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- Bárány, P, et al.
(författare)
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Muscle Abnormalities with Kidney Failure
- 2021
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Ingår i: Clinical journal of the American Society of Nephrology : CJASN. - 1555-905X. ; 16:11, s. 1613-1614
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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- Dai, L, et al.
(författare)
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Functional vitamin K insufficiency, vascular calcification and mortality in advanced chronic kidney disease: A cohort study
- 2021
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Ingår i: PloS one. - : Public Library of Science (PLoS). - 1932-6203. ; 16:2, s. e0247623-
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Tidskriftsartikel (refereegranskat)abstract
- Patients with chronic kidney disease (CKD) suffer from vitamin K deficiency and are at high risk of vascular calcification (VC) and premature death. We investigated the association of functional vitamin K deficiency with all-cause mortality and whether this association is modified by the presence of VC in CKD stage 5 (CKD G5). Plasma dephosphorylated-uncarboxylated matrix Gla-protein (dp-ucMGP), a circulating marker of functional vitamin K deficiency, and other laboratory and clinical data were determined in 493 CKD G5 patients. VC was assessed in subgroups by Agatston scoring of coronary artery calcium (CAC) and aortic valve calcium (AVC). Backward stepwise regression did not identify dp-ucMGP as an independent determinant of VC. During a median follow-up of 42 months, 93 patients died. Each one standard deviation increment in dp-ucMGP was associated with increased risk of all-cause mortality (sub-hazard ratio (sHR) 1.17; 95% confidence interval, 1.01–1.37) adjusted for age, sex, cardiovascular disease, diabetes, body mass index, inflammation, and dialysis treatment. The association remained significant when further adjusted for CAC and AVC in sub-analyses (sHR 1.22, 1.01–1.48 and 1.27, 1.01–1.60, respectively). In conclusion, functional vitamin K deficiency associates with increased mortality risk that is independent of the presence of VC in patients with CKD G5.
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- Levin, A., et al.
(författare)
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Novel insights into the disease transcriptome of human diabetic glomeruli and tubulointerstitium
- 2020
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Ingår i: Nephrology Dialysis Transplantation. - : Oxford University Press (OUP). - 0931-0509 .- 1460-2385. ; 35:12, s. 2059-2072
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Tidskriftsartikel (refereegranskat)abstract
- Background. Diabetic nephropathy (DN) is the most common cause of end-stage renal disease, affecting similar to 30% of the rapidly growing diabetic population, and strongly associated with cardiovascular risk. Despite this, the molecular mechanisms of disease remain unknown. Methods. RNA sequencing (RNAseq) was performed on paired, micro-dissected glomerular and tubulointerstitial tissue from patients diagnosed with DN [n = 19, 15 males, median (range) age: 61 (30-85) years, chronic kidney disease stages 1-4] and living kidney donors [n = 20, 12 males, median (range) age: 56 (30-70) years]. Results. Principal component analysis showed a clear separation between glomeruli and tubulointerstitium transcriptomes. Differential expression analysis identified 1550 and 4530 differentially expressed genes, respectively (adjusted P < 0.01). Gene ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses highlighted activation of inflammation and extracellular matrix (ECM) organization pathways in glomeruli, and immune and apoptosis pathways in tubulointerstitium of DN patients. Specific gene modules were associated with renal function in weighted gene co-expression network analysis. Increased messengerRNA (mRNA) expression of renal damage markers lipocalin 2 (LCN) and hepatitis A virus cellular receptor1 (HAVCR1) in the tubulointerstitial fraction was observed alongside higher urinary concentrations of the corresponding proteins neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule-1 (KIM-1) in DN patients. Conclusions. Here we present the first RNAseq experiment performed on paired glomerular and tubulointerstitial samples from DN patients. We show that prominent disease-specific changes occur in both compartments, including relevant cellular processes such as reorganization of ECM and inflammation (glomeruli) as well as apoptosis (tubulointerstitium). The results emphasize the potential of utilizing high-throughput transcriptomics to decipher disease pathways and treatment targets in this high-risk patient population.
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- Mukai, H, et al.
(författare)
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Lung Dysfunction and Mortality in Patients with Chronic Kidney Disease
- 2018
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Ingår i: Kidney & blood pressure research. - : S. Karger AG. - 1423-0143 .- 1420-4096. ; 43:2, s. 522-535
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Tidskriftsartikel (refereegranskat)abstract
- <b><i>Background/Aims:</i></b> Lung dysfunction associates with increased mortality but the impact of chronic kidney disease (CKD) is less clear. We evaluated lung function and its association with mortality among individuals with normal to severely reduced glomerular filtration rate (GFR). <b><i>Methods:</i></b> 404 individuals representing GFR category G1 (n=31; GFR >90 mL/min/1.73 m<sup>2</sup>), G2 (n=46), G3 (n=33), G4 (n=49) and G5 (n=245; GFR< 15 mL/min/1.73 m<sup>2</sup>) underwent spirometry yielding lung function indices forced vital capacity (FVC), forced expiratory volume in the first second (FEV<sub>1</sub>) and peak expiratory flow (PEF). Associations of lung function indices expressed as percentages of predicted values (%FEV<sub>1</sub>, %FVC and %PEF) with 5-year mortality were analyzed by competing-risk regression models. <b><i>Results:</i></b> The prevalence of obstructive (6% in G1 and 11% in G5) and especially restrictive (9% in G1 to 36% in G5) lung dysfunction increased with declining GFR and with higher comorbidity burden. In patients (n=22) with protein-energy wasting, inflammation and cardiovascular disease, the prevalence of restrictive lung function was 64%. The highest tertiles of % FEV<sub>1</sub> and %FVC associated with lower sub-hazard ratios (sHR) for all-cause mortality, 0.49 (95% CI, 0.27-0.88)) and 0.56 (95% CI, 0.32-0.98), and that of %FEV<sub>1</sub> also with lower cardiovascular mortality risk (sHR 0.16; 95%CI 0.04-0.69) after adjusting for multiple confounders. Restrictive lung dysfunction (FEV<sub>1</sub>/FVC ≥ 0.70, and %FVC < 80) associated with increased mortality risk (sHR 1.80, 95%CI, 1.04-3.13) while the association with obstructive lung impairment was not statistically significant. <b><i>Conclusion:</i></b> Lung dysfunction and in particular restrictive lung dysfunction associates with degree of renal function impairment and presence of comorbidities, and is an independent predictor of increased mortality in CKD patients.
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- Axelsson, J, et al.
(författare)
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Is fetuin-A/alpha2-Heremans-Schmid glycoprotein associated with the metabolic syndrome in patients with chronic kidney disease?
- 2008
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Ingår i: American journal of nephrology. - : S. Karger AG. - 1421-9670 .- 0250-8095. ; 28:4, s. 669-676
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Tidskriftsartikel (refereegranskat)abstract
- <i>Introduction:</i> Components of the metabolic syndrome are highly prevalent in chronic kidney disease (CKD) patients – some of which paradoxically appear to predict an improved outcome in this population. We hypothesized that the circulating calcification inhibitor fetuin-A/AHSG, which is also a natural inhibitor of the tyrosine kinase insulin receptor, could be one factor explaining the association between increased fat mass and a survival advantage in CKD and thus conducted an explorational study to provide preliminary data to support further research into this hypothesis. <i>Patients and Methods:</i> In a cross-sectional study, we evaluated 198 CKD stage 5 patients (GFR 6.8 ± 0.2 ml/min; 62% males, mean age 52 ± 1 years) close to the start of renal replacement therapy. We studied circulating AHSG (ELISA) and two common functional <i>AHSG</i> gene polymorphisms (at amino acids Thr248Met (C-T) and Thr256Ser (C-G) using Pyrosequencing®) and related these to multiple components of the metabolic syndrome. <i>Results:</i> Median circulating AHSG was lower (p < 0.01) in type-2 (0.22 g/l) and type-1 (0.16 g/l) diabetics as compared to non-diabetic CKD-5 patients (0.24 g/l). AHSG correlated with both total and truncal fat mass in type-2 diabetics (rho 0.37 and 0.39; p < 0.001, respectively), but not in type-1 diabetics or non-diabetics. Both SNPs significantly influenced circulating levels of AHSG, and were also associated with significant differences in serum triglycerides and HDL cholesterol. Furthermore, there were significant differences in the prevalence of metabolic syndrome criteria between the <i>AHSG</i> Thr256Ser (C-G) genotype groups, with a more atherogenic lipid profile in AHSG high producers (Thr/Thr homozygotes). In multivariate analysis, the association between circulating AHSG and fat mass remained significant also after adjustment for age, gender, inflammation (CRP >10 mg/l), and <i>AHSG</i> genotype. <i>Conclusions:</i> The present, explorational, study supports further, mechanistic, studies into a physiological link between AHSG and body fat mass in patients with CKD. As we observed an association between higher fat mass and elevated AHSG levels, these preliminary results may form the basis of further study to establish if the observed associations may be one reason why obesity has been reported to constitute a survival advantage in CKD.
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- Axelsson, J, et al.
(författare)
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Serum leptin and epoetin sensitivity - Reply
- 2006
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Ingår i: AMERICAN JOURNAL OF KIDNEY DISEASES. - : Elsevier BV. - 0272-6386. ; 47:2, s. 372-372
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 44. |
- Axelsson, J, et al.
(författare)
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Serum retinol-binding protein concentration and its association with components of the uremic metabolic syndrome in nondiabetic patients with chronic kidney disease stage 5
- 2009
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Ingår i: American journal of nephrology. - : S. Karger AG. - 1421-9670 .- 0250-8095. ; 29:5, s. 447-53
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Tidskriftsartikel (refereegranskat)abstract
- <i>Introduction:</i> Chronic kidney disease (CKD) is associated with insulin resistance also in the absence of overt diabetes mellitus. The liver-derived transport protein retinol-binding protein (RBP) has recently been proposed as a novel adipokine involved in the metabolism of glucose. Although RBP is elevated in type 2 diabetics with mild CKD, its role in advanced CKD is not well studied. We hypothesized that altered RBP levels in CKD could be one factor contributing to the uremic insulin resistance. <i>Patients and Methods:</i> In a cross-sectional study, we evaluated 141 nondiabetic stage 5 CKD patients (GFR 6.8 ± 2.0 ml/min; 62% males, mean age 52 ± 11 years) close to the start of renal replacement therapy. We studied circulating RBP (RIA), retinol and metabolic markers. Body composition was also assessed using DEXA and patients were divided according to truncal fat mass above (obese) or below (lean) the sex-specific median. A fasting plasma glucose ≥6.1 m<i>M</i> was defined as impaired glucose tolerance (IGT). <i>Results:</i> Serum RBP levels were significantly elevated in CKD as compared to previous reports in non-renal patients. Whereas levels of RBP did not differ between lean and obese patients without IGT, they were lower in lean CKD patients with IGT (5.9 ± 2.9 μ<i>M</i>) than in obese CKD patients with IGT (7.0 ± 2.9 μ<i>M</i>; p < 0.05). While RBP did not correlate with truncal or total fat mass or biomarkers of inflammation, in univariate analysis, we found weak correlations with HbA1c% (rho = 0.17; p < 0.05), fasting serum triglycerides (rho = 0.20; p < 0.001) and fasting apolipoprotein (Apo) A1 (rho = 0.29; p < 0.001). RBP also correlated negatively with ApoB (rho = –0.29; p < 0.001). In multivariate analysis, RBP was a significant and independent predictor of both HbA1c% and ApoA1 levels. Finally, RBP was strongly correlated with serum retinol, and calculating a retinol/RBP index further strengthened the observed correlations with HOMA-IR and HbA1c%. <i>Conclusions:</i> RBP is elevated in nondiabetic stage 5 CKD and correlates weakly with HbA1c and ApoA1. As RBP is thought to induce insulin resistance and directly affect lipoprotein metabolism in other disease states, these findings may support a role for RBP in contributing to the uremic metabolic syndrome, putatively by altering ApoA1 metabolism, but further studies are needed to test this hypothesis.
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