AIMS: Cystatin C is a well established marker of kidney function. There is evidence that cystatin C concentrations are also associated with mortality. The present analysis prospectively evaluated the associations of cystatin C with all-cause and cardiovascular (CV) mortality in a well-characterized cohort of persons undergoing angiography, but without overt renal insufficiency. METHODS: Cystatin C was available in 2998 persons (mean age: 62.7 ± 10.5 years; 30.3% women). Of those 2346 suffered from coronary artery disease (CAD) and 652 (controls) did not. Creatinine (mean ± SD: 83.1 ± 47.8 vs. 74.1 ± 24.7 μmol/L, p = 0.036) but not Cystatin C (mean ± SD: 1.02 ± 0.44 vs. 0.92 ± 0.26 mg/L, p = 0.065) was significantly higher in patients with CAD. After a median follow-up of 9.9 years, in total 898 (30%) deaths occurred, 554 (18.5%) due to CV disease and 326 (10.9%) due to non-CV causes. Multivariable-adjusted Cox analysis (adjusting for eGFR and established cardiovascular risk factors, lipid lowering therapy, angiographic coronary artery disease, and C-reactive protein) revealed that patients in the highest cystatin C quartile were at an increased risk for all-cause (hazard ratio (HR) 1.93, 95% CI 1.50-2.48) and CV mortality (HR 2.05 95% CI 1.48-2.84) compared to those in the lowest quartile. The addition of cystatin C to a model consisting of established cardiovascular risk factors increased the area under the receiver-operating characteristic curve for CV and all-cause mortality, but the difference was statistically not significant. However, reclassification analysis revealed significant improvement by addition of cystatin C for CV and all-cause mortality (p < 0.001), respectively. CONCLUSION: The concentration of cystatin C is strongly associated with long-term all-cause and cardiovascular mortality in patients referred to coronary angiography, irrespective of creatinine-based renal function.
AIMS: Cystatin C is a well established marker of kidney function. There is evidence that cystatin C concentrations are also associated with mortality. The present analysis prospectively evaluated the associations of cystatin C with all-cause and cardiovascular (CV) mortality in a well-characterized cohort of persons undergoing angiography, but without overt renal insufficiency. METHODS:Cystatin C was available in 2998 persons (mean age: 62.7 ± 10.5 years; 30.3% women). Of those 2346 suffered from coronary artery disease (CAD) and 652 (controls) did not. Creatinine (mean ± SD: 83.1 ± 47.8 vs. 74.1 ± 24.7 μmol/L, p = 0.036) but not Cystatin C (mean ± SD: 1.02 ± 0.44 vs. 0.92 ± 0.26 mg/L, p = 0.065) was significantly higher in patients with CAD. After a median follow-up of 9.9 years, in total 898 (30%) deaths occurred, 554 (18.5%) due to CV disease and 326 (10.9%) due to non-CV causes. Multivariable-adjusted Cox analysis (adjusting for eGFR and established cardiovascular risk factors, lipid lowering therapy, angiographic coronary artery disease, and C-reactive protein) revealed that patients in the highest cystatin C quartile were at an increased risk for all-cause (hazard ratio (HR) 1.93, 95% CI 1.50-2.48) and CV mortality (HR 2.05 95% CI 1.48-2.84) compared to those in the lowest quartile. The addition of cystatin C to a model consisting of established cardiovascular risk factors increased the area under the receiver-operating characteristic curve for CV and all-cause mortality, but the difference was statistically not significant. However, reclassification analysis revealed significant improvement by addition of cystatin C for CV and all-cause mortality (p < 0.001), respectively. CONCLUSION: The concentration of cystatin C is strongly associated with long-term all-cause and cardiovascular mortality in patients referred to coronary angiography, irrespective of creatinine-based renal function.
Authors: Rohit M Oemrawsingh; K Martijn Akkerhuis; Victor A Umans; Bas Kietselaer; Carl Schotborgh; Eelko Ronner; Timo Lenderink; Anho Liem; David Haitsma; Pim van der Harst; Folkert W Asselbergs; Arthur Maas; Anton J Oude Ophuis; Ben Ilmer; Rene Dijkgraaf; Robbert-Jan de Winter; S Hong Kie The; Alexander J Wardeh; Walter Hermans; Etienne Cramer; Ron H van Schaik; Imo E Hoefer; Pieter A Doevendans; Maarten L Simoons; Eric Boersma Journal: BMJ Open Date: 2016-12-23 Impact factor: 2.692
Authors: Rainer P Woitas; Hubert Scharnagl; Marcus E Kleber; Graciela E Delgado; Tanja B Grammer; Martin Pichler; Bernhard K Krämer; Winfried März; Tatjana Stojakovic Journal: PLoS One Date: 2017-02-16 Impact factor: 3.240
Authors: Sander W van der Laan; Tove Fall; Aicha Soumaré; Alexander Teumer; Sanaz Sedaghat; Jens Baumert; Delilah Zabaneh; Jessica van Setten; Ivana Isgum; Tessel E Galesloot; Johannes Arpegård; Philippe Amouyel; Stella Trompet; Melanie Waldenberger; Marcus Dörr; Patrik K Magnusson; Vilmantas Giedraitis; Anders Larsson; Andrew P Morris; Janine F Felix; Alanna C Morrison; Nora Franceschini; Joshua C Bis; Maryam Kavousi; Christopher O'Donnell; Fotios Drenos; Vinicius Tragante; Patricia B Munroe; Rainer Malik; Martin Dichgans; Bradford B Worrall; Jeanette Erdmann; Christopher P Nelson; Nilesh J Samani; Heribert Schunkert; Jonathan Marchini; Riyaz S Patel; Aroon D Hingorani; Lars Lind; Nancy L Pedersen; Jacqueline de Graaf; Lambertus A L M Kiemeney; Sebastian E Baumeister; Oscar H Franco; Albert Hofman; André G Uitterlinden; Wolfgang Koenig; Christa Meisinger; Annette Peters; Barbara Thorand; J Wouter Jukema; Bjørn Odvar Eriksen; Ingrid Toft; Tom Wilsgaard; N Charlotte Onland-Moret; Yvonne T van der Schouw; Stéphanie Debette; Meena Kumari; Per Svensson; Pim van der Harst; Mika Kivimaki; Brendan J Keating; Naveed Sattar; Abbas Dehghan; Alex P Reiner; Erik Ingelsson; Hester M den Ruijter; Paul I W de Bakker; Gerard Pasterkamp; Johan Ärnlöv; Michael V Holmes; Folkert W Asselbergs Journal: J Am Coll Cardiol Date: 2016-08-30 Impact factor: 24.094