, et al. (författare)
  • Association between catheter ablation of atrial fibrillation and mortality or stroke
  • 2024
  • Ingår i: Heart. - : BMJ PUBLISHING GROUP. - 1355-6037 .- 1468-201X. ; 110, s. 163-169
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective Catheter ablation of atrial fibrillation effectively reduces symptomatic burden. However, its long-term effect on mortality and stroke is unclear. We investigated if patients with atrial fibrillation who undergo catheter ablation have lower risk for all-cause mortality or stroke than patients who are managed medically. Methods We retrospectively included 5628 consecutive patients who underwent first-time catheter ablation for atrial fibrillation between 2008 and 2018 at three major Swedish electrophysiology units. Control individuals with an atrial fibrillation diagnosis but without previous stroke were selected from the Swedish National Patient Register, resulting in a control group of 48 676 patients. Propensity score matching was performed to produce two cohorts of equal size (n=3955) with similar baseline characteristics. The primary endpoint was a composite of all-cause mortality or stroke. Results Patients who underwent catheter ablation were healthier (mean CHA(2)DS(2)-VASc score 1.4 +/- 1.4 vs 1.6 +/- 1.5, p<0.001), had a higher median income (288 vs 212 1000 Swedish krona [KSEK]/year, p<0.001) and had more frequently received university education (45.1% vs 28.9%, p<0.001). Mean follow-up was 4.5 +/- 2.8 years. After propensity score matching, catheter ablation was associated with lower risk for the combined primary endpoint (HR 0.58, 95% CI 0.48 to 0.69). The result was mainly driven by a decrease in all-cause mortality (HR 0.51, 95% CI 0.41 to 0.63), with stroke reduction showing a trend in favour of catheter ablation (HR 0.75, 95% CI 0.53 to 1.07). Conclusions Catheter ablation of atrial fibrillation was associated with a reduction in the primary endpoint of all-cause mortality or stroke. This result was driven by a marked reduction in all-cause mortality.
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  • Brus, Elisabet, et al. (författare)
  • Bed agglomeration characteristics of biomass fuels using blast-furnace slag as bed material
  • 2004
  • Ingår i: Energy & Fuels. - Washington, D.C. : American Chemical Society (ACS). - 0887-0624 .- 1520-5029. ; 18:4, s. 1187-1193
  • Tidskriftsartikel (refereegranskat)abstract
    • Agglomeration of bed material may cause severe operating problems during fluidized bed combustion. The attack or coating layers that are formed on the bed particles during combustion play an important role in the agglomeration process. To reduce bed agglomeration tendencies, alternative bed materials may be used. In this paper, bed agglomeration characteristics during the combustion of biomass fuels using a relatively new bed material (iron blast-furnace slag) as well as ordinary quartz sand were determined. Controlled agglomeration tests lasting 40 h, using five representative biomass fuels (bark, olive residue, peat, straw, and reed canary grass) were conducted in a bench-scale fluidized bed. The bed materials and agglomerates were analyzed using SEM/EDS and X-ray diffraction. Chemical equilibrium calculations were performed to interpret the experimental findings. The results showed that blast-furnace slag had a lower tendency to agglomerate than quartz sand for most of the fuels. The quartz particles showed an inner attack layer more often than did the blast-furnace slag. The blast-furnace slag had a lower tendency to react with elements from the fuel. The outer coating layer had similar characteristics and thickness for both bed materials when the same fuel was combusted. However, the inner attack layer thickness was larger for quartz particles. SEM/EDS analyses of the agglomerates showed that the inner Ca-K-silicate-rich attack layer was responsible for the agglomeration of quartz sand. The composition of blast-furnace slag agglomerate was similar to the outer coating layer. Chemical equilibrium calculations showed that the original composition of the blast-furnace slag was close to the equilibrium composition, and hence there was no major driving force for reactions between that bed material and K and Ca from the fuel. The homogeneous silica-rich attack layer (with a low melting temperature) was not formed to the same extent for blast-furnace slag, thus explaining the lower bed agglomeration tendency.
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9.
  • Delanaye, Pierre, et al. (författare)
  • CKD : A Call for an Age-Adapted Definition
  • 2019
  • Ingår i: Journal of the American Society of Nephrology. - 1046-6673. ; 30:10, s. 1785-1805
  • Forskningsöversikt (refereegranskat)abstract
    • Current criteria for the diagnosis of CKD in adults include persistent signs of kidney damage, such as increased urine albumin-to-creatinine ratio or a GFR below the threshold of 60 ml/min per 1.73 m2 This threshold has important caveats because it does not separate kidney disease from kidney aging, and therefore does not hold for all ages. In an extensive review of the literature, we found that GFR declines with healthy aging without any overt signs of compensation (such as elevated single-nephron GFR) or kidney damage. Older living kidney donors, who are carefully selected based on good health, have a lower predonation GFR compared with younger donors. Furthermore, the results from the large meta-analyses conducted by the CKD Prognosis Consortium and from numerous other studies indicate that the GFR threshold above which the risk of mortality is increased is not consistent across all ages. Among younger persons, mortality is increased at GFR <75 ml/min per 1.73 m2, whereas in elderly people it is increased at levels <45 ml/min per 1.73 m2 Therefore, we suggest that amending the CKD definition to include age-specific thresholds for GFR. The implications of an updated definition are far reaching. Having fewer healthy elderly individuals diagnosed with CKD could help reduce inappropriate care and its associated adverse effects. Global prevalence estimates for CKD would be substantially reduced. Also, using an age-specific threshold for younger persons might lead to earlier identification of CKD onset for such individuals, at a point when progressive kidney damage may still be preventable.
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