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102. Clinical Characteristics and Treatment Patterns of Children and Adults With IgA Nephropathy or IgA Vasculitis: Findings From the CureGN Study

Author

Selewski, David T., primary, Ambruzs, Josephine M., additional, Appel, Gerald B., additional, Bomback, Andrew S., additional, Matar, Raed Bou, additional, Cai, Yi, additional, Cattran, Daniel C., additional, Chishti, Aftab S., additional, D'Agati, Vivette D., additional, D'Alessandri-Silva, Cynthia J., additional, Gbadegesin, Rasheed A., additional, Hogan, Jonathan J., additional, Iragorri, Sandra, additional, Jennette, J. Charles, additional, Julian, Bruce A., additional, Khalid, Myda, additional, Lafayette, Richard A., additional, Liapis, Helen, additional, Lugani, Francesca, additional, Mansfield, Sarah A., additional, Mason, Sherene, additional, Nachman, Patrick H., additional, Nast, Cynthia C., additional, Nester, Carla M., additional, Noone, Damien G., additional, Novak, Jan, additional, O'Shaughnessy, Michelle M., additional, Reich, Heather N., additional, Rheault, Michelle N., additional, Rizk, Dana V., additional, Saha, Manish K., additional, Sanghani, Neil S., additional, Sperati, C. John, additional, Sreedharan, Rajasree, additional, Srivastava, Tarak, additional, Swiatecka-Urban, Agnieszka, additional, Twombley, Katherine, additional, Vasylyeva, Tetyana L., additional, Weaver, Donald J., additional, Yin, Hong, additional, Zee, Jarcy, additional, Falk, Ronald J., additional, Gharavi, Ali G., additional, Gillespie, Brenda W., additional, Gipson, Debbie S., additional, Greenbaum, Larry A., additional, Holzman, Lawrence B., additional, Kretzler, Matthias, additional, Robinson, Bruce M., additional, Smoyer, William E., additional, Flessner, Michael, additional, Guay-Woodford, Lisa M., additional, Kiryluk, Krzysztof, additional, Gharavi, Ali, additional, Ahn, Wooin, additional, Avasare, Rupali S., additional, Babayev, Revekka, additional, Batal, Ibrahim, additional, Brown, Eric, additional, Campenot, Eric S., additional, Canetta, Pietro, additional, Chan, Brenda, additional, D’Agati, Vivette D., additional, Fernandez, Hilda, additional, Foroncewicz, Bartosz, additional, Ghiggeri, Gian Marco, additional, Hines, William H., additional, Jain, Namrata G., additional, Lin, Fangming, additional, Marasa, Maddalena, additional, Markowitz, Glen, additional, Mohan, Sumit, additional, Mucha, Krzysztof, additional, Nickolas, Thomas L., additional, Radhakrishnan, Jai, additional, Rao, Maya K., additional, Regunathan-Shenk, Renu, additional, Sanna-Cherchi, Simone, additional, Santoriello, Dominick, additional, Stokes, Michael B., additional, Yu, Natalie, additional, Valeri, Anthony M., additional, Zviti, Ronald, additional, Al-Uzri, Amira, additional, Ashoor, Isa, additional, Aviles, Diego, additional, Baracco, Rossana, additional, Barcia, John, additional, Bartosh, Sharon, additional, Belsha, Craig, additional, Braun, Michael C., additional, Chishti, Aftab, additional, Claes, Donna, additional, Cramer, Carl, additional, Davis, Keefe, additional, Erkan, Elif, additional, Feig, Daniel, additional, Freundlich, Michael, additional, Hanna, Melisha, additional, Hidalgo, Guillermo, additional, Jain, Amrish, additional, Kallash, Mahmoud, additional, Lane, Jerome C., additional, Mahan, John, additional, Mathews, Nisha, additional, Nester, Carla, additional, Pan, Cynthia, additional, Patel, Hiren, additional, Revell, Adelaide, additional, Steinke, Julia, additional, Wenderfer, Scott E., additional, Wong, Craig S., additional, Falk, Ronald, additional, Cook, William, additional, Derebail, Vimal, additional, Fogo, Agnes, additional, Gasim, Adil, additional, Gehr, Todd, additional, Harris, Raymond, additional, Kidd, Jason, additional, Laurin, Louis-Philippe, additional, Pendergraft, Will, additional, Pichette, Vincent, additional, Powell, Thomas Brian, additional, Renfrow, Matthew B., additional, Royal, Virginie, additional, Adler, Sharon, additional, Alpers, Charles, additional, Brown, Elizabeth, additional, Cattran, Daniel, additional, Choi, Michael, additional, Dell, Katherine M., additional, Dukkipati, Ram, additional, Fervenza, Fernando C., additional, Fornoni, Alessia, additional, Gadegbeku, Crystal, additional, Gipson, Patrick, additional, Hasely, Leah, additional, Hingorani, Sangeeta, additional, Hladunewich, Michelle A., additional, Hogan, Jonathan, additional, Jefferson, J. Ashley, additional, Jhaveri, Kenar, additional, Johnstone, Duncan B., additional, Kaskel, Frederick, additional, Kogan, Amy, additional, Kopp, Jeffrey, additional, Lemley, Kevin V., additional, Dieguez, Laura Malaga-, additional, Meyers, Kevin, additional, Neu, Alicia, additional, O’Shaughnessy, Michelle Marie, additional, O’Toole, John F., additional, Parekh, Rulan, additional, Reich, Heather, additional, Reidy, Kimberly, additional, Rondon, Helbert, additional, Sambandam, Kamalanathan K., additional, Sedor, John R., additional, Selewski, David T., additional, Sethna, Christine B., additional, Schelling, Jeffrey, additional, Swiatecka-Urban, Agnes, additional, Trachtman, Howard, additional, Tuttle, Katherine R., additional, Weisstuch, Joseph, additional, Zhdanova, Olga, additional, Gillespie, Brenda, additional, Barisoni, Laura, additional, Mansfield, Sarah, additional, Mariani, Laura, additional, and Wladkowski, Matthew, additional

Published
2018
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103. Redefining Nephrotic Syndrome in Molecular Terms: Outcome-associated molecular clusters and patient stratification with noninvasive surrogate biomarkers

Author

Mariani, Laura H., primary, Eddy, Sean, additional, Martini, Sebastian, additional, Eichinger, Felix, additional, Godfrey, Brad, additional, Nair, Viji, additional, Adler, Sharon G., additional, Appel, Gerry B., additional, Athavale, Ambarish, additional, Barisoni, Laura, additional, Brown, Elizabeth, additional, Cattran, Dan C., additional, Dell, Katherine M., additional, Derebail, Vimal, additional, Fervenza, Fernando C., additional, Fornoni, Alessia, additional, Gadegbeku, Crystal A., additional, Gibson, Keisha L., additional, Gipson, Deb, additional, Greenbaum, Lawrence A., additional, Hingorani, Sangeeta R., additional, Hlandunewich, Michelle A., additional, Hogan, John, additional, Holzman, Larry B., additional, Jefferson, J. Ashley, additional, Kaskel, Frederick J., additional, Kopp, Jeffrey B., additional, Lafayette, Richard A., additional, Lemley, Kevin V., additional, Lieske, John C., additional, Lin, Jen-Jar, additional, Myers, Kevin E., additional, Nachman, Patrick H., additional, Nast, Cindy C., additional, Neu, Alicia M., additional, Reich, Heather N., additional, Sambandam, Kamal, additional, Sedor, John R., additional, Sethna, Christine B., additional, Srivastava, Tarak, additional, Trachtman, Howard, additional, Tran, Cheryl, additional, Wang, Chia-shi, additional, and Kretzler, Matthias, additional

Published
2018
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104. An eQTL Landscape of Kidney Tissue in Human Nephrotic Syndrome

Author

Gillies, Christopher E., primary, Putler, Rosemary, additional, Menon, Rajasree, additional, Otto, Edgar, additional, Yasutake, Kalyn, additional, Nair, Viji, additional, Hoover, Paul, additional, Lieb, David, additional, Li, Shuqiang, additional, Eddy, Sean, additional, Fermin, Damian, additional, McNulty, Michelle T., additional, Hacohen, Nir, additional, Kiryluk, Krzysztof, additional, Kretzler, Matthias, additional, Wen, Xiaoquan, additional, Sampson, Matthew G., additional, Sedor, John, additional, Dell, Katherine, additional, Schachere, Marleen, additional, Lemley, Kevin, additional, Whitted, Lauren, additional, Srivastava, Tarak, additional, Haney, Connie, additional, Sethna, Christine, additional, Grammatikopoulos, Kalliopi, additional, Appel, Gerald, additional, Toledo, Michael, additional, Greenbaum, Laurence, additional, Wang, Chia-shi, additional, Lee, Brian, additional, Adler, Sharon, additional, Nast, Cynthia, additional, LaPage, Janine, additional, Athavale, Ambarish, additional, Neu, Alicia, additional, Boynton, Sara, additional, Fervenza, Fernando, additional, Hogan, Marie, additional, Lieske, John C., additional, Chernitskiy, Vladimir, additional, Kaskel, Frederick, additional, Kumar, Neelja, additional, Flynn, Patricia, additional, Kopp, Jeffrey, additional, Castro-Rubio, Eveleyn, additional, Blake, Jodi, additional, Trachtman, Howard, additional, Zhdanova, Olga, additional, Modersitzki, Frank, additional, Vento, Suzanne, additional, Lafayette, Richard, additional, Mehta, Kshama, additional, Gadegbeku, Crystal, additional, Johnstone, Duncan, additional, Cattran, Daniel, additional, Hladunewich, Michelle, additional, Reich, Heather, additional, Ling, Paul, additional, Romano, Martin, additional, Fornoni, Alessia, additional, Barisoni, Laura, additional, Bidot, Carlos, additional, Gipson, Debbie, additional, Williams, Amanda, additional, Pitter, Renee, additional, Nachman, Patrick, additional, Gibson, Keisha, additional, Grubbs, Sandra, additional, Froment, Anne, additional, Holzman, Lawrence, additional, Meyers, Kevin, additional, Kallem, Krishna, additional, Cerecino, Fumei, additional, Sambandam, Kamal, additional, Brown, Elizabeth, additional, Johnson, Natalie, additional, Jefferson, Ashley, additional, Hingorani, Sangeeta, additional, Tuttle, Kathleen, additional, Curtin, Laura, additional, Dismuke, S., additional, Cooper, Ann, additional, Freedman, Barry, additional, Lin, Jen Jar, additional, Gray, Stefanie, additional, Barisoni, Larua, additional, Gillespie, Brenda, additional, Mariani, Laura, additional, Song, Peter, additional, Troost, Johnathan, additional, Zee, Jarcy, additional, Herreshoff, Emily, additional, Kincaid, Colleen, additional, Lienczewski, Chrysta, additional, Mainieri, Tina, additional, Abbott, Kevin, additional, Roy, Cindy, additional, Urv, Tiina, additional, and Brooks, John, additional

Published
2018
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105. Gut Microbial Product Predicts Cardiovascular Risk in Chronic Kidney Disease Patients.

Author

Jadoon, Adil, Mathew, Anna V., Byun, Jaeman, Gadegbeku, Crystal A., Gipson, Debbie S., Afshinnia, Farsad, Pennathur, Subramaniam, Mathew, Anna V, Gadegbeku, Crystal A, Gipson, Debbie S, and for the Michigan Kidney Translational Core CPROBE Investigator Group

Subjects
LIQUID chromatography, CARDIOVASCULAR diseases, KIDNEY diseases, BLOOD plasma, GLOMERULAR filtration rate
Abstract

Background: The gut microbiota is altered in patients with chronic kidney disease (CKD), and cardiovascular risk increases with progressive CKD. This study examined the potential link between short chain fatty acids (SCFAs), which are produced by the gut microbiota, and cardiovascular outcomes in patients with CKD.Methods: SCFAs were measured using a targeted liquid chromatography-mass spectrometry platform in baseline plasma samples from 214 patients with CKD enrolled in the Clinical Phenotyping Resource and Biobank Core; 81 patients with coronary artery disease (CAD) and 133 without CAD were randomly assigned to training and validation subsets. The primary outcome was a history of CAD and the secondary outcome was a composite history of cardiovascular disease (CVD) at enrollment.Results: We found significantly higher levels of the SCFA valerate among patients with CAD as compared with patients without CAD in the training set (p < 0.001). The valerate concentrations were also significantly higher among subjects with composite outcomes of CVD compared to those without CVD (p = 0.006). These results were subsequently replicated in the validation set. Logistic regression analysis revealed a strong independent association between plasma valerate levels and CVD in both training and validation sets. When valerate was added to the base clinical model comprising of diabetes, hypertension, urinary protein-creatinine ratio, and estimated glomerular filtration rate, it increased the c-statistics for predicting CVD from 0.68 to 0.79 (p = 0.02) in the training set, an observation which was confirmed in the validation set. -Conclusion: This study provides evidence for alterations in gut-microbiota-derived SCFAs with advancing CKD, demonstrates the association of higher plasma valerate levels with pre-existing CVD, and reveals areas for future exploration of cardiovascular risk in patients with CKD. [ABSTRACT FROM AUTHOR]

Published
2018
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107. Growth Differentiation Factor–15 and Risk of CKD Progression

Author

Nair, Viji, primary, Robinson-Cohen, Cassianne, additional, Smith, Michelle R., additional, Bellovich, Keith A., additional, Bhat, Zeenat Yousuf, additional, Bobadilla, Maria, additional, Brosius, Frank, additional, de Boer, Ian H., additional, Essioux, Laurent, additional, Formentini, Ivan, additional, Gadegbeku, Crystal A., additional, Gipson, Debbie, additional, Hawkins, Jennifer, additional, Himmelfarb, Jonathan, additional, Kestenbaum, Bryan, additional, Kretzler, Matthias, additional, Magnone, Maria Chiara, additional, Perumal, Kalyani, additional, Steigerwalt, Susan, additional, Ju, Wenjun, additional, and Bansal, Nisha, additional

Published
2017
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108. Association Between Progression of Retinopathy and Concurrent Progression of Kidney Disease: Findings From the Chronic Renal Insufficiency Cohort (CRIC) Study.

Author

Grunwald, Juan E., Pistilli, Maxwell, Ying, Gui-Shuang, Daniel, Ebenezer, Maguire, Maureen, Xie, Dawei, Roy, Jason, Whittock-Martin, Revell, Parker Ostroff, Candace, Lo, Joan C., Townsend, Raymond R., Gadegbeku, Crystal A., Lash, James P., Fink, Jeffrey C., Rahman, Mahboob, Feldman, Harold I., Kusek, John W., and Chronic Renal Insufficiency Cohort Study Investigators

Published
2019
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109. Design of the Nephrotic Syndrome Study Network (NEPTUNE) to evaluate primary glomerular nephropathy by a multidisciplinary approach

Author

Hogan, Marie C., Hladunewich, Michelle, Nast, Cynthia C., Meyers, Kevin E.C., Sampson, Matthew G., Appel, Gerald B., Hingorani, Sangeeta R., Nachman, Patrick H., Lienczewski, Chrysta C., Dell, Katherine M., Greenbaum, Larry A., Gipson, Debbie S., Hernandez, Joel D., Choi, Michael J., Nelson, Peter J., Lemley, Kevin V., Kopp, Jeffrey B., Holzman, Lawrence B., Adler, Sharon G., Fervenza, Fernando C., Kaskel, Frederick J., Barisoni, Laura, Cattran, Daniel C., Hogan, Susan L., Neu, Alicia M., Hewitt, Stephen M., Gibson, Keisha L., Gadegbeku, Crystal A., Song, Peter X.K., Lieske, John C., Ojo, Akinlolu O., and Contreras, Gabriel

Abstract

The Nephrotic Syndrome Study Network (NEPTUNE) is a North American multi-center collaborative consortium established to develop a translational research infrastructure for Nephrotic Syndrome. This includes a longitudinal observational cohort study, a pilot and ancillary studies program, a training program, and a patient contact registry. NEPTUNE will enroll 450 adults and children with minimal change disease, focal segmental glomerulosclerosis and membranous nephropathy for detailed clinical, histopathologic, and molecular phenotyping at the time of clinically-indicated renal biopsy. Initial visits will include an extensive clinical history, physical examination, collection of urine, blood and renal tissue samples, and assessments of quality of life and patient-reported outcomes. Follow-up history, physical measures, urine and blood samples, and questionnaires will be obtained every 4 months in the first year and bi-annually, thereafter. Molecular profiles and gene expression data will be linked to phenotypic, genetic, and digitalized histologic data for comprehensive analyses using systems biology approaches. Analytical strategies were designed to transform descriptive information to mechanistic disease classification for Nephrotic Syndrome and to identify clinical, histological, and genomic disease predictors. Thus, understanding the complexity of the disease pathogenesis will guide further investigation for targeted therapeutic strategies.

Published
2013
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110. Retinopathy and Chronic Kidney Disease in the Chronic Renal Insufficiency Cohort Study (CRIC)

Author

Grunwald, Juan E., Alexander, Judith, Ying, Gui-Shuang, Maguire, Maureen, Daniel, Ebenezer, Whittock-Martin, Revell, Parker, Candace, McWilliams, Kathleen, Lo, Joan C., Go, Alan, Townsend, Raymond, Gadegbeku, Crystal A., Lash, James P., Fink, Jeffrey C., Rahman, Mahboob, Feldman, Harold, Kusek, John W., Xie, Dawei, and Jaar, Bernard G.

Subjects
Male, Diabetic Retinopathy, Reproducibility of Results, Retinal Vessels, Blood Pressure, Hypertensive Retinopathy, Middle Aged, Severity of Illness Index, Article, Proteinuria, Cross-Sectional Studies, Risk Factors, Diabetes Mellitus, Photography, Humans, Female, Renal Insufficiency, Chronic, Follow-Up Studies, Glomerular Filtration Rate
Abstract

To investigate the association between retinopathy and chronic kidney disease.In this observational, cross-sectional study, 2605 patients of the Chronic Renal Insufficiency Cohort (CRIC) study, a multicenter study of chronic kidney disease, were offered participation. Nonmydriatic fundus photographs of the disc and macula in both eyes were obtained in 1936 of these subjects. The photographs were reviewed in a masked fashion at a central photograph reading center using standard protocols. Presence and severity of retinopathy (diabetic, hypertensive, or other) and vessel diameter caliber were assessed by trained graders and a retinal specialist using protocols developed for large epidemiologic studies. Kidney function measurements and information on traditional and nontraditional risk factors for decreased kidney function were obtained from the CRIC study.Greater severity of retinopathy was associated with lower estimated glomerular filtration rate after adjustment for traditional and nontraditional risk factors. The presence of vascular abnormalities usually associated with hypertension was also associated with lower estimated glomerular filtration rate. We found no strong direct relationship between estimated glomerular filtration rate and average arteriolar or venular calibers.Our findings show a strong association between severity of retinopathy and its features and level of kidney function after adjustment for traditional and nontraditional risk factors for chronic kidney disease, suggesting that retinovascular pathology reflects renal disease.

Published
2012

112. Complete Remission in the Nephrotic Syndrome Study Network

Author

Gipson, Debbie S., primary, Troost, Jonathan P., additional, Lafayette, Richard A., additional, Hladunewich, Michelle A., additional, Trachtman, Howard, additional, Gadegbeku, Crystal A., additional, Sedor, John R., additional, Holzman, Lawrence B., additional, Moxey-Mims, Marva M., additional, Perumal, Kalyani, additional, Kaskel, Frederick J., additional, Nelson, Peter J., additional, Tuttle, Katherine R., additional, Bagnasco, Serena M., additional, Hogan, Marie C., additional, Dell, Katherine M., additional, Appel, Gerald B., additional, Lieske, John C., additional, Ilori, Titilayo O., additional, Sethna, Christine B., additional, Fervenza, Fernando C., additional, Hogan, Susan L., additional, Nachman, Patrick H., additional, Rosenberg, Avi Z., additional, Greenbaum, Larry A., additional, Meyers, Kevin E.C., additional, Hewitt, Stephen M., additional, Choi, Michael J., additional, Kopp, Jeffrey B., additional, Zhdanova, Olga, additional, Hodgin, Jeffrey B., additional, Johnstone, Duncan B., additional, Adler, Sharon G., additional, Avila-Casado, Carmen, additional, Neu, Alicia M., additional, Hingorani, Sangeeta R., additional, Lemley, Kevin V., additional, Nast, Cynthia C., additional, Brady, Tammy M., additional, Barisoni-Thomas, Laura, additional, Fornoni, Alessia, additional, Jennette, J. Charles, additional, Cattran, Daniel C., additional, Palmer, Matthew B., additional, Gibson, Keisha L., additional, Reich, Heather N., additional, Mokrzycki, Michele H., additional, Sambandam, Kamalanathan K., additional, Zilleruelo, Gaston E., additional, Licht, Christoph, additional, Sampson, Matthew G., additional, Song, Peter, additional, Mariani, Laura H., additional, and Kretzler, Matthias, additional

Published
2015
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113. Higher plasma CXCL12 levels predict incident myocardial infarction and death in chronic kidney disease: findings from the Chronic Renal Insufficiency Cohort study.

Author

Mehta, Nehal N, Mehta, Nehal N, Matthews, Gregory J, Krishnamoorthy, Parasuram, Shah, Rhia, McLaughlin, Catherine, Patel, Parth, Budoff, Matthew, Chen, Jing, Wolman, Melanie, Go, Alan, He, Jiang, Kanetsky, Peter A, Master, Stephen R, Rader, Daniel J, Raj, Dominic, Gadegbeku, Crystal A, Shah, Rachana, Schreiber, Marty, Fischer, Michael J, Townsend, Raymond R, Kusek, John, Feldman, Harold I, Foulkes, Andrea S, Reilly, Muredach P, Chronic Renal Insufficiency Cohort (CRIC) Study Investigators, Mehta, Nehal N, Mehta, Nehal N, Matthews, Gregory J, Krishnamoorthy, Parasuram, Shah, Rhia, McLaughlin, Catherine, Patel, Parth, Budoff, Matthew, Chen, Jing, Wolman, Melanie, Go, Alan, He, Jiang, Kanetsky, Peter A, Master, Stephen R, Rader, Daniel J, Raj, Dominic, Gadegbeku, Crystal A, Shah, Rachana, Schreiber, Marty, Fischer, Michael J, Townsend, Raymond R, Kusek, John, Feldman, Harold I, Foulkes, Andrea S, Reilly, Muredach P, and Chronic Renal Insufficiency Cohort (CRIC) Study Investigators

Abstract

AimsGenome-wide association studies revealed an association between a locus at 10q11, downstream from CXCL12, and myocardial infarction (MI). However, the relationship among plasma CXCL12, cardiovascular disease (CVD) risk factors, incident MI, and death is unknown.Methods and resultsWe analysed study-entry plasma CXCL12 levels in 3687 participants of the Chronic Renal Insufficiency Cohort (CRIC) Study, a prospective study of cardiovascular and kidney outcomes in chronic kidney disease (CKD) patients. Mean follow-up was 6 years for incident MI or death. Plasma CXCL12 levels were positively associated with several cardiovascular risk factors (age, hypertension, diabetes, hypercholesterolaemia), lower estimated glomerular filtration rate (eGFR), and higher inflammatory cytokine levels (P < 0.05). In fully adjusted models, higher study-entry CXCL12 was associated with increased odds of prevalent CVD (OR 1.23; 95% confidence interval 1.14, 1.33, P < 0.001) for one standard deviation (SD) increase in CXCL12. Similarly, one SD higher CXCL12 increased the hazard of incident MI (1.26; 1.09,1.45, P < 0.001), death (1.20; 1.09,1.33, P < 0.001), and combined MI/death (1.23; 1.13-1.34, P < 0.001) adjusting for demographic factors, known CVD risk factors, and inflammatory markers and remained significant for MI (1.19; 1.03,1.39, P = 0.01) and the combined MI/death (1.13; 1.03,1.24, P = 0.01) after further controlling for eGFR and urinary albumin:creatinine ratio.ConclusionsIn CKD, higher plasma CXCL12 was associated with CVD risk factors and prevalent CVD as well as the hazard of incident MI and death. Further studies are required to establish if plasma CXCL12 reflect causal actions at the vessel wall and is a tool for genomic and therapeutic trials.

Published
2014

114. Myeloperoxidase Levels and Its Product 3-Chlorotyrosine Predict Chronic Kidney Disease Severity and Associated Coronary Artery Disease.

Author

afshinnia, Farsad, Zeng, Lixia, Byun, Jaeman, Gadegbeku, Crystal a., Magnone, Maria Chiara, Whatling, Carl, Valastro, Barbara, Kretzler, Matthias, Pennathur, Subramaniam, and Michigan Kidney Translational Core CPROBE Investigator Group

Subjects
KIDNEY diseases, MYELOPEROXIDASE, CORONARY arteries, BLOOD proteins, MASS spectrometry, CHRONIC kidney failure complications, TYROSINE metabolism, CHRONIC kidney failure, COMPARATIVE studies, CORONARY disease, ENZYME-linked immunosorbent assay, RESEARCH methodology, MEDICAL cooperation, OXIDOREDUCTASES, RESEARCH, RESEARCH funding, TYROSINE, OXIDATIVE stress, EVALUATION research, SEVERITY of illness index
Abstract

Background: The role of myeloperoxidase in chronic kidney disease (CKD) and its association with coronary artery disease (CAD) is controversial. In this study, we compared myeloperoxidase and protein-bound 3-chlorotyrosine (ClY) levels in subjects with varying degrees of CKD and tested their associations with CAD.Methods: From Clinical Phenotyping Resource and Biobank Core, 111 patients were selected from CKD stages 1 to 5. Plasma myeloperoxidase level was measured using enzyme-linked-immunosorbent assay. Plasma protein-bound 3-ClY, a specific product of hypochlorous acid generated by myeloperoxidase was measured by liquid chromatography mass spectrometry.Results: We selected 29, 20, 24, 22, and 16 patients from stages 1 to 5 CKD, respectively. In a sex-adjusted general linear model, mean ± SD of myeloperoxidase levels decreased from 18.1 ± 12.3 pmol in stage 1 to 10.9 ± 4.7 pmol in stage 5 (p = 0.011). In patients with and without CAD, the levels were 19.1 ± 10.1 and 14.8 ± 8.7 pmol (p = 0.036). There was an increase in 3-ClY mean from 0.81 ± 0.36 mmol/mol-tyrosine in stage 1 to 1.42 ± 0.41 mmol/mol-tyrosine in stage 5 (p < 0.001). The mean 3-ClY levels in patients with and without CAD were 1.25 ± 0.44 and 1.04 ± 0.42 mmol/mol-tyrosine (p = 0.023), respectively. C-statistic of ClY when added to myeloperoxidase level to predict CKD stage 5 was 0.86, compared to 0.79 for the myeloperoxidase level alone (p = 0.0097).Conclusion: The myeloperoxidase levels decrease from stages 1 to 5, whereas activity increases. In contrast, both myeloperoxidase and ClY levels rise in the presence of CAD at various stages of CKD. Measuring both plasma myeloperoxidase and 3-CLY levels provide added value to determine the burden of myeloperoxidase-mediated oxidative stress. [ABSTRACT FROM AUTHOR]

Published
2017
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115. Integrative Biology Identifies Shared Transcriptional Networks in CKD

Author

Martini, Sebastian, primary, Nair, Viji, additional, Keller, Benjamin J., additional, Eichinger, Felix, additional, Hawkins, Jennifer J., additional, Randolph, Ann, additional, Böger, Carsten A., additional, Gadegbeku, Crystal A., additional, Fox, Caroline S., additional, Cohen, Clemens D., additional, and Kretzler, Matthias, additional

Published
2014
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116. Retinopathy and Progression of CKD

Author

Grunwald, Juan E., primary, Pistilli, Maxwell, additional, Ying, Gui-Shuang, additional, Daniel, Ebenezer, additional, Maguire, Maureen G., additional, Xie, Dawei, additional, Whittock-Martin, Revell, additional, Parker Ostroff, Candace, additional, Lo, Joan C., additional, Townsend, Raymond R., additional, Gadegbeku, Crystal A., additional, Lash, James P., additional, Fink, Jeffrey C., additional, Rahman, Mahboob, additional, Feldman, Harold I., additional, and Kusek, John W., additional

Published
2014
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117. Candidate Gene Association Study of Coronary Artery Calcification in Chronic Kidney Disease

Author

Ferguson, Jane F., primary, Matthews, Gregory J., additional, Townsend, Raymond R., additional, Raj, Dominic S., additional, Kanetsky, Peter A., additional, Budoff, Matthew, additional, Fischer, Michael J., additional, Rosas, Sylvia E., additional, Kanthety, Radhika, additional, Rahman, Mahboob, additional, Master, Stephen R., additional, Qasim, Atif, additional, Li, Mingyao, additional, Mehta, Nehal N., additional, Shen, Haiqing, additional, Mitchell, Braxton D., additional, O'Connell, Jeffrey R., additional, Shuldiner, Alan R., additional, Ho, Weang Kee, additional, Young, Robin, additional, Rasheed, Asif, additional, Danesh, John, additional, He, Jiang, additional, Kusek, John W., additional, Ojo, Akinlolu O., additional, Flack, John, additional, Go, Alan S., additional, Gadegbeku, Crystal A., additional, Wright, Jackson T., additional, Saleheen, Danish, additional, Feldman, Harold I., additional, Rader, Daniel J., additional, Foulkes, Andrea S., additional, and Reilly, Muredach P., additional

Published
2013
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118. FGF23 Modifies the Relationship Between Vitamin D and Cardiac Remodeling

Author

Ky, Bonnie, primary, Shults, Justine, additional, Keane, Martin G., additional, Sutton, Martin St. John, additional, Wolf, Myles, additional, Feldman, Harold I., additional, Reese, Peter P., additional, Anderson, Cheryl A., additional, Townsend, Raymond R., additional, Deo, Rajat, additional, Lo, Joan, additional, Gadegbeku, Crystal, additional, Carlow, Dean, additional, Sulik, Michael J., additional, and Leonard, Mary B., additional

Published
2013
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120. A Longitudinal Study of Left Ventricular Function and Structure from CKD to ESRD

Author

Bansal, Nisha, primary, Keane, Martin, additional, Delafontaine, Patrice, additional, Dries, Daniel, additional, Foster, Elyse, additional, Gadegbeku, Crystal A., additional, Go, Alan S., additional, Hamm, L. Lee, additional, Kusek, John W., additional, Ojo, Akinlolu O., additional, Rahman, Mahboob, additional, Tao, Kaixiang, additional, Wright, Jackson T., additional, Xie, Dawei, additional, and Hsu,, Chi-yuan, additional

Published
2013
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121. Kidney Function Can Improve in Patients with Hypertensive CKD

Author

Hu, Bo, primary, Gadegbeku, Crystal, additional, Lipkowitz, Michael S., additional, Rostand, Stephen, additional, Lewis, Julia, additional, Wright, Jackson T., additional, Appel, Lawrence J., additional, Greene, Tom, additional, Gassman, Jennifer, additional, and Astor, Brad C., additional

Published
2012
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122. Pathogenic Cycle Between the Endogenous Nitric Oxide Synthase Inhibitor Asymmetrical Dimethylarginine and the Leukocyte-Derived Hemoprotein Myeloperoxidase

Author

von Leitner, Eike-Christin, primary, Klinke, Anna, additional, Atzler, Dorothee, additional, Slocum, Jessica L., additional, Lund, Natalie, additional, Kielstein, Jan T., additional, Maas, Renke, additional, Schmidt-Haupt, Robin, additional, Pekarova, Michaela, additional, Hellwinkel, Olaf, additional, Tsikas, Dimitrios, additional, D'Alecy, Louis G., additional, Lau, Denise, additional, Willems, Stephan, additional, Kubala, Lukas, additional, Ehmke, Heimo, additional, Meinertz, Thomas, additional, Blankenberg, Stefan, additional, Schwedhelm, Edzard, additional, Gadegbeku, Crystal A., additional, Böger, Rainer H., additional, Baldus, Stephan, additional, and Sydow, Karsten, additional

Published
2011
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123. Correlates of Osteoprotegerin and Association with Aortic Pulse Wave Velocity in Patients with Chronic Kidney Disease

Author

Scialla, Julia J., primary, Leonard, Mary B., additional, Townsend, Raymond R., additional, Appel, Lawrence, additional, Wolf, Myles, additional, Budoff, Matt J., additional, Chen, Jing, additional, Lustigova, Eva, additional, Gadegbeku, Crystal A., additional, Glenn, Melanie, additional, Hanish, Asaf, additional, Raj, Dominic, additional, Rosas, Sylvia E., additional, Seliger, Stephen L., additional, Weir, Matthew R., additional, and Parekh, Rulan S., additional

Published
2011
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124. Central Pulse Pressure in Chronic Kidney Disease

Author

Townsend, Raymond R., primary, Chirinos, Julio A., additional, Parsa, Afshin, additional, Weir, Matthew A., additional, Sozio, Stephen M., additional, Lash, James P., additional, Chen, Jing, additional, Steigerwalt, Susan P., additional, Go, Alan S., additional, Hsu, Chi-yuan, additional, Rafey, Mohammed, additional, Wright, Jackson T., additional, Duckworth, Mark J., additional, Gadegbeku, Crystal A., additional, and Joffe, Marshall P., additional

Published
2010
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125. Prevalence of Ocular Fundus Pathology in Patients with Chronic Kidney Disease

Author

Grunwald, Juan E., primary, Alexander, Judith, additional, Maguire, Maureen, additional, Whittock, Revell, additional, Parker, Candace, additional, McWilliams, Kathleen, additional, Lo, Joan C., additional, Townsend, Raymond, additional, Gadegbeku, Crystal A., additional, Lash, James P., additional, Fink, Jeffrey C., additional, Rahman, Mahaboob, additional, Feldman, Harold, additional, Kusek, John, additional, and Ojo, Akinlolu, additional

Published
2010
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126. Aortic PWV in Chronic Kidney Disease: A CRIC Ancillary Study

Author

Townsend, Raymond R., primary, Wimmer, Neil J., additional, Chirinos, Julio A., additional, Parsa, Afshin, additional, Weir, Matthew, additional, Perumal, Kalyani, additional, Lash, James P., additional, Chen, Jing, additional, Steigerwalt, Susan P., additional, Flack, John, additional, Go, Alan S., additional, Rafey, Mohammed, additional, Rahman, Mahboob, additional, Sheridan, Angela, additional, Gadegbeku, Crystal A., additional, Robinson, Nancy A., additional, and Joffe, Marshall, additional

Published
2010
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127. Chronic Renal Insufficiency Cohort (CRIC) Study

Author

Lash, James P., primary, Go, Alan S., additional, Appel, Lawrence J., additional, He, Jiang, additional, Ojo, Akinlolu, additional, Rahman, Mahboob, additional, Townsend, Raymond R., additional, Xie, Dawei, additional, Cifelli, Denise, additional, Cohan, Janet, additional, Fink, Jeffrey C., additional, Fischer, Michael J., additional, Gadegbeku, Crystal, additional, Hamm, L. Lee, additional, Kusek, John W., additional, Landis, J. Richard, additional, Narva, Andrew, additional, Robinson, Nancy, additional, Teal, Valerie, additional, and Feldman, Harold I., additional

Published
2009
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130. 165

Author

Platel, Raylene, primary, Billecke, Scott, additional, Whitesall, Steven, additional, Perlman, Rachel L., additional, Jamerson, Kenneth A., additional, D’Alecy, Louis G., additional, and Gadegbeku, Crystal A., additional

Published
2007
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135. APOL1renal-risk variants associate with reduced cerebral white matter lesion volume and increased gray matter volume

Author

Freedman, Barry I., Gadegbeku, Crystal A., Bryan, R. Nick, Palmer, Nicholette D., Hicks, Pamela J., Ma, Lijun, Rocco, Michael V., Smith, S. Carrie, Xu, Jianzhao, Whitlow, Christopher T., Wagner, Benjamin C., Langefeld, Carl D., Hawfield, Amret T., Bates, Jeffrey T., Lerner, Alan J., Raj, Dominic S., Sadaghiani, Mohammad S., Toto, Robert D., Wright, Jackson T., Bowden, Donald W., Williamson, Jeff D., Sink, Kaycee M., Maldjian, Joseph A., Pajewski, Nicholas M., and Divers, Jasmin

Abstract

To assess apolipoprotein L1 gene (APOL1) renal-risk-variant effects on the brain, magnetic resonance imaging (MRI)-based cerebral volumes and cognitive function were assessed in 517 African American–Diabetes Heart Study (AA-DHS) Memory IN Diabetes (MIND) and 2568 hypertensive African American Systolic Blood Pressure Intervention Trial (SPRINT) participants without diabetes. Within these cohorts, 483 and 197 had cerebral MRI, respectively. AA-DHS participants were characterized as follows: 60.9% female, mean age of 58.6 years, diabetes duration 13.1 years, estimated glomerular filtration rate of 88.2 ml/min/1.73 m2, and a median spot urine albumin to creatinine ratio of 10.0 mg/g. In additive genetic models adjusting for age, sex, ancestry, scanner, intracranial volume, body mass index, hemoglobin A1c, statins, nephropathy, smoking, hypertension, and cardiovascular disease, APOL1renal-risk-variants were positively associated with gray matter volume (β = 3.4 × 10–3) and negatively associated with white matter lesion volume (β = –0.303) (an indicator of cerebral small vessel disease) and cerebrospinal fluid volume (β= –30707) (all significant), but not with white matter volume or cognitive function. Significant associations corresponding to adjusted effect sizes (β/SE) were observed with gray matter volume (0.16) and white matter lesion volume (–0.208), but not with cerebrospinal fluid volume (–0.251). Meta-analysis results with SPRINT Memory and Cognition in Decreased Hypertension (MIND) participants who had cerebral MRI were confirmatory. Thus, APOL1renal-risk-variants are associated with larger gray matter volume and lower white matter lesion volume suggesting lower intracranial small vessel disease.

Published
2016
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138. Physical Performance and Frailty in Chronic Kidney Disease.

Author

Reese, Peter P., Cappola, Anne R., Shults, Justine, Townsend, Raymond R., Gadegbeku, Crystal A., Anderson, Cheryl, Baker, Joshua F., Carlow, Dean, Sulik, Michael J., Lo, Joan C., Go, Alan S., Ky, Bonnie, Mariani, Laura, Feldman, Harold I., and Leonard, Mary B.

Abstract

Background: Poor physical performance and frailty are associated with elevated risks of death and disability. Chronic kidney disease (CKD) is also strongly associated with these outcomes. The risks of poor physical performance and frailty among CKD patients, however, are not well established. Methods: We measured the Short Physical Performance Battery (SPPB; a summary test of gait speed, chair raises and balance; range 0-12) and the five elements of frailty among 1,111 Chronic Renal Insufficiency Cohort participants. Adjusting for demographics and multiple comorbidities, we fit a linear regression model for the outcome of SPPB score and an ordinal logistic regression model for frailty status. Results: Median (interquartile range, IQR) age was 65 (57-71) years, median estimated glomerular filtration rate (eGFR) for non-dialysis patients was 49 (36-62) ml/min/1.73 m2, and median SPPB score was 9 (7-10). Seven percent of participants were frail and 43% were pre-frail. Compared with the SPPB score for eGFR >60 ml/min/1.73 m2, the SPPB was 0.51 points lower for eGFR 30-59; 0.61 points lower for eGFR 15-29, and 1.75 points lower for eGFR <15 (p < 0.01 for all comparisons). eGFR 30-59 (odds ratio, OR 1.45; p = 0.024), eGFR 15-29 (OR 2.02; p = 0.002) and eGFR <15 (OR 4.83; p < 0.001) were associated with worse frailty status compared with eGFR >60 ml/min/1.73 m2. Conclusions: CKD severity was associated with poor physical performance and frailty in a graded fashion. Future trials should determine if outcomes for CKD patients with frailty and poor physical performance are improved by targeted interventions. © 2013 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Published
2013
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139. Vitamin D and Subsequent Systolic Hypertension Among Women.

Author

Griffin, Flojaune C., Gadegbeku, Crystal A., and Sowers, MaryFran R.

Subjects
VITAMIN D deficiency, VITAMIN deficiency, HYPERTENSION in women, DISEASES in women, CAUCASIAN race, DISEASE risk factors
Abstract

BackgroundWe examined data from a cohort of Caucasian women for evidence of an association between serum vitamin D (25-hydroxyvitamin D (25(OH)D)) insufficiency and greater risk of systolic hypertension in the population-based longitudinal Michigan Bone Health and Metabolism Study (MBHMS).MethodsThe cohort includes 559 women aged 24-44 years in 1992; annual blood pressure (BP) measurements and data collection began in 1992 and is ongoing. A single-time serum 25(OH)D level was measured in 1993. Using logistic regression, vitamin D insufficiency (<80 nmol/l) was related to systolic hypertension (≥140 mm Hg) measures identified in 1993 and in 2007. Further, the relationship between vitamin D at baseline and the trajectory of systolic BP across the ensuing 14 years was assessed using longitudinal mixed modeling.ResultsVitamin D insufficiency was not significantly associated with concurrent systolic hypertension in 1993 (odds ratio (OR) 1.3; 95% confidence interval (CI) (0.32, 5.1)). However, vitamin D insufficiency was associated with increased risk of systolic hypertension in 2007 (OR 3.0; 95% CI (1.01, 8.7)) after adjusting for age, body fat percentage, antihypertensive medication use, and smoking. Baseline vitamin D status was not associated with rate of BP change over the 14-year period.ConclusionsConsistent with previous animal and human studies, we found a single-time measure of vitamin D among young adult women was associated with systolic hypertension 14 years later. These prospective results suggest the need for further study of the role vitamin D insufficiency in early adulthood as a risk factor in subsequent hypertension among women.American Journal of Hypertension (2011). doi:10.1038/ajh.2010.226 [ABSTRACT FROM AUTHOR]

Published
2011
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141. Aortic Pulse Pressure Is Associated With Carotid IMT in Chronic Kidney Disease: Report From Chronic Renal Insufficiency Cohort.

Author

DeLoach, Stephanie S., Appel, Lawrence J., Jing Chen, Joffe, Marshall M., Gadegbeku, Crystal A., Mohler III, Emile R., Parsa, Afshin, Perumal, Kalyani, Rafey, Mohammed A., Steigerwalt, Susan P., Teal, Valerie, Townsend, Raymond R., and Rosas, Sylvia E.

Subjects
CHRONIC kidney failure, KIDNEY diseases, CARDIOVASCULAR diseases, GLOMERULAR filtration rate
Abstract

BackgroundPatients with chronic kidney disease (CKD) have a disproportionate risk of cardiovascular disease. This study was designed to assess the association between two noninvasive measures of cardiovascular risk, pulse wave analysis (PWA), and carotid intima-media thickness (IMT), in a cohort of CKD patients enrolled in the Chronic Renal Insufficiency Cohort (CRIC) study.MethodsThree hundred and sixty-seven subjects with CKD enrolled in the CRIC study at the University of Pennsylvania site (mean age 59.9 years, blood pressure 129/74 mm Hg, estimated glomerular filtration rate 48 ml/min/1.73 m2, IMT 0.8 mm) had both carotid IMT and PWA measurements. Carotid ultrasound was also used to determine the presence of plaque. PWA was used to determine augmentation index (AI), amplification ratio (AMPR), aortic pulse pressure (C_PP), and central aortic systolic pressure (C_SP).ResultsIMT was significantly associated with all PWA-derived measures. However, on multivariable linear regression analysis, only AMPR (regression coefficient −0.072, P = 0.006), C_PP (regression coefficient 0.0025, P < 0.001), and C_SP (regression coefficient 0.0017, P < 0.001) remained significantly associated with IMT. The prevalence of carotid plaque in the cohort was 59%. Of the PWA-derived measures, only C_PP was significantly associated with the presence of carotid plaque (P < 0.001).ConclusionsPWA-derived measures are associated with carotid IMT and plaque in the CKD. Of these measures, C_PP was most associated with carotid IMT and plaque.American Journal of Hypertension 2009; doi:10.1038/ajh.2009.156 [ABSTRACT FROM AUTHOR]

Published
2009
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143. Effects of Intravenously Administered Iron on Systemic Blood Pressure in Hemodialysis Patients.

Author

Ullian, Michael E. and Gadegbeku, Crystal A.

Subjects
*INTRAVENOUS therapy, *HEMODIALYSIS, *BLOOD pressure, *IRON deficiency diseases, *HYPOTENSION, *DIALYSIS (Chemistry)
Abstract

Background/Aims: Although maintenance of iron stores by intravenous iron infusion has become increasingly common in chronic hemodialysis patients, the effects of intravenous iron on blood pressure are not clear. Methods: In 52 mostly African-American patients in an urban setting, we reviewed blood pressure data over the course of hemodialysis on days that intravenous iron was administered and on control days. Results: The drop in blood pressure from the beginning to the end of hemodialysis was more pronounced when iron was not administered (9.9 ± 1.2 mm Hg) compared to when iron was administered (4.1 ± 1.7 mm Hg; p < 0.01). In a subset of chronic hemodialysis patients, blood pressure was actually higher at the end of hemodialysis compared to at the onset (9.6% of control hemodialysis sessions and 32.7% of sessions in which iron was administered; p < 0.01). The incidence of intra-dialytic hypotension and related symptoms was similar on iron and non-iron days. Conclusion: Intravenous iron therapy, well entrenched in clinical practice for the treatment of the anemia of end-stage renal disease, may reduce the incidence and magnitude of post-dialytic hypotension. Copyright © 2004 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Published
2004
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144. Fibroblast growth factor 23 is elevated before parathyroid hormone and phosphate in chronic kidney disease

Author

Isakova, Tamara, Wahl, Patricia, Vargas, Gabriela S., Gutiérrez, Orlando M., Scialla, Julia, Xie, Huiliang, Appleby, Dina, Nessel, Lisa, Bellovich, Keith, Chen, Jing, Hamm, Lee, Gadegbeku, Crystal, Horwitz, Edward, Townsend, Raymond R., Anderson, Cheryl A.M., Lash, James P., Hsu, Chi-yuan, Leonard, Mary B., Wolf, Myles, and on behalf of the Chronic Renal Insufficiency Cohort (CRIC) Study Group

Subjects
Male, Fibroblast growth factor 23, medicine.medical_specialty, Time Factors, 030232 urology & nephrology, Parathyroid hormone, 030204 cardiovascular system & hematology, urologic and male genital diseases, Severity of Illness Index, Article, Phosphates, Phosphorus metabolism, 03 medical and health sciences, Hyperphosphatemia, 0302 clinical medicine, Predictive Value of Tests, FGF23, Internal medicine, medicine, Humans, Prospective Studies, Renal Insufficiency, Chronic, Aged, phosphate, Hyperparathyroidism, business.industry, Middle Aged, medicine.disease, United States, Up-Regulation, Fibroblast Growth Factors, Fibroblast Growth Factor-23, stomatognathic diseases, Endocrinology, Parathyroid Hormone, Nephrology, Phosphorus, Dietary, Female, Hyperparathyroidism, Secondary, Secondary hyperparathyroidism, Renal phosphate excretion, business, Biomarkers, chronic kidney disease, Glomerular Filtration Rate, Kidney disease
Abstract

Fibroblast growth factor 23 (FGF23) regulates phosphorus metabolism and is a strong predictor of mortality in dialysis patients. FGF23 has been proposed as an early biomarker of disordered phosphorus metabolism in earlier stages of chronic kidney disease (CKD), but data from large, well-characterized CKD cohorts are lacking. We measured FGF23 in baseline samples from 3,879 participants in the Chronic Renal Insufficiency Cohort study, a nationally representative, diverse CKD cohort with mean (± sd) estimated glomerular filtration rate (eGFR) of 42.8 ± 13.5 ml/min/1.73m2. Serum phosphate (3.7 ± 0.7 mg/dl) and parathyroid hormone (PTH; median 54, interquartile range [IQR] 35 – 89 pg/ml) levels were in the normal range, but FGF23 (median 145, IQR 96 – 239 RU/ml) was markedly greater than in healthy populations and increased significantly with decreasing eGFR. FGF23 excess, defined as ≥ 100 RU/ml, was more common than secondary hyperparathyroidism (≥ 65 pg/ml) and hyperphosphatemia (≥ 4.6 mg/dl) in all strata of eGFR, and the eGFR threshold at which the slope of FGF23 increased (57.8; 95%CI: 55.4 – 60.8 ml/min/1.73m2) was higher than the corresponding threshold for PTH (46.9; 95%CI: 45.5 – 51.4 ml/min/1.73m2). Thus, increased FGF23 is a common manifestation of CKD that develops earlier than increases in phosphate or PTH. These findings provide additional support for use of FGF23 as a sensitive early screening test to identify disordered phosphorus metabolism in CKD patients with normal serum phosphate levels.

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145. Candidate Gene Association Study of Coronary Artery Calcification in Chronic Kidney Disease Findings From the CRIC Study (Chronic Renal Insufficiency Cohort)

Author

Ferguson, Jane F., Matthews, Gregory J., Townsend, Raymond R., Raj, Dominic S., Kanetsky, Peter A., Budoff, Matthew, Fischer, Michael J., Rosas, Sylvia E., Kanthety, Radhika, Rahman, Mahboob, Master, Stephen R., Qasim, Atif, Li, Mingyao, Mehta, Nehal N., Shen, Haiqing, Mitchell, Braxton D., O'Connell, Jeffrey R., Shuldiner, Alan R., Ho, Weang Kee, Young, Robin, Rasheed, Asif, Danesh, John, He, Jiang, Kusek, John W., Ojo, Akinlolu O., Flack, John, Go, Alan S., Gadegbeku, Crystal A., Wright, Jackson T., Saleheen, Danish, Feldman, Harold I., Rader, Daniel J., Foulkes, Andrea S., and Reilly, Muredach P.

Subjects
Chronic Renal Insufficiency Cohort Study (CRIC), coronary artery calcification (CAC), cardiovascular system, nutritional and metabolic diseases, risk factors, cardiovascular diseases, chronic kidney disease (CKD), single nucleotide polymorphisms (SNPs), candidate genes, myocardial infarction (MI)
Abstract

ObjectivesThis study sought to identify loci for coronary artery calcification (CAC) in patients with chronic kidney disease (CKD).BackgroundCKD is associated with increased CAC and subsequent coronary heart disease (CHD), but the mechanisms remain poorly defined. Genetic studies of CAC in CKD may provide a useful strategy for identifying novel pathways in CHD.MethodsWe performed a candidate gene study (∼2,100 genes; ∼50,000 single nucleotide polymorphisms [SNPs]) of CAC within the CRIC (Chronic Renal Insufficiency Cohort) study (N = 1,509; 57% European, 43% African ancestry). SNPs with preliminary evidence of association with CAC in CRIC were examined for association with CAC in the PennCAC (Penn Coronary Artery Calcification) (N = 2,560) and AFCS (Amish Family Calcification Study) (N = 784) samples. SNPs with suggestive replication were further analyzed for association with myocardial infarction (MI) in the PROMIS (Pakistan Risk of Myocardial Infarction Study) (N = 14,885).ResultsOf 268 SNPs reaching p < 5 × 10−4 for CAC in CRIC, 28 SNPs in 23 loci had nominal support (p < 0.05 and in same direction) for CAC in PennCAC or AFCS. Besides chr9p21 and COL4A1, known loci for CHD, these included SNPs having reported genome-wide association study association with hypertension (e.g., ATP2B1). In PROMIS, 4 of the 23 suggestive CAC loci (chr9p21, COL4A1, ATP2B1, and ABCA4) had significant associations with MI, consistent with their direction of effect on CAC.ConclusionsWe identified several loci associated with CAC in CKD that also relate to MI in a general population sample. CKD imparts a high risk of CHD and may provide a useful setting for discovery of novel CHD genes and pathways.

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147. A Unifying Approach for GFR Estimation: Recommendations of the NKF-ASN Task Force on Reassessing the Inclusion of Race in Diagnosing Kidney Disease

Author

Delgado, Cynthia, Baweja, Mukta, Crews, Deidra C., Eneanya, Nwamaka D., Gadegbeku, Crystal A., Inker, Lesley A., Mendu, Mallika L., Miller, W. Greg, Moxey-Mims, Marva M., Roberts, Glenda V., St. Peter, Wendy L., Warfield, Curtis, and Powe, Neil R.

Abstract

In response to a national call for reevaluation of the use of race in clinical algorithms, the National Kidney Foundation (NKF) and the American Society of Nephrology (ASN) established a Task Force to reassess inclusion of race in the estimation of glomerular filtration rate (eGFR) in the United States and its implications for diagnosis and management of patients with, or at risk for, kidney diseases.

Published
2021
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148. Clustering-based spatial analysis (CluSA) framework through graph neural network for chronic kidney disease prediction using histopathology images.

Author

Lee, Joonsang, Warner, Elisa, Shaikhouni, Salma, Bitzer, Markus, Kretzler, Matthias, Gipson, Debbie, Pennathur, Subramaniam, Bellovich, Keith, Bhat, Zeenat, Gadegbeku, Crystal, Massengill, Susan, Perumal, Kalyani, Saha, Jharna, Yang, Yingbao, Luo, Jinghui, Zhang, Xin, Mariani, Laura, Hodgin, Jeffrey B., and Rao, Arvind

Subjects
*CHRONIC kidney failure, *MACHINE learning, *HISTOPATHOLOGY, *KIDNEYS, *RENAL biopsy, *KIDNEY physiology
Abstract

Machine learning applied to digital pathology has been increasingly used to assess kidney function and diagnose the underlying cause of chronic kidney disease (CKD). We developed a novel computational framework, clustering-based spatial analysis (CluSA), that leverages unsupervised learning to learn spatial relationships between local visual patterns in kidney tissue. This framework minimizes the need for time-consuming and impractical expert annotations. 107,471 histopathology images obtained from 172 biopsy cores were used in the clustering and in the deep learning model. To incorporate spatial information over the clustered image patterns on the biopsy sample, we spatially encoded clustered patterns with colors and performed spatial analysis through graph neural network. A random forest classifier with various groups of features were used to predict CKD. For predicting eGFR at the biopsy, we achieved a sensitivity of 0.97, specificity of 0.90, and accuracy of 0.95. AUC was 0.96. For predicting eGFR changes in one-year, we achieved a sensitivity of 0.83, specificity of 0.85, and accuracy of 0.84. AUC was 0.85. This study presents the first spatial analysis based on unsupervised machine learning algorithms. Without expert annotation, CluSA framework can not only accurately classify and predict the degree of kidney function at the biopsy and in one year, but also identify novel predictors of kidney function and renal prognosis. [ABSTRACT FROM AUTHOR]

Published
2023
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149. Tissue transcriptome-driven identification of epidermal growth factor as a chronic kidney disease biomarker

Author

Ju, Wenjun, Nair, Viji, Smith, Shahaan, Zhu, Li, Shedden, Kerby, Song, Peter X. K., Mariani, Laura H., Eichinger, Felix H., Berthier, Celine C., Randolph, Ann, Lai, Jennifer Yi-Chun, Zhou, Yan, Hawkins, Jennifer J., Bitzer, Markus, Sampson, Matthew G., Thier, Martina, Solier, Corinne, Duran-Pacheco, Gonzalo C., Duchateau-Nguyen, Guillemette, Essioux, Laurent, Schott, Brigitte, Formentini, Ivan, Magnone, Maria C., Bobadilla, Maria, Cohen, Clemens D., Bagnasco, Serena M., Barisoni, Laura, Lv, Jicheng, Zhang, Hong, Wang, Hai-Yan, Brosius, Frank C., Gadegbeku, Crystal A., and Kretzler, Matthias

Abstract

Renal and urinary EGF can serve as biomarkers for prediction of outcomes in chronic kidney disease.

Published
2015
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150. Apixaban for Patients With Atrial Fibrillation on Hemodialysis: A Multicenter Randomized Controlled Trial.

Author

Pokorney, Sean D., Chertow, Glenn M., Al-Khalidi, Hussein R., Gallup, Dianne, Dignacco, Pat, Mussina, Kurt, Bansal, Nisha, Gadegbeku, Crystal A., Garcia, David A., Garonzik, Samira, Lopes, Renato D., Mahaffey, Kenneth W., Matsuda, Kelly, Middleton, John P., Rymer, Jennifer A., Sands, George H., Thadhani, Ravi, Thomas, Kevin L., Washam, Jeffrey B., and Winkelmayer, Wolfgang C.

Subjects
*ATRIAL fibrillation, *INTERNATIONAL normalized ratio, *HEMODIALYSIS, *CHRONIC kidney failure, *APIXABAN, *HEMODIALYSIS patients
Abstract

Background: There are no randomized data evaluating the safety or efficacy of apixaban for stroke prevention in patients with end-stage kidney disease on hemodialysis and with atrial fibrillation (AF).Methods: The RENAL-AF trial (Renal Hemodialysis Patients Allocated Apixaban Versus Warfarin in Atrial Fibrillation) was a prospective, randomized, open-label, blinded-outcome evaluation (PROBE) of apixaban versus warfarin in patients receiving hemodialysis with AF and a CHA2DS2-VASc score ≥2. Patients were randomly assigned 1:1 to 5 mg of apixaban twice daily (2.5 mg twice daily for patients ≥80 years of age, weight ≤60 kg, or both) or dose-adjusted warfarin. The primary outcome was time to major or clinically relevant nonmajor bleeding. Secondary outcomes included stroke, mortality, and apixaban pharmacokinetics. Pharmacokinetic sampling was day 1, day 3, and month 1.Results: From January 2017 through January 2019, 154 patients were randomly assigned to apixaban (n=82) or warfarin (n=72). The trial stopped prematurely because of enrollment challenges. Time in therapeutic range (international normalized ratio, 2.0-3.0) for warfarin-treated patients was 44% (interquartile range, 23%-59%). The 1-year rates for major or clinically relevant nonmajor bleeding were 32% and 26% in apixaban and warfarin groups, respectively (hazard ratio, 1.20 [95% CI, 0.63-2.30]), whereas 1-year rates for stroke or systemic embolism were 3.0% and 3.3% in apixaban and warfarin groups, respectively. Death was the most common major event in the apixaban (21 patients [26%]) and warfarin (13 patients [18%]) arms. The pharmacokinetic substudy enrolled the target 50 patients. Median steady-state 12-hour area under the curve was 2475 ng/mL×h (10th to 90th percentiles, 1342-3285) for 5 mg of apixaban twice daily and 1269 ng/mL×h (10th to 90th percentiles, 615-1946) for 2.5 mg of apixaban twice daily. There was substantial overlap between minimum apixaban blood concentration, 12-hour area under the curve, and maximum apixaban blood concentration for patients with and without a major or clinically relevant nonmajor bleeding event.Conclusions: There was inadequate power to draw any conclusion regarding rates of major or clinically relevant nonmajor bleeding comparing apixaban and warfarin in patients with AF and end-stage kidney disease on hemodialysis. Clinically relevant bleeding events were ≈10-fold more frequent than stroke or systemic embolism among this population on anticoagulation, highlighting the need for future randomized studies evaluating the risks versus benefits of anticoagulation among patients with AF and end-stage kidney disease on hemodialysis.Registration: URL: https://www.Clinicaltrials: gov; Unique identifier: NCT02942407. [ABSTRACT FROM AUTHOR]

Published
2022
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