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67. Phenotypic features of vascular calcification in chronic kidney disease.

Author

Dai, L., Debowska, M., Lukaszuk, T., Bobrowski, L., Barany, P., Söderberg, M., Thiagarajan, D., Frostegård, J., Wennberg, L., Lindholm, B., Qureshi, A. R., Waniewski, J., and Stenvinkel, P.

Subjects
CHRONIC kidney failure, KIDNEY calcification, KIDNEY exchange, ABSOLUTE value, BONE metabolism, CHRONICALLY ill
Abstract

Background: Patients with chronic kidney disease stage 5 (CKD5) are predisposed to vascular calcification (VC), but the combined effect of factors associated with VC was sparsely investigated. We applied the relaxed linear separability (RLS) feature selection model to identify features that concomitantly associate with VC in CKD5 patients.Methods: Epigastric arteries collected during surgery from living donor kidney transplant recipients were examined to score the histological extent of medial VC. Sixty-two phenotypic features in 152 patients were entered into RLS model to differentiate between no-minimal VC (n = 93; score 0-1) and moderate-extensive VC (n = 59; score 2-3). The subset of features associated with VC was selected on the basis of cross-validation procedure. The strength of association of the selected features with VC was expressed by the absolute value of 'RLS factor'.Results: Among 62 features, a subset of 17 features provided optimal prediction of VC with 89% of patients correctly classified into their groups. The 17 features included traditional risk factors (diabetes, age, cholesterol, BMI and male sex) and markers of bone metabolism, endothelial function, metabolites, serum antibodies and mitochondrial-derived peptide. Positive RLS factors range from 1.26 to 4.05 indicating features associated with increased risk of VC, and negative RLS factors range from -0.95 to -1.83 indicating features associated with reduced risk of VC.Conclusion: The RLS model identified 17 features including novel biomarkers and traditional risk factors that together concomitantly associated with medial VC. These results may inform further investigations of factors promoting VC in CKD5 patients. [ABSTRACT FROM AUTHOR]

Published
2020
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74. The use of echocardiography in observational clinical trials: the EURECA-m registry

Author

Sicari, R, Gargani, L, Wiecek, A, Covic, A, Goldsmith, D, Suleymanlar, G, Ortiz, A, Massy, Z, Martinez Catelao, A, Lindholm, B, Heine, GH, Fliser, D, Mallamaci, F, London, G, Zoccali, C, EUropean Renal, Cardiovascular Medicine working group of the European Renal Association European Dialysis Transplantation Association, PARATI, GIANFRANCO, Sicari, R, Gargani, L, Wiecek, A, Covic, A, Goldsmith, D, Suleymanlar, G, Parati, G, Ortiz, A, Massy, Z, Martinez Catelao, A, Lindholm, B, Heine, G, Fliser, D, Mallamaci, F, London, G, Zoccali, C, European, R, and Cardiovascular Medicine working group of the European Renal Association European Dialysis Transplantation, A

Subjects
medicine.medical_specialty, Pathology, medicine.medical_treatment, Population, Disease, core lab, Renal Dialysis, medicine, Humans, Registries, Intensive care medicine, education, Dialysis, Protocol (science), Transplantation, education.field_of_study, Clinical Trials as Topic, business.industry, clinical trial, MED/11 - MALATTIE DELL'APPARATO CARDIOVASCOLARE, Clinical trial, Europe, Clinical research, Nephrology, Cardiovascular Diseases, Echocardiography, Kidney Failure, Chronic, Observational study, business
Abstract

Echocardiography is the most widely used non-invasive imaging technique due to its availability, low cost, transportability and lack of ionizing radiations. However, it suffers from the main limitation of being highly subjective and operator-dependent. Furthermore, specifically, population or disease-dependent issues exist which should be addressed when this technique is applied in multicenter studies. As to the population of patients with end-stage renal disease (ESRD) maintained on chronic dialysis, indexation of echocardiographic parameters and timing of echocardiography in relationship to dialysis represent a specific, main issue that needs to be carefully considered and standardized. Scientific societies recommend the set-up of core laboratories in order to reduce inter- and intra-observer variability when an echocardiographic parameter is considered as an end-point in clinical research. Several studies have shown the superiority of interpretation given by echocardiography core-lab reading. These advantages are counterbalanced by higher costs and complexity. The EURECA-m registry by the EURECA-m working group, an ERA-EDTA initiative, aimed at promoting the scientific collaboration among professionals in the field of cardiovascular and renal medicine. The registry involves several centers in Europe and one of its aims is to measure conventional echocardiographic parameters in ESRD patients on chronic dialysis. A central reading protocol has been set up for the registry in order to give robustness to the echo studies.

Published
2012

75. Excess protein intake relative to fiber and cardiovascular events in elderly men with chronic kidney disease

Author

Xu, H., Rossi, M., Campbell, K. L., Sencion, G. L., Ärnlöv, Johan, Cederholm, Tommy, Sjögren, Per, Riserus, Ulf, Lindholm, B., Carrero, J. J., Xu, H., Rossi, M., Campbell, K. L., Sencion, G. L., Ärnlöv, Johan, Cederholm, Tommy, Sjögren, Per, Riserus, Ulf, Lindholm, B., and Carrero, J. J.

Abstract

Background and aims: The elevated cardiovascular (CVD) risk observed in chronic kidney disease (CKD) may be partially alleviated through diet. While protein intake may link to CVD events in this patient population, dietary fiber has shown cardioprotective associations. Nutrients are not consumed in isolation; we hypothesize that CVD events in CKD may be associated with dietary patterns aligned with an excess of dietary protein relative to fiber. Methods and Results: Prospective cohort study from the Uppsala Longitudinal Study of Adult Men. Included were 390 elderly men aged 70-71 years with CKD and without clinical history of CVD. Protein and fiber intake, as well as its ratio, were calculated from 7-day dietary records. Cardiovascular events were registered prospectively during a median follow-up of 9.1 (inter-quartile range, 4.5-10.7) years. The median dietary intake of protein and fiber was 66.7 (60.7-71.1) and 16.6 (14.5-19.1) g/day respectively and the protein-to-fiber intake ratio was 4.0 (3.5-4.7). Protein-to-fiber intake ratio was directly associated with serum C-reactive protein levels. During follow-up, 164 first-time CVD events occurred (incidence rate 54.5/1000 per year). Protein-fiber intake ratio was an independent risk factor for CVD events [adjusted hazard ratio, HR per standard deviation increase (95% confidence interval, CI) 1.33 (1.08, 1.64)]. Although in opposing directions, dietary protein [1.18 (0.97, 1.44)], dietary fiber alone [0.81 (0.64, 1.02)], were not significantly associated with CVD events. Conclusions: An excess of dietary protein relative to fiber intake was associated with the incidence of cardiovascular events in a homogeneous population of older men with CKD.

Published
2016
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76. Lipophilic index, kidney function, and kidney function decline

Author

Xu, H., Ärnlöv, Johan, Sandhagen, Bo, Risérus, Ulf, Lindholm, B., Lind, Lars, Carrero, J. J., Xu, H., Ärnlöv, Johan, Sandhagen, Bo, Risérus, Ulf, Lindholm, B., Lind, Lars, and Carrero, J. J.

Abstract

Background and aims: Unhealthy dietary fats are associated with faster kidney function decline. The cell membrane composition of phospholipid fatty acids (FAs) is a determinant of membrane fluidity and rheological properties. These properties, which have been linked to kidney damage, are thought to be reflected by the lipophilic index (LI). We prospectively investigated the associations of LI with kidney function and its decline. Methods and results: Observational study from the Prospective Investigation of Vasculature in Uppsala Seniors including 975 men and women with plasma phospholipid FAs composition and cystatin-C estimate glomerular filtration rate (eGFR). Of these, 780 attended reexamination after 5 years, and eGFR changes were assessed. Participants with a 5-year eGFR reduction >= 30% were considered chronic kidney disease (CKD) progressors (n = 198). LI was calculated as the sum of the products of the FA proportions with the respective FAs melting points. Blood rheology/viscosity measurements were performed in a random subsample of 559 subjects at baseline. Increased LI showed a statistically significant but overall weak association with blood, plasma viscosity (both Spearman rho = 0.16, p < 0.01), and erythrocyte deformability (rho = -0.09, p < 0.05). In cross-sectional analyses, LI associated with lower eGFR (regression coefficient 3.00 ml/min/1.73 m(2) 1-standard deviation (SD) increment in LI, 95% CI: -4.31, -1.69, p < 0.001). In longitudinal analyses, LI associated with a faster eGFR decline (-2.13 [95% CI -3.58, -0.69] ml/min/1.73 m(2), p < 0.01) and with 32% increased odds of CKD progression (adjusted OR 1.32 [95%, CI 1.05-1.65]). Conclusions: A high LI was associated with lower kidney function, kidney function decline, and CKD progression.

Published
2016
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77. Increased lipoprotein binding to arterial proteoglycans and normal macrophage cholesterol efflux capacity define the pro-atherogenic feature of CKD dyslipidemia

Author

Pedrelli, M., primary, Stenvinkel, P., additional, Minniti, M.E., additional, Emma, K., additional, Dikkers, A., additional, Ebtehaj, S., additional, Gomaraschi, M., additional, Barany, P., additional, Qureshi, A.R., additional, Camejo, G., additional, Lindholm, B., additional, Öörni, K., additional, Tietge, U., additional, Calabresi, L., additional, Hurt-Camejo, E., additional, and Parini, P., additional

Published
2016
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79. Dietary acid load, kidney function, osteoporosis, and risk of fractures in elderly men and women

Author

Jia, T, Byberg, Liisa, Lindholm, B, Larsson, T E, Lind, Lars, Michaëlsson, Karl, Carrero, J J, Jia, T, Byberg, Liisa, Lindholm, B, Larsson, T E, Lind, Lars, Michaëlsson, Karl, and Carrero, J J

Abstract

Because kidney dysfunction reduces the ability to excrete dietary acid excess, we hypothesized that underlying kidney function may have confounded the mixed studies linking dietary acid load with the risk of osteoporosis and fractures in the community. In a relatively large survey of elderly men and women, we report that dietary acid load did neither associate with DEXA-estimated bone mineral density nor with fracture risk. Underlying kidney function did not modify these null findings. Our results do not support the dietary acid-base hypothesis of bone loss. INTRODUCTION: Impaired renal function reduces the ability to excrete dietary acid excess. We here investigate the association between dietary acid load and bone mineral density (BMD), osteoporosis, and fracture risk by renal function status. METHODS: An observational study was conducted in 861 community-dwelling 70-year-old men and women (49 % men) with complete dietary data from the Prospective Investigation of the Vasculature in Uppsala Seniors (PIVUS). The exposure was dietary acid load as estimated from 7-day food records by the net endogenous acid production (NEAP) and potential renal acid load (PRAL) algorithms. Renal function assessed by cystatin C estimated glomerular filtration rate was reduced in 21 % of the individuals. Study outcomes were BMD and osteoporosis state (assessed by DEXA) and time to fracture (median follow-up of 9.2 years). RESULTS: In cross-section, dietary acid load had no significant associations with BMD or with the diagnosis of osteoporosis. During follow-up, 131 fractures were validated. Neither NEAP (adjusted hazard ratios (HR) (95 % confidence interval (CI)), 1.01 (0.85-1.21), per 1 SD increment) nor PRAL (adjusted HR (95 % CI), 1.07 (0.88-1.30), per 1 SD increment) associated with fracture risk. Further multivariate adjustment for kidney function or stratification by the presence of kidney disease did not modify these null associations. CONCLUSIONS: The hypothesis that dietary a

Published
2015
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80. Genetic fine mapping and genomic annotation defines causal mechanisms at type 2 diabetes susceptibility loci

Author

Gaulton, K. (Kyle), Ferreira, T. (Teresa), Lee, Y. (Yeji), Raimondo, A. (Anne), Mägi, R. (Reedik), Reschen, M.E. (Michael E.), Mahajan, A. (Anubha), Locke, A. (Adam), Rayner, N.W. (Nigel William), Robertson, N.R. (Neil), Scott, R.A. (Robert), Prokopenko, I. (Inga), Scott, L.J. (Laura), Green, T. (Todd), Sparsø, T. (Thomas), Thuillier, D. (Dorothee), Yengo, L. (Loic), Grallert, H. (Harald), Wahl, S. (Simone), Frånberg, M. (Mattias), Strawbridge, R.J. (Rona), Kestler, H. (Hans), Chheda, H. (Himanshu), Eisele, L. (Lewin), Gustafsson, S. (Stefan), Steinthorsdottir, V. (Valgerdur), Thorleifsson, G. (Gudmar), Qi, L. (Lu), Karssen, L.C. (Lennart), Leeuwen, E.M. (Elisa) van, Willems, S.M. (Sara), Li, M. (Man), Chen, H. (Han), Fuchsberger, C. (Christian), Kwan, P. (Phoenix), Ma, C. (Clement), Linderman, M. (Michael), Lu, Y. (Yingchang), Thomsen, S.K. (Soren K.), Rundle, J.K. (Jana K.), Beer, N.L. (Nicola L.), Bunt, M. (Martijn) van de, Chalisey, A. (Anil), Kang, H.M. (Hyun Min), Voight, B.F. (Benjamin), Abecasis, G.R. (Gonçalo), Almgren, P. (Peter), Baldassarre, D. (Damiano), Balkau, B. (Beverley), Benediktsson, R. (Rafn), Blüher, M. (Matthias), Boeing, H. (Heiner), Bonnycastle, L.L. (Lori), Bottinger, E.P. (Erwin P.), Burtt, N.P. (Noël), Carey, J. (Jason), Charpentier, G. (Guillaume), Chines, P.S. (Peter), Cornelis, M. (Marilyn), Couper, D.J. (David J.), Crenshaw, A. (Andrew), Dam, R.M. (Rob) van, Doney, A.S.F. (Alex), Dorkhan, M. (Mozhgan), Edkins, T. (Ted), Eriksson, J.G. (Johan G.), Esko, T. (Tõnu), Eury, E. (Elodie), Fadista, J. (João), Flannick, J. (Jason), Fontanillas, P. (Pierre), Fox, C.S. (Caroline), Franks, P.W. (Paul W.), Gertow, K. (Karl), Gieger, C. (Christian), Gigante, B. (Bruna), Gottesman, R.F. (Rebecca), Grant, G.B. (George), Grarup, N. (Niels), Groves, C.J. (Christopher J.), Hassinen, M. (Maija), Have, C.T. (Christian T.), Herder, C. (Christian), Holmen, O.L. (Oddgeir), Hreidarsson, A.B. (Astradur), Humphries, S.E. (Steve E.), Hunter, D.J. (David J.), Jackson, A.U. (Anne), Jonsson, A. (Anna), Jørgensen, M.E. (Marit E.), Jørgensen, T. (Torben), Kao, W.H.L. (Wen), Kerrison, N.D. (Nicola D.), Kinnunen, L. (Leena), Klopp, N. (Norman), Kong, A. (Augustine), Kovacs, P. (Peter), Kraft, P. (Peter), Kravic, J. (Jasmina), Langford, C. (Cordelia), Leander, K. (Karin), Liang, L. (Liming), Lichtner, P. (Peter), Lindgren, C.M. (Cecilia M.), Lindholm, B. (Bengt), Linneberg, A. (Allan), Liu, C.-T. (Ching-Ti), Lobbens, S. (Stéphane), Luan, J. (Jian'fan), Lyssenko, V. (Valeriya), Männistö, S. (Satu), McLeod, O. (Olga), Meyer, J. (Jobst), Mihailov, E. (Evelin), Mirza, G. (Ghazala), Mühleisen, T.W. (Thomas), Müller-Nurasyid, M. (Martina), Navarro, C. (Carmen), Nöthen, M.M. (Markus), Oskolkov, N.N. (Nikolay N.), Owen, K.R. (Katharine), Palli, D. (Domenico), Pechlivanis, S. (Sonali), Peltonen, L. (Leena Johanna), Perry, J.R.B. (John), Platou, C.P. (Carl), Roden, M. (Michael), Ruderfer, D. (Douglas), Rybin, D. (Denis), Van Der Schouw, Y.T. (Yvonne T.), Sennblad, B. (Bengt), Sigurosson, G. (Gunnar), Stancáková, A. (Alena), Steinbach, D., Storm, P. (Petter), Strauch, K. (Konstantin), Stringham, H.M. (Heather), Sun, Q., Thorand, B. (Barbara), Tikkanen, E. (Emmi), Tönjes, A. (Anke), Trakalo, J. (Joseph), Tremoli, E. (Elena), Tuomi, T. (Tiinamaija), Wennauer, R. (Roman), Wiltshire, S. (Steven), Wood, A.R. (Andrew), Zeggini, E. (Eleftheria), Dunham, I. (Ian), Birney, E. (Ewan), Pasquali, L. (Lorenzo), Ferrer, J. (Jorge), Loos, R.J.F. (Ruth), Dupuis, J. (Josée), Florez, J.C. (Jose), Boerwinkle, E.A. (Eric), Pankow, J.S. (James), Duijn, C.M. (Cornelia) van, Sijbrands, E.J.G. (Eric), Meigs, J.B. (James B.), Hu, F.B. (Frank), Thorsteinsdottir, U. (Unnur), Zwart, J-A. (John-Anker), Lakka, T.A. (Timo), Rauramaa, R. (Rainer), Stumvoll, M. (Michael), Pedersen, N.L. (Nancy L.), Lind, L. (Lars), Keinanen-Kiukaanniemi, S. (Sirkka), Korpi-Hyövälti, E. (Eeva), Saaristo, T. (Timo), Saltevo, J. (Juha), Kuusisto, J. (Johanna), Laakso, M. (Markku), Metspalu, A. (Andres), Erbel, R. (Raimund), Jöckel, K.-H. (Karl-Heinz), Moebus, S. (Susanne), Ripatti, S. (Samuli), Salomaa, V. (Veikko), Ingelsson, E. (Erik), Boehm, B.O. (Bernhard), Bergman, R.N. (Richard N.), Collins, F.S. (Francis S.), Mohlke, K.L. (Karen L.), Koistinen, H. (Heikki), Tuomilehto, J. (Jaakko), Hveem, K. (Kristian), Njølstad, I. (Inger), Deloukas, P. (Panagiotis), Donnelly, P.J. (Peter J.), Frayling, T.M. (Timothy), Hattersley, A.T. (Andrew), Faire, U. (Ulf) de, Hamsten, A. (Anders), Illig, T. (Thomas), Peters, A. (Annette), Cauchi, S. (Stephane), Sladek, R. (Rob), Froguel, P. (Philippe), Hansen, T. (Torben), Pedersen, O. (Oluf), Morris, A.D. (Andrew), Palmer, C.N.A. (Collin N. A.), Kathiresan, S. (Sekar), Melander, O. (Olle), Nilsson, P.M. (Peter M.), Groop, L. (Leif), Barroso, I.E. (Inês), Langenberg, C. (Claudia), Wareham, N.J. (Nicholas J.), O'Callaghan, C.A. (Christopher A.), Gloyn, A.L. (Anna), Altshuler, D. (David), Boehnke, M. (Michael), Teslovich, T.M. (Tanya M.), McCarthy, M.I. (Mark), Morris, A.P. (Andrew), Gaulton, K. (Kyle), Ferreira, T. (Teresa), Lee, Y. (Yeji), Raimondo, A. (Anne), Mägi, R. (Reedik), Reschen, M.E. (Michael E.), Mahajan, A. (Anubha), Locke, A. (Adam), Rayner, N.W. (Nigel William), Robertson, N.R. (Neil), Scott, R.A. (Robert), Prokopenko, I. (Inga), Scott, L.J. (Laura), Green, T. (Todd), Sparsø, T. (Thomas), Thuillier, D. (Dorothee), Yengo, L. (Loic), Grallert, H. (Harald), Wahl, S. (Simone), Frånberg, M. (Mattias), Strawbridge, R.J. (Rona), Kestler, H. (Hans), Chheda, H. (Himanshu), Eisele, L. (Lewin), Gustafsson, S. (Stefan), Steinthorsdottir, V. (Valgerdur), Thorleifsson, G. (Gudmar), Qi, L. (Lu), Karssen, L.C. (Lennart), Leeuwen, E.M. (Elisa) van, Willems, S.M. (Sara), Li, M. (Man), Chen, H. (Han), Fuchsberger, C. (Christian), Kwan, P. (Phoenix), Ma, C. (Clement), Linderman, M. (Michael), Lu, Y. (Yingchang), Thomsen, S.K. (Soren K.), Rundle, J.K. (Jana K.), Beer, N.L. (Nicola L.), Bunt, M. (Martijn) van de, Chalisey, A. (Anil), Kang, H.M. (Hyun Min), Voight, B.F. (Benjamin), Abecasis, G.R. (Gonçalo), Almgren, P. (Peter), Baldassarre, D. (Damiano), Balkau, B. (Beverley), Benediktsson, R. (Rafn), Blüher, M. (Matthias), Boeing, H. (Heiner), Bonnycastle, L.L. (Lori), Bottinger, E.P. (Erwin P.), Burtt, N.P. (Noël), Carey, J. (Jason), Charpentier, G. (Guillaume), Chines, P.S. (Peter), Cornelis, M. (Marilyn), Couper, D.J. (David J.), Crenshaw, A. (Andrew), Dam, R.M. (Rob) van, Doney, A.S.F. (Alex), Dorkhan, M. (Mozhgan), Edkins, T. (Ted), Eriksson, J.G. (Johan G.), Esko, T. (Tõnu), Eury, E. (Elodie), Fadista, J. (João), Flannick, J. (Jason), Fontanillas, P. (Pierre), Fox, C.S. (Caroline), Franks, P.W. (Paul W.), Gertow, K. (Karl), Gieger, C. (Christian), Gigante, B. (Bruna), Gottesman, R.F. (Rebecca), Grant, G.B. (George), Grarup, N. (Niels), Groves, C.J. (Christopher J.), Hassinen, M. (Maija), Have, C.T. (Christian T.), Herder, C. (Christian), Holmen, O.L. (Oddgeir), Hreidarsson, A.B. (Astradur), Humphries, S.E. (Steve E.), Hunter, D.J. (David J.), Jackson, A.U. (Anne), Jonsson, A. (Anna), Jørgensen, M.E. (Marit E.), Jørgensen, T. (Torben), Kao, W.H.L. (Wen), Kerrison, N.D. (Nicola D.), Kinnunen, L. (Leena), Klopp, N. (Norman), Kong, A. (Augustine), Kovacs, P. (Peter), Kraft, P. (Peter), Kravic, J. (Jasmina), Langford, C. (Cordelia), Leander, K. (Karin), Liang, L. (Liming), Lichtner, P. (Peter), Lindgren, C.M. (Cecilia M.), Lindholm, B. (Bengt), Linneberg, A. (Allan), Liu, C.-T. (Ching-Ti), Lobbens, S. (Stéphane), Luan, J. (Jian'fan), Lyssenko, V. (Valeriya), Männistö, S. (Satu), McLeod, O. (Olga), Meyer, J. (Jobst), Mihailov, E. (Evelin), Mirza, G. (Ghazala), Mühleisen, T.W. (Thomas), Müller-Nurasyid, M. (Martina), Navarro, C. (Carmen), Nöthen, M.M. (Markus), Oskolkov, N.N. (Nikolay N.), Owen, K.R. (Katharine), Palli, D. (Domenico), Pechlivanis, S. (Sonali), Peltonen, L. (Leena Johanna), Perry, J.R.B. (John), Platou, C.P. (Carl), Roden, M. (Michael), Ruderfer, D. (Douglas), Rybin, D. (Denis), Van Der Schouw, Y.T. (Yvonne T.), Sennblad, B. (Bengt), Sigurosson, G. (Gunnar), Stancáková, A. (Alena), Steinbach, D., Storm, P. (Petter), Strauch, K. (Konstantin), Stringham, H.M. (Heather), Sun, Q., Thorand, B. (Barbara), Tikkanen, E. (Emmi), Tönjes, A. (Anke), Trakalo, J. (Joseph), Tremoli, E. (Elena), Tuomi, T. (Tiinamaija), Wennauer, R. (Roman), Wiltshire, S. (Steven), Wood, A.R. (Andrew), Zeggini, E. (Eleftheria), Dunham, I. (Ian), Birney, E. (Ewan), Pasquali, L. (Lorenzo), Ferrer, J. (Jorge), Loos, R.J.F. (Ruth), Dupuis, J. (Josée), Florez, J.C. (Jose), Boerwinkle, E.A. (Eric), Pankow, J.S. (James), Duijn, C.M. (Cornelia) van, Sijbrands, E.J.G. (Eric), Meigs, J.B. (James B.), Hu, F.B. (Frank), Thorsteinsdottir, U. (Unnur), Zwart, J-A. (John-Anker), Lakka, T.A. (Timo), Rauramaa, R. (Rainer), Stumvoll, M. (Michael), Pedersen, N.L. (Nancy L.), Lind, L. (Lars), Keinanen-Kiukaanniemi, S. (Sirkka), Korpi-Hyövälti, E. (Eeva), Saaristo, T. (Timo), Saltevo, J. (Juha), Kuusisto, J. (Johanna), Laakso, M. (Markku), Metspalu, A. (Andres), Erbel, R. (Raimund), Jöckel, K.-H. (Karl-Heinz), Moebus, S. (Susanne), Ripatti, S. (Samuli), Salomaa, V. (Veikko), Ingelsson, E. (Erik), Boehm, B.O. (Bernhard), Bergman, R.N. (Richard N.), Collins, F.S. (Francis S.), Mohlke, K.L. (Karen L.), Koistinen, H. (Heikki), Tuomilehto, J. (Jaakko), Hveem, K. (Kristian), Njølstad, I. (Inger), Deloukas, P. (Panagiotis), Donnelly, P.J. (Peter J.), Frayling, T.M. (Timothy), Hattersley, A.T. (Andrew), Faire, U. (Ulf) de, Hamsten, A. (Anders), Illig, T. (Thomas), Peters, A. (Annette), Cauchi, S. (Stephane), Sladek, R. (Rob), Froguel, P. (Philippe), Hansen, T. (Torben), Pedersen, O. (Oluf), Morris, A.D. (Andrew), Palmer, C.N.A. (Collin N. A.), Kathiresan, S. (Sekar), Melander, O. (Olle), Nilsson, P.M. (Peter M.), Groop, L. (Leif), Barroso, I.E. (Inês), Langenberg, C. (Claudia), Wareham, N.J. (Nicholas J.), O'Callaghan, C.A. (Christopher A.), Gloyn, A.L. (Anna), Altshuler, D. (David), Boehnke, M. (Michael), Teslovich, T.M. (Tanya M.), McCarthy, M.I. (Mark), and Morris, A.P. (Andrew)

Abstract

We performed fine mapping of 39 established type 2 diabetes (T2D) loci in 27,206 cases and 57,574 controls of European ancestry. We identified 49 distinct association signals at these loci, including five mapping in or near KCNQ1. 'Credible sets' of the variants most likely to drive each distinct signal mapped predominantly to noncoding sequence, implying that association with T2D is mediated through gene regulation. Credible set variants were enriched for overlap with FOXA2 chromatin immunoprecipitation binding sites in human islet and liver cells, including at MTNR1B, where fine mapping implicated rs10830963 as driving T2D association. We confirmed that the T2D risk allele for this SNP increases FOXA2-bound enhancer activity in islet- and liver-derived cells. We observed allele-specific differences in NEUROD1 binding in islet-derived cells, consistent with evidence that the T2D risk allele increases islet MTNR1B expression. Our study demonstrates how integration of genetic and genomic information can define molecular mechanisms through which variants underlying association signals exert their effects on disease.

Published
2015
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85. Elevated levels of plasma osteoprotegerin are associated with all-cause mortality risk and atherosclerosis in patients with stages 3 to 5 chronic kidney disease

Author

Nascimento, M. M., Hayashi, Shirley Y., Riella, M. C., Lindholm, B., Nascimento, M. M., Hayashi, Shirley Y., Riella, M. C., and Lindholm, B.

Abstract

Osteoprotegerin (OPG) regulates bone mass by inhibiting osteoclast differentiation and activation, and plays a role in vascular calcification. We evaluated the relationship between osteoprotegerin levels and inflammatory markers, atherosclerosis, and mortality in patients with stages 3-5 chronic kidney disease. A total of 145 subjects (median age 61 years, 61% men; 36 patients on hemodialysis, 55 patients on peritoneal dialysis, and 54 patients with stages 3-5 chronic kidney disease) were studied. Clinical characteristics, markers of mineral metabolism (including fibroblast growth factor-23 [FGF-23]) and inflammation (high-sensitivity C-reactive protein [hsCRP] and interleukin-6 [IL-6]), and the intima-media thickness (IMT) in the common carotid arteries were measured at baseline. Cardiac function was assessed by color tissue Doppler echocardiography. After 36 months follow-up, the survival rate by Kaplan-Meier analysis was significantly different according to OPG levels (chi(2) = 14.33; P = 0.002). Increased OPG levels were positively associated with IL-6 (r = 0.38, P<0.001), FGF-23 (r = 0.26, P<0.001) and hsCRP (r = 0.0.24, P = 0.003). In addition, OPG was positively associated with troponin I (r = 0.54, P<0.001) and IMT (r = 0.39, P<0.0001). Finally, in Cox analysis, only OPG (HR = 1.07, 95% CI = 1.02-1.13) and hsCRP (HR = 1.02, 95% CI = 1.01-1.04) were independently associated with increased risk of death. These results suggested that elevated levels of serumOPG might be associated with atherosclerosis and all-cause mortality in patients with chronic kidney disease., QC 20150109

Published
2014
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86. Assessment of arterial stiffness for clinical and epidemiological studies: methodological considerations for validation and entry into the European Renal and Cardiovascular Medicine registry.

Author

Boutouyrie, P, Fliser, D, Goldsmith, D, Covic, A, Wiecek, A, Ortiz, A, Martinez Castelao, A, Lindholm, B, Massy, Z, Suleymanlar, G, Sicari, R, Gargani, L, Parati, G, Mallamaci, F, Zoccali, C, London, G, Massy, ZA, London, GM, PARATI, GIANFRANCO, Boutouyrie, P, Fliser, D, Goldsmith, D, Covic, A, Wiecek, A, Ortiz, A, Martinez Castelao, A, Lindholm, B, Massy, Z, Suleymanlar, G, Sicari, R, Gargani, L, Parati, G, Mallamaci, F, Zoccali, C, London, G, Massy, ZA, London, GM, and PARATI, GIANFRANCO

Abstract

Epidemiological studies have highlighted the role of arterial stiffness as a risk factor for development of cardiovascular (CV) diseases. Moreover, aortic stiffness has been shown to be a significant predictive factor of all-cause and CV mortality in different populations including patients with endstage renal disease. Pulse-wave velocity (PWV) is the most widely used technique to assess arterial stiffness. Although PWV can be measured on any artery or between any arterial sites, only carotid-to-femoral PWV, representing stiffness of the aorta and iliofemoral axes, has been shown to have predictive value for morbidity and mortality. The several available commercial devices differ according to the type of signal (pressure, distension, flow) or by recording both sites simultaneously or using ECG synchronization. It is also possible to directly measure arterial diameter changes during the cardiac cycle and link them to local pulse–pressure changes, which provides the pressure–diameter relationship and stress–strain relationship if arterial wall thickness is also measured. These techniques are based on high-precision vascular echo tracking or magnetic resonance imaging and applanation tonometry. This paper summarizes the basic principles of arterial haemodynamics and various methodologies to assess stiffness and the latest consensus recommendations for clinical applications.

Published
2014

92. Systemic and intraperitoneal interleukin‐6 system during the first year of peritoneal dialysis

Author

Pecoits-Filho, R., Carvalho, M. J., Peter Stenvinkel, Lindholm, B., and Heimbürger, O.

Abstract

Perit Dial Int. 2006 Jan-Feb;26(1):53-63. Systemic and intraperitoneal interleukin-6 system during the first year of peritoneal dialysis. Pecoits-Filho R, Carvalho MJ, Stenvinkel P, Lindholm B, Heimbürger O. Division of Renal Medicine and Baxter Novum, Karolinska Institutet, K-56, Huddinge University Hospital, 141 86 Stockholm, Sweden. roberto.pecoits-filho@klinvet.ki.se Comment in: Perit Dial Int. 2006 Jan-Feb;26(1):35-7. Abstract OBJECTIVE: To investigate if intraperitoneal and systemic interleukin-6 (IL-6) and soluble IL-6 receptor (sIL-6R) are related to each other and to peritoneal solute transport rate (PSTR). DESIGN: Longitudinal study in retrospectively selected patients. SETTING: Peritoneal dialysis (PD) unit of a university-based hospital. PATIENTS AND METHODS: 31 PD patients on treatment with conventional glucose-based solutions participated in a longitudinal study. IL-6 and sIL-6R were measured in plasma and overnight effluent, both at baseline and after 12 +/- 2 months on PD. C-reactive protein (CRP) and serum albumin were used as surrogate markers of inflammation. PSTR of small solutes was evaluated using the dialysate-to-plasma ratio (D/P) of creatinine after a 4-hour dwell; PSTR of large solutes was evaluated using the 24-hour D/P ratio of albumin. RESULTS: D/P creat increased over time (0.67 +/- 0.15 vs 0.80 +/- 0.11, p < 0.0001) and correlated to D/P albumin only at the baseline evaluation. Patients with plasma IL-6 > or = median had higher (p < 0.005) D/P creat at baseline [0.74 (0.62 - 0.87)] compared to patients with IL-6 < median [0.57 (0.47 - 0.66)]. Dialysate IL-6 at baseline was also higher (p < 0.05) in patients with plasma IL-6 > or = median [24.7 (16.5 - 38.5) pg/mL] compared to patients with IL-6 < median [14.1 (10 - 25.7) pg/mL]. Neither CRP nor albumin changed over time on PD, although they were closely linked to plasma IL-6 levels. A strong positive correlation was found between D/P creat and dialysate IL-6 (rho = 0.77, p < 0.0001) at baseline, but not at 1 year. In contrast, there was a significant correlation between D/P creat and dialysate sIL-6R (rho = 0.39, p < 0.05) at 1 year, but not at baseline. At 1 year, 17 patients with increasing PSTR had higher increases in dialysate IL-6 (28 +/- 26 vs -21 +/- 78 pg/mL, p < 0.05) and levels of dialysate sIL-6R (693 +/- 392 vs 394 +/- 274 pg/mL, p = 0.05) compared to patients with stable PSTR (n = 11). Patients who had peritonitis presented higher baseline serum IL-6 concentration (6.8 +/- 1.0 pg/mL) compared with patients without peritonitis (4.0 +/- 0.6 pg/mL, p < 0.05). Finally, both at baseline and after 1 year, there were significant correlations between plasma and dialysate IL-6 (rho = 0.46, p < 0.05, and rho = 0.40, p < 0.05) respectively. CONCLUSIONS: These findings indicate that, (1) intraperitoneal and systemic inflammation increase in PD patients during the first year of therapy; (2) intraperitoneal and systemic inflammation may be interrelated and the IL-6 system may be the link; (3) the IL-6 system (both intraperitoneal and systemic) is associated with PSTR, particularly in the early phase of PD treatment, in which small and large solute transport are linked. Signs of a transition between acute and chronic inflammation were observed in the follow-up evaluation. Inflammation may, at least in part, be responsible for the development of a high PSTR, and this could be one reason for the high mortality in patients with high PSTR. PMID: 16538876 [PubMed - indexed for MEDLINE

Published
2006

94. Effect of hepatitis C serology on C-reactive protein in a cohort of brazilian hemodialysis patients

Author

Nascimento, M. M., Bruchfeld, A., Suliman, Mohamed E., Hayashi, Shirley Y., Pecoits-Filho, Roberto, Manfro, Roberto Ceratti, Pachaly, Maria A., Renner, L., Stenvinkel, P., Riella, Miguel Carlos, and Lindholm, B.

Subjects
Hepatite C, Hemodialysis, Diálise renal, Proteina C-reativa, Interleucina-6, C-reactive protein
Abstract

Hepatitis C (HCV) is not an uncommon feature in hemodialysis (HD) patients and may be a cause of systemic inflammation. Plasma cytokine interleukin-6 (IL-6) is mainly produced by circulating and peripheral cells and induces the hepatic synthesis of C-reactive protein (CRP), which is the main acute phase reactant. The aim of this study was to investigate the influence of HCV on two markers of systemic inflammation, serum CRP and IL-6, in HD patients. The study included 118 HD patients (47% males, age 47 ± 13 years, 9% diabetics) who had been treated by standard HD for at least 6 months. The patients were divided into two groups depending on the presence (HCV+) or absence (HCV-) of serum antibodies against HCV. Serum albumin (S-Alb), plasma high sensitivity CRP (hsCRP), IL-6, and alanine aminotransferase (ALT) were measured and the values were compared with those for 22 healthy controls. Median hsCRP and IL-6 values and hsCRP/IL-6 ratio were: 3.5 vs 2.1 mg/l, P < 0.05; 4.3 vs 0.9 pg/ml, P < 0.0001, and 0.8 vs 2.7, P < 0.0001, for patients and controls, respectively. Age, gender, S-Alb, IL-6 and hsCRP did not differ between the HCV+ and HCV- patients. However, HCV+ patients had higher ALT (29 ± 21 vs 21 ± 25 IU/l) and had been on HD for a longer time (6.1 ± 3.0 vs 4.0 ± 2.0 years, P < 0.0001). Moreover, HCV+ patients had a significantly lower median hsCRP/IL-6 ratio (0.7 vs 0.9, P < 0.05) compared to the HCV- group. The lower hsCRP/IL-6 ratio in HCV+ patients than in HCV- patients suggests that hsCRP may be a less useful marker of inflammation in HCV+ patients and that a different cut-off value for hsCRP for this population of patients on HD may be required to define inflammation.

Published
2005

98. CKD NUTRITION

Author

Yoshifuji, A., primary, Wakino, S., additional, Irie, J., additional, Minakuchi, H., additional, Hasegawa, K., additional, Tokuyama, H., additional, Hayashi, K., additional, Itoh, H., additional, Xu, H., additional, Huang, X., additional, Riserus, U., additional, Cederholm, T., additional, Arnlov, J., additional, Sjogren, P., additional, Lindholm, B., additional, Carrero, J. J., additional, Poesen, R., additional, Windey, K., additional, Evenepoel, P., additional, De Preter, V., additional, Verbeke, K., additional, Meijers, B., additional, De Roij Van Zuijdewijn, C. L., additional, Nube, M. J., additional, Bots, M. L., additional, Blankestijn, P. J., additional, Van Den Dorpel, M. A., additional, Ter Wee, P. M., additional, Grooteman, M. P., additional, Masereeuw, R., additional, and Van Den Broek, P. H., additional

Published
2014
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99. PERITONEAL DIALYSIS 2

Author

Vlahu, C. A., primary, De Graaff, M., additional, Struijk, D. G., additional, Krediet, R. T., additional, Shin, H.-S., additional, Ryu, E.-S., additional, Choi, H.-S., additional, Ryu, D.-R., additional, Choi, K.-B., additional, Kang, D.-H., additional, Sanchez-Alvarez, E., additional, Rodriguez-Suarez, C., additional, Galvan-.Hernandez, J. A., additional, Kim, Y. L., additional, Kee, Y. K., additional, Lee, M. J., additional, Oh, H. J., additional, Park, J. T., additional, Han, S. H., additional, Yoo, T.-H., additional, Kang, S.-W., additional, Zhu, F., additional, Abbas, S. R., additional, Bologa, R., additional, Lanto, B., additional, Kotanko, P., additional, Parikova, A., additional, Smit, W., additional, Rroji ( Molla), M., additional, Seferi, S., additional, Cafka, M., additional, Thereska, N., additional, Huang, C.-C., additional, Wang, I.-K., additional, Shiao, Y.-T., additional, Teixeira, L., additional, Sousa, I., additional, Rodrigues, A., additional, Mendonca, D., additional, Ueda, A., additional, Iwase, M., additional, Usui, T., additional, Hirayama, A., additional, Nagai, K., additional, Saito, C., additional, Yamagata, K., additional, La Milia, V., additional, Pontoriero, G., additional, Locatelli, F., additional, Kim, S. M., additional, Kim, T. Y., additional, Lee, J. E., additional, Teta, D., additional, Guillodo, M.-P., additional, Kolko-Labadens, A., additional, Lasseur, C., additional, Levannier, M., additional, Panaye, M., additional, Fouque, D., additional, HAMADA, C., additional, Hara, K., additional, Kang, S. H., additional, Cho, K. H., additional, Park, J. W., additional, Yoon, K. W., additional, Do, J. Y., additional, Dogan, I., additional, Biro Dr, B., additional, Zakar Dr, G., additional, Foldine, Z., additional, Staudt, S., additional, Martins, A. R., additional, Vizinho, R., additional, Branco, P. Q., additional, Gaspar, M. A., additional, Barata, J. D., additional, Sikorska, D., additional, Klysz, P., additional, Posnik, B., additional, Baum, E., additional, Hoppe, K., additional, Schwermer, K., additional, Wanic-Kossowska, M., additional, Frankiewicz, D., additional, Pawlaczyk, K., additional, Lindholm, B., additional, Oko, A., additional, Busuioc, M., additional, Trolliet, P., additional, Guerraoui, A., additional, Caillette-Beaudoin, A., additional, Hallonet, P., additional, Yang, J.-O., additional, Gursu, M., additional, Topcuoglu, D., additional, Koc, L. K., additional, Yucel, L., additional, Sumnu, A., additional, Cebeci, E., additional, Doner, B., additional, Ozkan, O., additional, Behlul, A., additional, Koc, L., additional, Ozturk, S., additional, Kazancioglu, R., additional, Casas Parra, A. I. I., additional, Gonzalez, M. T. T., additional, Sandoval, D. A., additional, Carlota, G. C., additional, Grinyo, J. M. M., additional, Tseng, C.-H., additional, Chao, C.-T., additional, Yen, C.-J., additional, Chiang, C.-K., additional, Hung, K.-Y., additional, Huang, J.-W., additional, Al Wakeel, J. S., additional, Al Ghonaim, M., additional, Al Suwaida, A., additional, Al Harbi, A., additional, Makoshi, Z., additional, Abdullah, S., additional, Matsushita, Y., additional, Basic-Jukic, N., additional, Coen-Herak, D., additional, Martinovic, Z., additional, Radi -Antoli , M., additional, Kes, P., additional, Wu, T.-J., additional, Chen, J.-S., additional, Lin, S.-H., additional, Shiang, J.-C., additional, Wu, C.-C., additional, Munteanu, D., additional, Gemene, M., additional, Mircescu, G., additional, Opatrna, S., additional, Popperlova, A., additional, Tesar, V., additional, Rychlik, I., additional, Viklicky, O., additional, Jin, K., additional, Park, B.-S., additional, Jeong, H. J., additional, Kim, Y.-W., additional, Hogas, S., additional, Voroneanu, L., additional, Onofriescu, M., additional, Nistor, I., additional, Apetrii, M., additional, Siriopol, D., additional, Cujba, M., additional, Hogas, M., additional, and Covic, A., additional

Published
2014
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