17 results on '"GCKD Investigators"'
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2. Rare genetic variants affecting urine metabolite levels link population variation to inborn errors of metabolism
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Yurong Cheng, Pascal Schlosser, Johannes Hertel, Peggy Sekula, Peter J. Oefner, Ute Spiekerkoetter, Johanna Mielke, Daniel F. Freitag, Miriam Schmidts, GCKD Investigators, Florian Kronenberg, Kai-Uwe Eckardt, Ines Thiele, Yong Li, and Anna Köttgen
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Science - Abstract
Metabolites are indicators of health and disease; genetic studies can reveal variants influencing their levels. Here, the authors investigate the contribution of rare, exonic variants on the levels of urine metabolites and generate predictions on metabolic consequences underlying metabolic disease.
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- 2021
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3. Author Correction: Rare genetic variants affecting urine metabolite levels link population variation to inborn errors of metabolism
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Yurong Cheng, Pascal Schlosser, Johannes Hertel, Peggy Sekula, Peter J. Oefner, Ute Spiekerkoetter, Johanna Mielke, Daniel F. Freitag, Miriam Schmidts, GCKD Investigators, Florian Kronenberg, Kai-Uwe Eckardt, Ines Thiele, Yong Li, and Anna Köttgen
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Science - Published
- 2021
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4. Apolipoprotein A-IV concentrations and cancer in a large cohort of chronic kidney disease patients: results from the GCKD study
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Barbara Kollerits, Simon Gruber, Inga Steinbrenner, Johannes P. Schwaiger, Hansi Weissensteiner, Sebastian Schönherr, Lukas Forer, Fruzsina Kotsis, Ulla T. Schultheiss, Heike Meiselbach, Christoph Wanner, Kai-Uwe Eckardt, Florian Kronenberg, and for the GCKD Investigators
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Apolipoprotein A-IV ,Kidney function ,Cancer ,Inflammation ,Prospective study ,Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,RC254-282 - Abstract
Abstract Background Chronic kidney disease (CKD) is highly connected to inflammation and oxidative stress. Both favour the development of cancer in CKD patients. Serum apolipoprotein A-IV (apoA-IV) concentrations are influenced by kidney function and are an early marker of kidney impairment. Besides others, it has antioxidant and anti-inflammatory properties. Proteomic studies and small case–control studies identified low apoA-IV as a biomarker for various forms of cancer; however, prospective studies are lacking. We therefore investigated whether serum apoA-IV is associated with cancer in the German Chronic Kidney Disease (GCKD) study. Methods These analyses include 5039 Caucasian patients from the prospective GCKD cohort study followed for 6.5 years. Main inclusion criteria were an eGFR of 30–60 mL/min/1.73m2 or an eGFR > 60 mL/min/1.73m2 in the presence of overt proteinuria. Results Mean apoA-IV concentrations of the entire cohort were 28.9 ± 9.8 mg/dL (median 27.6 mg/dL). 615 patients had a history of cancer before the enrolment into the study. ApoA-IV concentrations above the median were associated with a lower odds for a history of cancer (OR = 0.79, p = 0.02 when adjusted age, sex, smoking, diabetes, BMI, albuminuria, statin intake, and eGFRcreatinine). During follow-up 368 patients developed an incident cancer event and those with apoA-IV above the median had a lower risk (HR = 0.72, 95%CI 0.57–0.90, P = 0.004). Finally, 62 patients died from such an incident cancer event and each 10 mg/dL higher apoA-IV concentrations were associated with a lower risk for fatal cancer (HR = 0.62, 95%CI 0.44–0.88, P = 0.007). Conclusions Our data indicate an association of high apoA-IV concentrations with reduced frequencies of a history of cancer as well as incident fatal and non-fatal cancer events in a large cohort of patients with CKD. Graphical Abstract
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- 2024
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5. Heart failure in a cohort of patients with chronic kidney disease: the GCKD study.
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Hanna Beck, Stephanie I Titze, Silvia Hübner, Martin Busch, Georg Schlieper, Ulla T Schultheiss, Christoph Wanner, Florian Kronenberg, Vera Krane, Kai-Uwe Eckardt, Anna Köttgen, and GCKD Investigators
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Medicine ,Science - Abstract
BACKGROUND AND AIMS:Chronic kidney disease (CKD) is a risk factor for development and progression of heart failure (HF). CKD and HF share common risk factors, but few data exist on the prevalence, signs and symptoms as well as correlates of HF in populations with CKD of moderate severity. We therefore aimed to examine the prevalence and correlates of HF in the German Chronic Kidney Disease (GCKD) study, a large observational prospective study. METHODS AND RESULTS:We analyzed data from 5,015 GCKD patients aged 18-74 years with an estimated glomerular filtration rate (eGFR) of 500 mg/d). We evaluated a definition of HF based on the Gothenburg score, a clinical HF score used in epidemiological studies (Gothenburg HF), and self-reported HF. Factors associated with HF were identified using multivariable adjusted logistic regression. The prevalence of Gothenburg HF was 43% (ranging from 24% in those with eGFR >90 to 59% in those with eGFR
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- 2015
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6. Correction: Heart Failure in a Cohort of Patients with Chronic Kidney Disease: The GCKD Study.
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Hanna Beck, Stephanie I Titze, Silvia Hübner, Martin Busch, Georg Schlieper, Ulla T Schultheiss, Christoph Wanner, Florian Kronenberg, Vera Krane, Kai-Uwe Eckardt, Anna Köttgen, and GCKD Investigators
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Medicine ,Science - Published
- 2015
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7. Correction: Apolipoprotein A-IV concentrations and cancer in a large cohort of chronic kidney disease patients: results from the GCKD study
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Barbara Kollerits, Simon Gruber, Inga Steinbrenner, Johannes P. Schwaiger, Hansi Weissensteiner, Sebastian Schönherr, Lukas Forer, Fruzsina Kotsis, Ulla T. Schultheiss, Heike Meiselbach, Christoph Wanner, Kai-Uwe Eckardt, Florian Kronenberg, and for the GCKD Investigators
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Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,RC254-282 - Published
- 2024
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8. Association of the metabolic syndrome with mortality and major adverse cardiac events: A large chronic kidney disease cohort
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Gckd Investigators, Florian Kronenberg, Lorenz M Pammer, Martin Busch, Jan Lipovsek, Helena Stockmann, Kai-Uwe Eckardt, Ulla T. Schultheiss, Barbara Kollerits, Fruzsina Kotsis, Claudia Lamina, and Heike Meiselbach
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medicine.medical_specialty ,Population ,Insulin resistance ,Risk Factors ,Internal medicine ,Internal Medicine ,medicine ,Humans ,Prospective Studies ,Mortality ,Renal Insufficiency, Chronic ,education ,Prospective cohort study ,Triglycerides ,Metabolic Syndrome ,education.field_of_study ,business.industry ,Cholesterol, HDL ,Hazard ratio ,medicine.disease ,Glucose ,Cardiovascular Diseases ,Hypertension ,Cohort ,Albuminuria ,medicine.symptom ,Metabolic syndrome ,business ,Glomerular Filtration Rate ,Kidney disease - Abstract
Background Metabolic syndrome with its key components insulin resistance, central obesity, dyslipidaemia, and hypertension is associated with a high risk for cardiovascular events and all-cause mortality in the general population. However, evidence that these findings apply to patients with chronic kidney disease (CKD) with moderately reduced estimated glomerular filtration rate and/or albuminuria is limited. Objectives We aimed to investigate the association between metabolic syndrome and its components with all-cause mortality and cardiovascular outcomes in CKD patients. Methods Prospective observation of a cohort of 5110 CKD patients from the German Chronic Kidney Disease study with 3284 (64.3%) of them having a metabolic syndrome at baseline. Results During the follow-up of 6.5 years, 605 patients died and 650 patients experienced major cardiovascular events. After extended data adjustment, patients with a metabolic syndrome had a higher risk for all-cause mortality (hazard ratio [HR] = 1.26, 95% confidence interval [CI]: 1.04-1.54) and cardiovascular events (HR = 1.48, 95% CI: 1.22-1.79). The risk increased steadily with a growing number of metabolic syndrome components (increased waist circumference, glucose, triglycerides, hypertension and decreased HDL cholesterol): HR per component = 1.09 (95% CI: 1.02-1.17) for all-cause mortality, and 1.23 (95% CI: 1.15-1.32) for cardiovascular events. This resulted in hazard ratios between 1.50 and 2.50 in the case of four or five components present. Analysis of individual components of metabolic syndrome showed that the glucose component led to the highest increase in risk for all-cause mortality (HR = 1.68, 95% CI: 1.38-2.03) and cardiovascular events (HR = 1.81, 95% CI: 1.51-2.18), followed by the HDL cholesterol and triglyceride components. Conclusions We observed a high prevalence of metabolic syndrome among patients with moderate CKD. Metabolic syndrome increases the risk for all-cause mortality and cardiovascular events. The glucose and lipid components seem to be the main drivers for the association with outcomes.
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- 2021
9. Uromodulin and its association with urinary metabolites: the German Chronic Kidney Disease Study
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Bächle, Helena, Sekula, Peggy, Schlosser, Pascal, Steinbrenner, Inga, Cheng, Yurong, Kotsis, Fruzsina, Meiselbach, Heike, Stockmann, Helena, Schönherr, Sebastian, GCKD investigators, ?, Eckardt, Kai-Uwe, Devuyst, Olivier, Scherberich, Jürgen, Köttgen, Anna, Schultheiss, Ulla T, and University of Zurich
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570 Life sciences ,biology ,610 Medicine & health ,10052 Institute of Physiology - Published
- 2022
10. Educational Attainment Is Associated With Kidney and Cardiovascular Outcomes in the German CKD (GCKD) Cohort
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Winitzki, Doris, Zacharias, Helena U., Nadal, Jennifer, Baid-Agrawal, Seema, Schaeffner, Elke, Schmid, Matthias, Busch, Martin, Bergmann, Manuela M., Schultheiss, Ulla, Kotsis, Fruzsina, Stockmann, Helena, Meiselbach, Heike, Wolf, Gunter, Krane, Vera, Sommerer, Claudia, Eckardt, Kai-Uwe, Schneider, Markus P., Schlieper, Georg Rainer, Flöge, Jürgen, Saritas, Turgay, and German Chronic Kidney Disease (GCKD) Investigators
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Nephrology - Abstract
Kidney international / Reports 7(5), 1004-1015 (2022). doi:10.1016/j.ekir.2022.02.001, Published by Elsevier, Amsterdam
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- 2022
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11. Frequent LPA KIV-2 Variants Lower Lipoprotein(a) Concentrations and Protect Against Coronary Artery Disease
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Schachtl-Riess, Johanna F., Kheirkhah, Azin, Grüneis, Rebecca, Di Maio, Silvia, Schoenherr, Sebastian, Streiter, Gertraud, Losso, Jamie Lee, Paulweber, Bernhard, Eckardt, Kai-Uwe, Köttgen, Anna, Lamina, Claudia, Kronenberg, Florian, Coassin, Stefan, For The GCKD Investigators, Meiselbach, Heike, Schneider, Markus P., Schiffer, Mario, Prokosch, Hans-Ulrich, Bärthlein, Barbara, Beck, Andreas, Reis, André, Ekici, Arif B., Becker, Susanne, Becker-Grosspitsch, Dinah, Alberth-Schmidt, Ulrike, Hausknecht, Birgit, Weigel, Anke, Walz, Gerd, Schultheiß, Ulla T., Kotsis, Fruzsina, Meder, Simone, Mitsch, Erna, Reinhard, Ursula, Floege, Jürgen, Saritas, Turgay, Schaeffner, Elke, Baid-Agrawal, Seema, Theisen, Kerstin, Haller, Hermann, Menne, Jan, Zeier, Martin, Sommerer, Claudia, Theilinger, Johanna, Wolf, Gunter, Busch, Martin, Paul, Rainer, Sitter, Thomas, Wanner, Christoph, Krane, Vera, Börner-Klein, Antje, Bauer, Britta, Raschenberger, Julia, Kollerits, Barbara, Forer, Lukas, Schönherr, Sebastian, Weissensteiner, Hansi, Oefner, Peter J., Gronwald, Wolfram, Schmid, Matthias, and Nadal, Jennifer
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medicine.medical_specialty ,610 Medizin ,Coronary Artery Disease ,Mendelian randomization ,cardiovascular disease ,cohort study ,copy number variation ,genetic variability ,lipoprotein(a) ,Coronary artery disease ,Kringles ,Internal medicine ,Medicine ,Humans ,Copy-number variation ,Genetic variability ,Prospective Studies ,Risk factor ,ddc:610 ,biology ,business.industry ,Genetic Variation ,Lipoprotein(a) ,medicine.disease ,biology.protein ,Cardiology ,lipids (amino acids, peptides, and proteins) ,biological phenomena, cell phenomena, and immunity ,Cardiology and Cardiovascular Medicine ,business ,Lipoprotein ,Cohort study - Abstract
Background: Lipoprotein(a) (Lp(a)) concentrations are a major independent risk factor for coronary artery disease (CAD) and are mainly determined by variation in LPA. Up to 70% of the LPA coding sequence is located in the hypervariable kringle IV type 2 (KIV-2) region. It is hardly accessible by conventional technologies, but may contain functional variants. Objectives: This study sought to investigate the new, very frequent splicing variant KIV-2 4733G>A on Lp(a) and CAD. Methods: We genotyped 4733G>A in the GCKD (German Chronic Kidney Disease) study (n = 4,673) by allele-specific polymerase chain reaction, performed minigene assays, identified proxy single nucleotide polymorphisms and used them to characterize its effect on CAD by survival analysis in UK Biobank (n = 440,234). Frequencies in ethnic groups were assessed in the 1000 Genomes Project. Results: The 4733G>A variant (38.2% carrier frequency) was found in most isoform sizes. It reduces allelic expression without abolishing protein production, lowers Lp(a) by 13.6 mg/dL (95% CI: 12.5-14.7; P < 0.0001) and is the strongest variance-explaining factor after the smaller isoform. Splicing of minigenes was modified. Compound heterozygosity (4.6% of the population) for 4733G>A and 4925G>A, another KIV-2 splicing mutation, reduces Lp(a) by 31.8 mg/dL and most importantly narrows the interquartile range by 9-fold (from 42.1 to 4.6 mg/dL) when compared to the wild type. In UK Biobank 4733G>A alone and compound heterozygosity with 4925G>A reduced HR for CAD by 9% (95% CI: 7%-11%) and 12% (95% CI: 7%-16%) (both P < 0.001). Frequencies in ethnicities differ notably. Conclusions: Functional variants in the previously inaccessible LPA KIV-2 region cooperate in determining Lp(a) variance and CAD risk. Even a moderate but lifelong genetic Lp(a) reduction translates to a noticeable CAD risk reduction.
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- 2021
12. Association of mitochondrial DNA copy number with metabolic syndrome and type 2 diabetes in 14 176 individuals
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Fazzini, Federica, Lamina, Claudia, Meiselbach, Heike, Schönherr, Sebastian, Forer, Lukas, Weissensteiner, Hansi, Pramstaller, Peter P., Eckardt, Kai-Uwe, Hicks, Andrew A., Kronenberg, Florian, GCKD Investigators, Raftopoulou, Athina, Schneider, Markus, Schiffer, Mario, Prokosch, Hans-Ulrich, Bärthlein, Barbara, Beck, Andreas, Kraska, Detlef, Reis, André, Ekici, Arif B., Becker, Susanne, Koller, Adriana, Becker-Grosspitsch, Dinah, Alberth-Schmidt, Ulrike, Hausknecht, Birgit, Weigel, Anke, Walz, Gerd, Köttgen, Anna, Schultheiß, Ulla T., Kotsis, Fruzsina, Meder, Simone, Mitsch, Erna, Fuchsberger, Christian, Reinhard, Ursula, Flöge, Jürgen, Saritas, Turgay, Schaeffner, Elke, Baid-Agrawal, Seema, Theisen, Kerstin, Haller, Hermann, Menne, Jan, Zeier, Martin, Sommerer, Claudia, Pattaro, Cristian, Theilinger, Johanna, Wolf, Gunter, Busch, Martin, Paul, Rainer, Sitter, Thomas, Wanner, Christoph, Krane, Vera, Börner-Klein, Antje, Bauer, Britta, Del Greco, Fabiola M., Raschenberger, Julia, Kollerits, Barbara, Oefner, Peter, Gronwald, Wolfram, Schmid, Matthias, Nadal, Jennifer, Döttelmayer, Patricia, Fendt, Liane, and Fritz, Josef
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Male ,0301 basic medicine ,medicine.medical_specialty ,Mitochondrial DNA ,DNA Copy Number Variations ,chronic kidney disease, diabetes, metabolic syndrome, mitochondrial DNA copy number ,610 Medizin ,Type 2 diabetes ,030204 cardiovascular system & hematology ,Mitochondrion ,DNA, Mitochondrial ,Body Mass Index ,03 medical and health sciences ,0302 clinical medicine ,Internal medicine ,Diabetes mellitus ,Internal Medicine ,Humans ,Medicine ,Prospective Studies ,Triglycerides ,Aged ,Metabolic Syndrome ,ddc:610 ,diabetes ,business.industry ,Original Articles ,Middle Aged ,medicine.disease ,Obesity ,mitochondrial DNA copy number ,Cross-Sectional Studies ,030104 developmental biology ,Endocrinology ,Diabetes Mellitus, Type 2 ,Original Article ,Female ,Waist Circumference ,Metabolic syndrome ,business ,Body mass index ,chronic kidney disease ,Kidney disease - Abstract
Journal of internal medicine 290(1), 190-202 (2021). doi:10.1111/joim.13242, Published by Wiley-Blackwell, Oxford [u.a.]
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- 2021
13. Author Correction: Rare genetic variants affecting urine metabolite levels link population variation to inborn errors of metabolism
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Peter J. Oefner, Yurong Cheng, Ines Thiele, Ute Spiekerkoetter, Kai-Uwe Eckardt, Daniel F. Freitag, Miriam Schmidts, Gckd Investigators, Yong Li, Peggy Sekula, Johannes Hertel, Florian Kronenberg, Anna Köttgen, Pascal Schlosser, and Johanna Mielke
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Genetics ,Multidisciplinary ,Metabolite ,Science ,Population variation ,Genetic variants ,General Physics and Astronomy ,Genome-wide association study ,General Chemistry ,Metabolism ,Urine ,Biology ,General Biochemistry, Genetics and Molecular Biology ,chemistry.chemical_compound ,chemistry - Published
- 2021
14. Mitochondrial DNA copy number is associated with mortality and infections in a large cohort of patients with chronic kidney disease
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Fazzini, Federica, Lamina, Claudia, Eckardt, Kai-Uwe, Köttgen, Anna, Kronenberg, Florian, GCKD Investigators, Meiselbach, Heike, Schneider, Markus, Dienemann, Thomas, Prokosch, Hans-Ulrich, Bärthlein, Barbara, Fendt, Liane, Beck, Andreas, Ganslandt, Thomas, Reis, André, Ekici, Arif B., Avendaño, Susanne, Becker-Grosspitsch, Dinah, Alberth-Schmidt, Ulrike, Hausknecht, Birgit, Zitzmann, Rita, Weigel, Anke, Schultheiss, Ulla T., Walz, Gerd, Schultheiß, Ulla, Kotsis, Fruzsina, Meder, Simone, Mitsch, Erna, Reinhard, Ursula, Flöge, Jürgen, Schlieper, Georg, Saritas, Turgay, Ernst, Sabine, Beaujean, Nicole, Schaeffner, Elke, Baid-Agrawal, Seema, Theisen, Kerstin, Haller, Hermann, Menne, Jan, Zeier, Martin, Sommerer, Claudia, Woitke, Rebecca, Hicks, Andrew A., Wolf, Gunter, Busch, Martin, Fuß, Rainer, Sitter, Thomas, Blank, Claudia, Wanner, Christoph, Krane, Vera, Börner-Klein, Antje, Bauer, Britta, Raschenberger, Julia, Kollerits, Barbara, Forer, Lukas, Schönherr, Sebastian, Weissensteiner, Hansi, Oefner, Peter, Gronwald, Wolfram, Zacharias, Helena, Schmid, Matthias, and Nadal, Jennifer
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Male ,DNA Copy Number Variations ,Kaplan-Meier Estimate ,Middle Aged ,Infections ,Prognosis ,DNA, Mitochondrial ,Mitochondria ,Hospitalization ,Oxidative Stress ,Cardiovascular Diseases ,Risk Factors ,Cause of Death ,Germany ,Prevalence ,Humans ,Female ,Prospective Studies ,Renal Insufficiency, Chronic ,Aged ,Follow-Up Studies ,Proportional Hazards Models - Abstract
Kidney international 96(2), 480-488 (2019). doi:10.1016/j.kint.2019.04.021, Published by Elsevier, New York, NY
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- 2019
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15. Rare genetic variants affecting urine metabolite levels link population variation to inborn errors of metabolism.
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Cheng, Yurong, Schlosser, Pascal, Hertel, Johannes, Sekula, Peggy, Oefner, Peter J., Spiekerkoetter, Ute, Mielke, Johanna, Freitag, Daniel F., Schmidts, Miriam, GCKD Investigators, Kronenberg, Florian, Eckardt, Kai-Uwe, Thiele, Ines, Li, Yong, and Köttgen, Anna
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INBORN errors of metabolism ,GENES ,POPULATION genetics ,GENE knockout ,METABOLIC disorders ,AMINO acid metabolism ,URINE - Abstract
Metabolite levels in urine may provide insights into genetic mechanisms shaping their related pathways. We therefore investigate the cumulative contribution of rare, exonic genetic variants on urine levels of 1487 metabolites and 53,714 metabolite ratios among 4864 GCKD study participants. Here we report the detection of 128 significant associations involving 30 unique genes, 16 of which are known to underlie inborn errors of metabolism. The 30 genes are strongly enriched for shared expression in liver and kidney (odds ratio = 65, p-FDR = 3e−7), with hepatocytes and proximal tubule cells as driving cell types. Use of UK Biobank whole-exome sequencing data links genes to diseases connected to the identified metabolites. In silico constraint-based modeling of gene knockouts in a virtual whole-body, organ-resolved metabolic human correctly predicts the observed direction of metabolite changes, highlighting the potential of linking population genetics to modeling. Our study implicates candidate variants and genes for inborn errors of metabolism. Metabolites are indicators of health and disease; genetic studies can reveal variants influencing their levels. Here, the authors investigate the contribution of rare, exonic variants on the levels of urine metabolites and generate predictions on metabolic consequences underlying metabolic disease. [ABSTRACT FROM AUTHOR]
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- 2021
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16. Heart failure in a cohort of patients with chronic kidney disease: the GCKD study
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Beck, Hanna, Titze, Stephanie I., Hübner, Silvia, Busch, Martin, Schlieper, Georg Rainer, Schultheiss, Ulla T., Wanner, Christoph, Kronenberg, Florian, Krane, Vera, Eckardt, Kai-Uwe, Köttgen, Anna, GCKD Investigators, Titze, Stephanie, Prokosch, Hans-Ulrich, Bärthlein, Barbara, Reis, André, Ekici, Arif B., Gefeller, Olaf, Hilgers, Karl F., Avendaño, Susanne, Becker-Grosspitsch, Dinah, Hauck, Nina, Seuchter, Susanne A., Hausknecht, Birgit, Rittmeier, Marion, Weigel, Anke, Beck, Andreas, Ganslandt, Thomas, Knispel, Sabine, Dressel, Thomas, Malzer, Martina, Flöge, Jürgen, Eitner, Frank, Findeisen, Katharina, Arweiler, Elfriede Christel, Ernst, Sabine, Unger, Mario, Lipski, Stefan, Schaeffner, Elke, Baid-Agrawal, Seema, Petzold, Kerstin, Schindler, Ralf, Schultheiss, Ulla, Meder, Simone, Mitsch, Erna, Reinhard, Ursula, Walz, Gerd, Haller, Hermann, Lorenzen, Johan, Kielstein, Jan T., Otto, Petra, Sommerer, Claudia, Föllinger, Claudia, Zeier, Martin, Wolf, Gunter, Paul, Katharina, Dittrich, Lisett, Sitter, Thomas, Hilge, Robert, Blank, Claudia, Schmiedeke, Daniel, Toncar, Sebastian, Cavitt, Daniela, Schönowsky, Karina, Börner-Klein, Antje, Raschenberger, Julia, Kollerits, Barbara, Forer, Lukas, Schönherr, Sebastian, Weißensteiner, Hansi, Oefner, Peter, Gronwald, Wolfram, Zacharias, Helena, Schmid, Matthias, and GCKD Investigators
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medicine.medical_specialty ,Anemia ,610 Medizin ,Renal function ,lcsh:Medicine ,Medizinische Fakultät ,Internal medicine ,Epidemiology ,Medicine ,ddc:610 ,Risk factor ,Prospective cohort study ,lcsh:Science ,Multidisciplinary ,business.industry ,lcsh:R ,medicine.disease ,Endocrinology ,Heart failure ,Cohort ,lcsh:Q ,business ,Research Article ,Kidney disease - Abstract
PLoS one 10(4), e0122552 (2015). doi:10.1371/journal.pone.0122552, Published by PLoS, Lawrence, Kan.
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- 2015
17. Author Correction: Rare genetic variants affecting urine metabolite levels link population variation to inborn errors of metabolism.
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Cheng, Yurong, Schlosser, Pascal, Hertel, Johannes, Sekula, Peggy, Oefner, Peter J., Spiekerkoetter, Ute, Mielke, Johanna, Freitag, Daniel F., Schmidts, Miriam, GCKD Investigators, Kronenberg, Florian, Eckardt, Kai-Uwe, Thiele, Ines, Li, Yong, and Köttgen, Anna
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INBORN errors of metabolism ,GENETIC variation ,URINE - Abstract
The original version of the Supplementary Data associated with this Article included two incorrect column labels in Supplementary Data 3 and 6 files. The HTML has been updated to include a corrected version of Supplementary Data 3 and 6; the original version of Supplementary Data 3 and 6 with the incorrectly labelled column headers can be found as Supplementary Information associated with this Correction. [Extracted from the article]
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- 2021
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