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3. Unbiased kidney-centric molecular categorization of chronic kidney disease as a step towards precision medicine

Author

Reznichenko, Anna, Nair, Viji, Eddy, Sean, Fermin, Damian, Tomilo, Mark, Slidel, Timothy, Ju, Wenjun, Henry, Ian, Badal, Shawn S., Wesley, Johnna D., Liles, John T., Moosmang, Sven, Williams, Julie M., Quinn, Carol Moreno, Bitzer, Markus, Hodgin, Jeffrey B., Barisoni, Laura, Karihaloo, Anil, Breyer, Matthew D., Duffin, Kevin L., Patel, Uptal D., Magnone, Maria Chiara, Bhat, Ratan, and Kretzler, Matthias

Published
2024
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4. 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

Published
2023
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6. Corrigendum: Identification and validation of urinary CXCL9 as a biomarker for diagnosis of acute interstitial nephritis

Author

Moledina, Dennis G., Obeid, Wassim, Smith, Rex N., Rosales, Ivy, Sise, Meghan E., Moeckel, Gilbert, Kashgarian, Michael, Kuperman, Michael, Campbell, Kirk N., Lefferts, Sean, Meliambro, Kristin, Bitzer, Markus, Perazella, Mark A., Luciano, Randy L., Pober, Jordan S., Cantley, Lloyd G., Colvin, Robert B., Wilson, F. Perry, and Parikh, Chirag R.

Subjects
Proteins, Kidney diseases -- Diagnosis, Health care industry
Abstract

In the abstract and the legend for Figure 1, the descriptions of the Olink Proteomics assays utilized were incorrect. The correct descriptions appear below. The HTML and PDF versions of [...]

Published
2024
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7. Precision Medicine in Nephrology: An Integrative Framework of Multidimensional Data in the Kidney Precision Medicine Project

Author

Lake, Blue, Zhang, Kun, Lecker, Stewart, Morales, Alexander, Bogen, Steve, Amodu, Afolarin A., Beck, Laurence, Henderson, Joel, Ilori, Titlayo, Maikhor, Shana, Onul, Ingrid, Schmidt, Insa, Verma, Ashish, Waikar, Sushrut, Yadati, Pranav, Yu, Guanghao, Colona, Mia R., McMahon, Gearoid, Hacohen, Nir, Greka, Anna, Hoover, Paul J., Marshall, Jamie L., Aulisio, Mark, Bush, William, Chen, Yijiang, Crawford, Dana, Madabhushi, Anant, Viswanathan, Vidya S., Bush, Lakeshia, Cooperman, Leslie, Gadegbeku, Crystal, Herlitz, Leal, Jolly, Stacey, Nguyen, Jane, O’Malley, Charles, O’Toole, John, Palmer, Ellen, Poggio, Emilio, Spates-Harden, Kassandra, Sedor, John, Sendrey, Dianna, Taliercio, Jonathan, Appelbaum, Paul, Balderes, Olivia, Barasch, Jonathan, Berroue, Cecilia, Bomback, Andrew, Canetta, Pietro A., D’Agati, Vivette, Kiryluk, Krzysztof, Kudose, Satoru, Mehl, Karla, Sabatello, Maya, Shang, Ning, de Pinho Gonçalves, Joana, Lardenoije, Roy, Migas, Lukasz, Van de Plas, Raf, Rennke, Helmut, Azeloglu, Evren, Campbell, Kirk, Coca, Steven, He, Cijang, He, John, Iyengar, Srinivas Ravi, Lefferts, Seanee, Nadkarni, Girish, Patel, Marissa, Tokita, Joji, Ward, Stephen, Xiong, Yuguang, Verdoes, Abraham, Sabo, Angela, Barwinska, Daria, Gisch, Debora Lidia, Williams, James, Kelly, Katherine, Dunn, Kenneth, Asghari, Mahla, Eadon, Michael, Ferkowicz, Michael, Dagher, Pierre, Ferreira, Ricardo Melo, Winfree, Seth, Bledsoe, Sharon, Wofford, Stephanie, El-Achkar, Tarek, Sutton, Timothy, Bowen, William, Cheng, Ying-Hua, Slade, Austen, Record, Elizabeth, Cheng, Yinghua, Borner, Katy, Herr, Bruce, Jain, Yashvardhan, Quardokus, Ellen, Atta, Mohamed, Bernard, Lauren, Menez, Steven, Parikh, Chirag, Corona Villalobos, Celia Pamela, Wang, Ashley, Wen, Yumeng, Xu, Alan, Chen, Sarah, Donohoe, Isabel, Johansen, Camille, Rosas, Sylvia, Sun, Jennifer, Ardayfio, Joseph, Bebiak, Jack, Campbell, Taneisha, Fox, Monica, Knight, Richard, Koewler, Robert, Pinkeney, Roy, Saul, John, Shpigel, Anna, Prasad, Pottumarthi, Madhavan, Sethu M., Parikh, Samir, Rovin, Brad, Shapiro, John P., Anderton, Christopher, Lukowski, Jessica, Pasa-Tolic, Ljiljana, Velickovic, Dusan, Oliver, George, Mao, Weiguang, Sealfon, Rachel, Troyanskaya, Olga, Pollack, Ari, Goltsev, Yury, Ginley, Brandon, Anjani, Kavya, Laszik, Zoltan G., Mukatash, Tariq, Nolan, Garry, Beyda, David, Bracamonte, Erika, Brosius, Frank, Campos, Baltazar, Marquez, Nicole, Mendoza, Katherine, Scott, Raymond, Thajudeen, Bijin, Tsosie, Rebecca, Woodhead, Gregory, Saunders, Milda, Alloway, Rita R., Lee, Paul J., Rike, Adele, Shi, Tiffany, Woodle, E. Steve, Bjornstad, Petter, Hsieh, Elena, Kendrick, Jessica, Pyle, Laura, Thurman, Joshua, Vinovskis, Carissa, Wrobel, Julia, Lucarelli, Nicholas, Sarder, Pinaki, Bui, James, Carmona-Powell; Ron Gaba, Eunice, Kelly, Tanika, Lash, James, Meza, Natalie, Redmond, Devona, Renteria, Amada, Ricardo, Ana, Setty, Suman, Srivastava, Anand, Alakwaa, Fadhl, Ascani, Heather, Balis, Ul, Bitzer, Markus, Blanc, Victoria, Bonevich, Nikki, Conser, Ninive, Demeke, Dawit, Dull, Rachel, Eddy, Sean, Frey, Renee, Hartman, John, He, Yongqun Oliver, Hodgin, Jeffrey, Kretzler, Matthias, Lienczewski, Chrysta, Luo, Jinghui, Mariani, Laura, McCown, Phillip, Menon, Rajasree, Nair, Viji, Otto, Edgar, Reamy, Rebecca, Rose, Michael, Schaub, Jennifer, Steck, Becky, Wright, Zachary, Coleman, Alyson, Henderson-Brown; Jerica Berge, Dorisann, Caramori, Maria Luiza, Adeyi, Oyedele, Nachman, Patrick, Safadi, Sami, Flanagan, Siobhan, Ma, Sisi, Klett, Susan, Wolf, Susan, Harindhanavudhi, Tasma, Rao, Via, Bream, Peter, Froment, Anne, Kelley, Sara, Mottl, Amy, Chaudhury; Evan Zeitler, Prabir Roy, Bender, Filitsa, Elder, Michele, Gilliam, Matthew, Hall, Daniel E., Kellum, John A., Murugan, Raghavan, Palevsky, Paul, Rosengart, Matthew, Tan, Roderick, Tublin, Mitchell, Winters, James, Bansal, Shweta, Montellano, Richard, Pamreddy, Annapurna, Sharma, Kumar, Venkatachalam, Manjeri, Ye, Hongping, Zhang, Guanshi, Basit, Mujeeb, Cai, Qi, Hendricks, Allen, Hedayati, Susan, Kermani, Asra, Lee, Simon C., Ma, Shihong, Miller, Richard Tyler, Moe, Orson W., Park, Harold, Patel, Jiten, Pillai, Anil, Sambandam, Kamalanathan, Torrealba, Jose, Toto, Robert D., Vazquez, Miguel, Wang, Nancy, Wen, Natasha, Zhang, Dianbo, Alpers, Charles, Berglund, Ashley, Berry, Brooke, Blank, Kristina, Brown, Keith, Carson, Jonas, Daniel, Stephen, de Boer, Ian H., Dighe, Ashveena L., Dowd, Frederick, Grewenow, Stephanie M., Himmelfarb, Jonathan, Hoofnagle, Andrew, Jefferson, Nichole, Larson, Brandon, Limonte, Christine, McClelland, Robyn, Mooney, Sean, Nam, Yunbi, Park, Christopher, Phuong, Jimmy, Rezaei, Kasra, Roberts, Glenda, Sarkisova, Natalya, Shankland, Stuart, Snyder, Jaime, Stutzke, Christy, Tuttle, Katherine, Wangperawong, Artit, Wilcox, Adam, Williams, Kayleen, Young, Bessie, Allen, Jamie, Caprioli, Richard M., de Caestecker, Mark, Djambazova, Katerina, Dufresne, Martin, Farrow, Melissa, Fogo, Agnes, Sharman, Kavya, Spraggins, Jeffrey, Basta, Jeannine, Conlon, Kristine, Diettman, Sabine M., Gaut, Joseph, Kaushal, Madhurima, Jain, Sanjay, Knoten, Amanda, Minor, Brittany, Nwanne, Gerald, Vijayan, Anitha, Zhang, Bo, Arora, Tanima, Cantley, Lloyd, Victoria Castro, Angela M., Kakade, Vijayakumar, Moeckel, Gilbert, Moledina, Dennis, Shaw, Melissa, Wilson, Francis P., El-Achkar, Tarek M., and Eadon, Michael T.

Published
2024
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8. Molecular Signatures of Glomerular Neovascularization in a Patient with Diabetic Kidney Disease

Author

Ferkowicz, Michael J., Verma, Ashish, Barwinska, Daria, Melo Ferreira, Ricardo, Henderson, Joel M., Kirkpatrick, Mary, Silva, Paolo S., Steenkamp, Devin W., Phillips, Carrie L., Waikar, Sushrut S., Sutton, Timothy A., Lake, Blue, Zhang, Kun, Lecker, Stewart, Morales, Alexander, Stillman, Isaac, Bogen, Steve, Amodu, Afolarin A., Beck, Laurence, Henderson, Joel, Ilori, Titlayo, Maikhor, Shana, Onul, Ingrid, Schmidt, Insa, Verma, Ashish, Waikar, Sushrut, Yadati, Pranav, Yu, Guanghao, Colona, Mia R., McMahon, Gearoid, Weins, Astrid, Hacohen, Nir, Greka, Anna, Hoover, Paul J., Marshall, Jamie L., Aulisio, Mark, Bush, William, Chen, Yijiang, Crawford, Dana, Madabhushi, Anant, Viswanathan, Vidya S., Bush, Lakeshia, Cooperman, Leslie, Gadegbeku, Crystal, Herlitz, Leal, Jolly, Stacey, Nguyen, Jane, O’Malley, Charles, O’Toole, John, Palmer, Ellen, Poggio, Emilio, Spates-Harden, Kassandra, Sedor, John, Sendrey, Dianna, Taliercio, Jonathan, Appelbaum, Paul, Balderes, Olivia, Barasch, Jonathan, Berroue, Cecilia, Bomback, Andrew, Canetta, Pietro A., D’Agati, Vivette, Kiryluk, Krzysztof, Kudose, Satoru, Mehl, Karla, Sabatello, Maya, Shang, Ning, Varela, German, de Pinho Gonçalves, Joana, Lardenoije, Roy, Migas, Lukasz, Van de Plas, Raf, Barisoni, Laura, Rennke, Helmut, Azeloglu, Evren, Campbell, Kirk, Coca, Steven, He, Cijang, He, John, Iyengar, Srinivas Ravi, Lefferts, Seanee, Nadkarni, Girish, Patel, Marissa, Tokita, Joji, Ward, Stephen, Xiong, Yuguang, Verdoes, Abraham, Sabo, Angela, Barwinska, Daria, Gisch, Debora Lidia, Williams, James, Kelly, Katherine, Dunn, Kenneth, Asghari, Mahla, Eadon, Michael, Ferkowicz, Michael, Dagher, Pierre, Ferreira, Ricardo Melo, Winfree, Seth, Bledsoe, Sharon, Wofford, Stephanie, El-Achkar, Tarek, Sutton, Timothy, Bowen, William, Cheng, Ying-Hua, Slade, Austen, Record, Elizabeth, Cheng, Yinghua, Borner, Katy, Herr, Bruce, Jain, Yashvardhan, Quardokus, Ellen, Atta, Mohamed, Bernard, Lauren, Menez, Steven, Parikh, Chirag, Corona Villalobos, Celia Pamela, Wang, Ashley, Wen, Yumeng, Xu, Alan, Chen, Sarah, Donohoe, Isabel, Johansen, Camille, Rosas, Sylvia, Sun, Jennifer, Ardayfio, Joseph, Bebiak, Jack, Brown, Keith, Campbell, Taneisha, Fox, Monica, Hayashi, Lynda, Jefferson, Nichole, Richard Knight, Jennifer Jones, Koewler, Robert, Pinkeney, Roy, Saul, John, Shpigel, Anna, Stutzke, Christy, Prasad, Pottumarthi, Madhavan, Sethu M., Parikh, Samir, Rovin, Brad, Shapiro, John P., Anderton, Christopher, Lukowski, Jessica, Pasa-Tolic, Ljiljana, Velickovic, Dusan, Oliver, George, Mao, Weiguang, Sealfon, Rachel, Troyanskaya, Olga, Wong, Aaron, Pollack, Ari, Goltsev, Yury, Ginley, Brandon, Lutnick, Brendon, Anjani, Kavya, Laszik, Zoltan G., Mukatash, Tariq, Nolan, Garry, Beyda, David, Bracamonte, Erika, Brosius, Frank, Campos, Baltazar, Marquez, Nicole, Mendoza, Katherine, Scott, Raymond, Thajudeen, Bijin, Tsosie, Rebecca, Woodhead, Gregory, Saunders, Milda, Alloway, Rita R., Lee, Paul J., Rike, Adele, Shi, Tiffany, Woodle, E. Steve, Bjornstad, Petter, Hsieh, Elena, Kendrick, Jessica, Pyle, Laura, Thurman, Joshua, Vinovskis, Carissa, Wrobel, Julia, Lucarelli, Nicholas, Sarder, Pinaki, Bui, James, Carmona-Powell, Eunice, Gaba, Ron, Kelly, Tanika, Lash, James, Meza, Natalie, Redmond, Devona, Renteria, Amada, Ricardo, Ana, Setty, Suman, Srivastava, Anand, Alakwaa, Fadhl, Ascani, Heather, Balis, Ul, Bitzer, Markus, Blanc, Victoria, Bonevich, Nikki, Conser, Ninive, Demeke, Dawit, Dull, Rachel, Eddy, Sean, Frey, Renee, Hartman, John, He, Yongqun Oliver, Hodgin, Jeffrey, Kretzler, Matthias, Lienczewski, Chrysta, Luo, Jinghui, Mariani, Laura, McCown, Phillip, Menon, Rajasree, Nair, Viji, Otto, Edgar, Reamy, Rebecca, Rose, Michael, Schaub, Jennifer, Steck, Becky, Wright, Zachary, Coleman, Alyson, Henderson-Brown, Dorisann, Berge, Jerica, Caramori, Maria Luiza, Adeyi, Oyedele, Nachman, Patrick, Safadi, Sami, Flanagan, Siobhan, Ma, Sisi, Klett, Susan, Wolf, Susan, Harindhanavudhi, Tasma, Rao, Via, Bream, Peter, Froment, Anne, Kelley, Sara, Mottl, Amy, Roy-Chaudhury, Prabir, Zeitler, Evan, Bender, Filitsa, Elder, Michele, Gilliam, Matthew, Hall, Daniel E., Kellum, John A., Murugan, Raghavan, Palevsky, Paul, Rosengart, Matthew, Tan, Roderick, Tublin, Mitchell, Winters, James, Bansal, Shweta, Montellano, Richard, Pamreddy, Annapurna, Sharma, Kumar, Venkatachalam, Manjeri, Ye, Hongping, Zhang, Guanshi, Basit, Mujeeb, Cai, Qi, Hendricks, Allen, Hedayati, Susan, and Asra

Published
2024
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9. Low concentrations of medium-sized HDL particles predict incident CVD in chronic kidney disease patients

Author

Kretzler, Matthias, Gipson, Debbie, Bitzer, Markus, Gadegbeku, Crystal, Bellovich, Keith, Bhat, Zeenat, Massengill, Susan, Perumal, Kalyani, Appel, Lawrence J., Cohen, Debbie L., Lash, James P., Nelson, Robert G., Rahman, Mahboob, Shah, Vallabh O., Unruh, Mark L., Shao, Baohai, Afshinnia, Farsad, Mathew, Anna V., Ronsein, Graziella E., Thornock, Carissa, Irwin, Angela D., Kansal, Mayank, Rao, Panduranga S., Dobre, Mirela, Al-Kindi, Sadeer, Weir, Matthew R., Go, Alan, He, Jiang, Chen, Jing, Feldman, Harold, Bornfeldt, Karin E., and Pennathur, Subramaniam

Published
2023
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10. The Extracellular RNA Communication Consortium: Establishing Foundational Knowledge and Technologies for Extracellular RNA Research

Author

Das, Saumya, Consortium, The Extracellular RNA Communication, Abdel-Mageed, Asim B, Adamidi, Catherine, Adelson, P David, Akat, Kemal M, Alsop, Eric, Ansel, K Mark, Arango, Jorge, Aronin, Neil, Avsaroglu, Seda Kilinc, Azizian, Azadeh, Balaj, Leonora, Ben-Dov, Iddo Z, Bertram, Karl, Bitzer, Markus, Blelloch, Robert, Bogardus, Kimberly A, Breakefield, Xandra Owens, Calin, George A, Carter, Bob S, Charest, Al, Chen, Clark C, Chitnis, Tanuja, Coffey, Robert J, Courtright-Lim, Amanda, Datta, Amrita, DeHoff, Peter, Diacovo, Thomas G, Erle, David J, Etheridge, Alton, Ferrer, Marc, Franklin, Jeffrey L, Freedman, Jane E, Galas, David J, Galeev, Timur, Gandhi, Roopali, Garcia, Aitor, Gerstein, Mark Bender, Ghai, Vikas, Ghiran, Ionita Calin, Giraldez, Maria D, Goga, Andrei, Gogakos, Tasos, Goilav, Beatrice, Gould, Stephen J, Guo, Peixuan, Gupta, Mihir, Hochberg, Fred, Huang, Bo, Huentelman, Matt, Hunter, Craig, Hutchins, Elizabeth, Jackson, Andrew R, Kalani, M Yashar S, Kanlikilicer, Pinar, Karaszti, Reka Agnes, Van Keuren-Jensen, Kendall, Khvorova, Anastasia, Kim, Yong, Kim, Hogyoung, Kim, Taek Kyun, Kitchen, Robert, Kraig, Richard P, Krichevsky, Anna M, Kwong, Raymond Y, Laurent, Louise C, Lee, Minyoung, L’Etoile, Noelle, Levy, Shawn E, Li, Feng, Li, Jenny, Li, Xin, Lopez-Berestein, Gabriel, Lucero, Rocco, Mateescu, Bogdan, Matin, AC, Max, Klaas EA, McManus, Michael T, Mempel, Thorsten R, Meyer, Cindy, Milosavljevic, Aleksandar, Mondal, Debasis, Mukamal, Kenneth Jay, Murillo, Oscar D, Muthukumar, Thangamani, Nickerson, Deborah A, O’Donnell, Christopher J, Patel, Dinshaw J, Patel, Tushar, Patton, James G, Paul, Anu, Peskind, Elaine R, Phelps, Mitch A, Putterman, Chaim, Quesenberry, Peter J, Quinn, Joseph F, Raffai, Robert L, and Ranabothu, Saritha

Subjects
Genetics, Biomarkers, Cell-Free Nucleic Acids, Extracellular Vesicles, Humans, Knowledge Bases, MicroRNAs, RNA, Extracellular RNA Communication Consortium, Biological Sciences, Medical and Health Sciences, Developmental Biology
Abstract

The Extracellular RNA Communication Consortium (ERCC) was launched to accelerate progress in the new field of extracellular RNA (exRNA) biology and to establish whether exRNAs and their carriers, including extracellular vesicles (EVs), can mediate intercellular communication and be utilized for clinical applications. Phase 1 of the ERCC focused on exRNA/EV biogenesis and function, discovery of exRNA biomarkers, development of exRNA/EV-based therapeutics, and construction of a robust set of reference exRNA profiles for a variety of biofluids. Here, we present progress by ERCC investigators in these areas, and we discuss collaborative projects directed at development of robust methods for EV/exRNA isolation and analysis and tools for sharing and computational analysis of exRNA profiling data.

Published
2019

11. Unsupervised machine learning for identifying important visual features through bag-of-words using histopathology data from chronic kidney disease

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

Published
2022
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12. Identification and validation of urinary CXCL9 as a biomarker for diagnosis of acute interstitial nephritis

Author

Moledina, Dennis G., Obeid, Wassim, Smith, Rex N., Rosales, Ivy, Sise, Meghan E., Moeckel, Gilbert, Kashgarian, Michael, Kuperman, Michael, Campbell, Kirk N., Lefferts, Sean, Meliambro, Kristin, Bitzer, Markus, Perazella, Mark A., Luciano, Randy L., Pober, Jordan S., Cantley, Lloyd G., Colvin, Robert B., Wilson, F. Perry, and Parikh, Chirag R.

Subjects
Nephritis -- Diagnosis -- Development and progression, Biological markers -- Physiological aspects -- Health aspects -- Identification and classification, Chemokines -- Physiological aspects -- Health aspects -- Identification and classification, Health care industry
Abstract

BACKGROUND. Acute tubulointerstitial nephritis (AIN) is one of the few causes of acute kidney injury with diagnosis- specific treatment options. However, due to the need to obtain a kidney biopsy for histological confirmation, AIN diagnosis can be delayed, missed, or incorrectly assumed. Here, we identify and validate urinary CXCL9, an IFN-[gamma]-induced chemokine involved in lymphocyte chemotaxis, as a diagnostic biomarker for AIN. METHODS. In a prospectively enrolled cohort with pathologist-adjudicated histological diagnoses, termed the discovery cohort, we tested the association of 180 immune proteins measured by an aptamer- based assay with AIN and validated the top protein, CXCL9, using sandwich immunoassay. We externally validated these findings in 2 cohorts with biopsy- confirmed diagnoses, termed the validation cohorts, and examined mRNA expression differences in kidney tissue from patients with AIN and individuals in the control group. RESULTS. In aptamer-based assay, urinary CXCL9 was 7.6-fold higher in patients with AIN than in individuals in the control group (P = 1.23 * [10.sup.-5]). Urinary CXCL9 measured by sandwich immunoassay was associated with AIN in the discovery cohort (n = 204; 15% AIN) independently of currently available clinical tests for AIN (adjusted odds ratio for highest versus lowest quartile: 6.0 [1.8-20]). Similar findings were noted in external validation cohorts, where CXCL9 had an AUC of 0.94 (0.86-1.00) for AIN diagnosis. CXCL9 mRNA expression was 3.9-fold higher in kidney tissue from patients with AIN (n = 19) compared with individuals in the control group (n = 52; P = 5.8 * [10.sup.-6]). CONCLUSION. We identified CXCL9 as a diagnostic biomarker for AIN using aptamer- based urine proteomics, confirmed this association using sandwich immunoassays in discovery and external validation cohorts, and observed higher expression of this protein in kidney biopsies from patients with AIN. FUNDING. This study was supported by National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) awards K23DK117065 (DGM), K08DK113281 (KM), R01DK128087 (DGM), R01DK126815 (DGM and LGC), R01DK126477 (KNC), UH3DK114866 (CRP, DGM, and FPW), R01DK130839 (MES), and P30DK079310 (the Yale O'Brien Center). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health., Introduction Sudden loss of kidney function, termed acute kidney injury (AKI), is common, affecting 1 in 5 hospitalized patients and is associated with adverse long-term outcomes, including chronic kidney disease, [...]

Published
2023
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13. Identification and validation of urinary CXCL9 as a biomarker for diagnosis of acute interstitial nephritis

Author

Moledina, Dennis G., primary, Obeid, Wassim, additional, Smith, Rex N., additional, Rosales, Ivy, additional, Sise, Meghan E., additional, Moeckel, Gilbert, additional, Kashgarian, Michael, additional, Kuperman, Michael, additional, Campbell, Kirk N., additional, Lefferts, Sean, additional, Meliambro, Kristin, additional, Bitzer, Markus, additional, Perazella, Mark A., additional, Luciano, Randy L., additional, Pober, Jordan S., additional, Cantley, Lloyd G., additional, Colvin, Robert B., additional, Wilson, F. Perry, additional, and Parikh, Chirag R., additional

Published
2024
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14. SGLT2 inhibitors mitigate kidney tubular metabolic and mTORC1 perturbations in youth-onset type 2 diabetes

Author

Schaub, Jennifer A., AlAkwaa, Fadhl M., McCown, Phillip J., Naik, Abhijit S., Nair, Viji, Eddy, Sean, Menon, Rajasree, Otto, Edgar A., Demeke, Dawit, Hartman, John, Fermin, Damian, O'Connor, Christopher L., Subramanian, Lalita, Bitzer, Markus, Harned, Roger, Ladd, Patricia, Pyle, Laura, Pennathur, Subramaniam, Inoki, Ken, Hodgin, Jeffrey B., Brosius, Frank C., III, Nelson, Robert G., Kretzler, Matthias, and Bjornstad, Petter

Subjects
Hypoglycemic agents -- Usage -- Physiological aspects, Type 2 diabetes -- Drug therapy -- Complications and side effects, Pediatric research, Diabetic nephropathies -- Risk factors -- Development and progression -- Prevention, Health care industry
Abstract

The molecular mechanisms of sodium-glucose cotransporter-2 (SGLT2) inhibitors (SGLT2i) remain incompletely understood. Single-cell RNA sequencing and morphometric data were collected from research kidney biopsies donated by young persons with type 2 diabetes (T2D), aged 12 to 21 years, and healthy controls (HCs). Participants with T2D were obese and had higher estimated glomerular filtration rates and mesangial and glomerular volumes than HCs. Ten T2D participants had been prescribed SGLT2i (T2Di[+]) and 6 not (T2Di[-]). Transcriptional profiles showed SGLT2 expression exclusively in the proximal tubular (PT) cluster with highest expression in T2Di(-) patients. However, transcriptional alterations with SGLT2i treatment were seen across nephron segments, particularly in the distal nephron. SGLT2i treatment was associated with suppression of transcripts in the glycolysis, gluconeogenesis, and tricarboxylic acid cycle pathways in PT, but had the opposite effect in thick ascending limb. Transcripts in the energy-sensitive mTORC1-signaling pathway returned toward HC levels in all tubular segments in T2Di(+), consistent with a diabetes mouse model treated with SGLT2i. Decreased levels of phosphorylated S6 protein in proximal and distal tubules in T2Di(+) patients confirmed changes in mTORC1 pathway activity. We propose that SGLT2i treatment benefits the kidneys by mitigating diabetes-induced metabolic perturbations via suppression of mTORC1 signaling in kidney tubules., Introduction The incedence of youth-onset type 2 diabetes (T2D) is rapidly rising among children and adolescents globally (1). It is associated with a more severe clinical course than youth-onset type [...]

Published
2023
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18. Upregulated PD-1 signaling antagonizes glomerular health in aged kidneys and disease

Author

Pippin, Jeffrey W., Kaverina, Natalya, Wang, Yuliang, Eng, Diana G., Zeng, Yuting, Tran, Uyen, Loretz, Carol J., Chang, Anthony, Akilesh, Shreeram, Poudel, Chetan, Perry, Hannah S., O'Connor, Christopher, Vaughan, Joshua C., Bitzer, Markus, Wessely, Oliver, and Shankland, Stuart J.

Subjects
Aging -- Physiological aspects -- Health aspects, Immunity -- Physiological aspects -- Health aspects, Kidney diseases -- Risk factors -- Development and progression, Health care industry
Abstract

With an aging population, kidney health becomes an important medical and socioeconomic factor. Kidney aging mechanisms are not well understood. We previously showed that podocytes isolated from aged mice exhibit increased expression of programmed cell death protein 1 (PD-1) surface receptor and its 2 ligands (PD-L1 and PD-L2). PDCD1 transcript increased with age in microdissected human glomeruli, which correlated with lower estimated glomerular filtration rate and higher segmental glomerulosclerosis and vascular arterial intima-to-lumen ratio. In vitro studies in podocytes demonstrated a critical role for PD-1 signaling in cell survival and in the induction of a senescence- associated secretory phenotype. To prove PD-1 signaling was critical to podocyte aging, aged mice were injected with anti-PD- 1 antibody. Treatment significantly improved the aging phenotype in both kidney and liver. In the glomerulus, it increased the life span of podocytes, but not that of parietal epithelial, mesangial, or endothelial cells. Transcriptomic and immunohistochemistry studies demonstrated that anti-PD-1 antibody treatment improved the health span of podocytes. Administering the same anti-PD-1 antibody to young mice with experimental focal segmental glomerulosclerosis (FSGS) lowered proteinuria and improved podocyte number. These results suggest a critical contribution of increased PD-1 signaling toward both kidney and liver aging and in FSGS., Introduction The US population is aging, and the number of Americans aged 65 and older will more than double over the next 40 years (US Census Bureau); Eurostat forecasts that [...]

Published
2022
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19. Genetic Analysis of Obesity-Induced Diabetic Nephropathy in BTBR Mice.

Author

Keller, Mark P., O’Connor, Chris, Bitzer, Markus, Schueler, Kathryn L., Stapleton, Donald S., Emfinger, Christopher H., Broman, Aimee Teo, Hodgin, Jeffrey B., and Attie, Alan D.

Subjects
DIABETIC nephropathies, LOCUS (Genetics), CHRONIC kidney failure, SINGLE nucleotide polymorphisms, MICE, MISSENSE mutation
Abstract

Diabetic nephropathy (DN) is the leading cause of end-stage renal disease in the U.S. and has a significant impact on human suffering. Leptin-deficient BTBR (BTBRob/ob) mice develop hallmark features of obesity-induced DN, whereas leptin-deficient C57BL/6J (B6ob/ob) mice do not. To identify genetic loci that underlie this strain difference, we constructed an F2 intercross between BTBRob/ob and B6ob/ob mice. We isolated kidneys from 460 F2 mice and histologically scored them for percent mesangial matrix and glomerular volume (∼50 glomeruli per mouse), yielding ∼45,000 distinct measures in total. The same histological measurements were made in kidneys from B6 and BTBR mice, either lean or obese (Lepob/ob), at 4 and 10 weeks of age, allowing us to assess the contribution of strain, age, and obesity to glomerular pathology. All F2 mice were genotyped for ∼5,000 single nucleotide polymorphisms (SNPs), ∼2,000 of which were polymorphic between B6 and BTBR, enabling us to identify a quantitative trait locus (QTL) on chromosome 7, with a peak at ∼30 Mbp, for percent mesangial matrix, glomerular volume, and mesangial volume. The podocyte-specific gene nephrin (Nphs1) is physically located at the QTL and contains high-impact SNPs in BTBR, including several missense variants within the extracellular immunoglobulin-like domains. Article Highlights: Diabetes is the leading cause of end-stage renal disease. We previously discovered that the BTBR mouse strain carrying the ob mutation at the leptin gene is an excellent model of human diabetic nephropathy and has been widely adopted by basic scientists and the pharmaceutical industry. Genetic factors play a role in susceptibility to diabetic nephropathy. We carried out a linkage study in a sample of mice generated from an intercross between the BTBR and C57BL/6J strains carrying the ob mutation. We identified a single locus and provided evidence that the leading candidate gene at this locus is nephrin. [ABSTRACT FROM AUTHOR]

Published
2024
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20. Spatial Heterogeneity of Glomerular Phenotypes Impacts Kidney Biopsy Findings

Author

Schaub, Jennifer A., primary, O’Connor, Christopher L., additional, Dailey, Meghan, additional, Hlynka, Andrew W., additional, Chang, Yurui, additional, Postiff, Deborah, additional, Kaffenberger, Samuel, additional, Palapattu, Ganesh, additional, Gillespie, Brenda W., additional, Hodgin, Jeffrey, additional, Shedden, Kerby, additional, and Bitzer, Markus, additional

Published
2023
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21. Inhibiting NLRP3 signaling in aging podocytes improves their life- and health-span

Author

Kaverina, Natalya, primary, Schweickart, R. Allen, additional, Chan, Gek Cher, additional, Maggiore, Joseph C., additional, Eng, Diana G., additional, Zeng, Yuting, additional, McKinzie, Sierra R., additional, Perry, Hannah S., additional, Ali, Adilijiang, additional, O’Connor, Christopher, additional, Pereira, Beatriz Maria Veloso, additional, Theberge, Ashleigh B., additional, Vaughan, Joshua C., additional, Loretz, Carol J., additional, Chang, Anthony, additional, Hukriede, Neil A., additional, Bitzer, Markus, additional, Pippin, Jeffrey W., additional, Wessely, Oliver, additional, and Shankland, Stuart J., additional

Published
2023
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22. Low concentrations of medium-sized HDL particles predict incident CVD in chronic kidney disease patients

Author

Shao, Baohai, primary, Afshinnia, Farsad, additional, Mathew, Anna V., additional, Ronsein, Graziella E., additional, Thornock, Carissa, additional, Irwin, Angela D., additional, Kansal, Mayank, additional, Rao, Panduranga S., additional, Dobre, Mirela, additional, Al-Kindi, Sadeer, additional, Weir, Matthew R., additional, Go, Alan, additional, He, Jiang, additional, Chen, Jing, additional, Feldman, Harold, additional, Bornfeldt, Karin E., additional, Pennathur, Subramaniam, additional, Kretzler, Matthias, additional, Gipson, Debbie, additional, Bitzer, Markus, additional, Gadegbeku, Crystal, additional, Bellovich, Keith, additional, Bhat, Zeenat, additional, Massengill, Susan, additional, Perumal, Kalyani, additional, Appel, Lawrence J., additional, Cohen, Debbie L., additional, Lash, James P., additional, Nelson, Robert G., additional, Rahman, Mahboob, additional, Shah, Vallabh O., additional, and Unruh, Mark L., additional

Published
2023
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26. Endoplasmic reticulum-associated degradation is required for nephrin maturation and kidney glomerular filtration function

Author

Yoshida, Sei, Wei, Xiaoqiong, Zhang, Gensheng, O'Connor, Christopher L., Torres, Mauricio, Zhou, Zhangsen, Lin, Liangguang, Menon, Rajasree, Xu, Xiaoxi, Zheng, Wenyue, Xiong, Yi, Otto, Edgar, Tang, Chih-Hang Anthony, Hua, Rui, Verma, Rakesh, Mori, Hiroyuki, Zhang, Yang, Hu, Chih-Chi Andrew, Liu, Ming, Garg, Puneet, Hodgin, Jeffrey B., Sun, Shengyi, Bitzer, Markus, and Qi, Ling

Subjects
Genetic disorders -- Development and progression, Endoplasmic reticulum -- Health aspects -- Physiological aspects, Proteolysis -- Research, Kidney glomerulus -- Health aspects -- Physiological aspects, Nephrotic syndrome -- Development and progression -- Genetic aspects, Epithelial cells -- Health aspects -- Physiological aspects, Health care industry
Abstract

Podocytes are key to the glomerular filtration barrier by forming a slit diaphragm between interdigitating foot processes; however, the molecular details and functional importance of protein folding and degradation in the ER remain unknown. Here, we show that the SEL1L-HRD1 protein complex of ER-associated degradation (ERAD) is required for slit diaphragm formation and glomerular filtration function. SEL1L-HRD1 ERAD is highly expressed in podocytes of both mouse and human kidneys. Mice with podocyte-specific Sel1L deficiency develop podocytopathy and severe congenital nephrotic syndrome with an impaired slit diaphragm shortly after weaning and die prematurely, with a median lifespan of approximately 3 months. We show mechanistically that nephrin, a type 1 membrane protein causally linked to congenital nephrotic syndrome, is an endogenous ERAD substrate. ERAD deficiency attenuated the maturation of nascent nephrin, leading to its retention in the ER. We also show that various autosomal-recessive nephrin disease mutants were highly unstable and broken down by SEL1L-HRD1 ERAD, which attenuated the pathogenicity of the mutants toward the WT allele. This study uncovers a critical role of SEL1L-HRD1 ERAD in glomerular filtration barrier function and provides insights into the pathogenesis associated with autosomal-recessive disease mutants., Introduction The key function of the kidneys is the ultrafiltration of blood in the glomerulus, where podocytes, specialized differentiated epithelial cells, wrap around capillaries of the glomerulus via a unique [...]

Published
2021
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28. CluSA: Clustering-based Spatial Analysis framework through Graph Neural Network for Chronic Kidney Disease Prediction using Histopathology Images

Author

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

Published
2022
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30. Multi-scalar data integration links glomerular angiopoietin-tie signaling pathway activation with progression of diabetic kidney disease

Author

Liu, Jiahao, primary, Nair, Viji, primary, Zhao, Yi-yang, primary, Chang, Dong-yuan, primary, Limonte, Christine, primary, Bansal, Nisha, primary, Fermin, Damian, primary, Eichinger, Felix, primary, Tanner, Emily C., primary, Bellovich, Keith A., primary, Steigerwalt, Susan, primary, Bhat, Zeenat, primary, Hawkins, Jennifer J., primary, Subramanian, Lalita, primary, Rosas, Sylvia E., primary, Sedor, John R., primary, Vasquez, Miguel A., primary, Waikar, Sushrut S., primary, Bitzer, Markus, primary, Pennathur, Subramaniam, primary, Brosius, Frank C., primary, Boer, Ian De, primary, Chen, Min, primary, Kretzler, Matthias, primary, and Ju, Wenjun, primary

Published
2022
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31. Bone marrow-derived immature myeloid cells are a main source of circulating suPAR contributing to proteinuric kidney disease

Author

Hahm, Eunsil, Wei, Changli, Fernandez, Isabel, Li, Jing, Tardi, Nicholas J, Tracy, Melissa, Wadhwani, Shikha, Cao, Yanxia, Peev, Vasil, Zloza, Andrew, Lusciks, Jevgenijs, Hayek, Salim S, O'Connor, Christopher, Bitzer, Markus, Gupta, Vineet, Sever, Sanja, Sykes, David B, Scadden, David T, and Reiser, Jochen

Subjects
Glycoproteins -- Health aspects, Kidney diseases -- Genetic aspects -- Development and progression -- Risk factors, Gene expression -- Health aspects, Biological sciences, Health
Abstract

Author(s): Eunsil Hahm [1]; Changli Wei [1]; Isabel Fernandez [1]; Jing Li [1]; Nicholas J Tardi [1]; Melissa Tracy [1]; Shikha Wadhwani [1]; Yanxia Cao [1]; Vasil Peev [1]; Andrew [...]

Published
2017
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33. The Michigan O’Brien Kidney Research Center: transforming translational kidney research through systems biology

Author

Bitzer, Markus, primary, Ju, Wenjun, additional, Subramanian, Lalita, additional, Troost, Jonathan P., additional, Tychewicz, Joseph, additional, Steck, Becky, additional, Wiggins, Roger C., additional, Gipson, Debbie S., additional, Gadegbeku, Crystal A., additional, Brosius, Frank C., additional, Kretzler, Matthias, additional, and Pennathur, Subramaniam, additional

Published
2022
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34. SGLT2 inhibition mitigates perturbations in nephron segment-specific metabolic transcripts and mTOR pathway activity in kidneys of young persons with type 2 diabetes

Author

Schaub, Jennifer A., primary, AlAkwaa, Fadhl M., additional, McCown, Phillip J., additional, Naik, Abhijit S., additional, Nair, Viji, additional, Eddy, Sean, additional, Menon, Rajasree, additional, Otto, Edgar A., additional, Hartman, John, additional, Fermin, Damian, additional, O’Connor, Christopher, additional, Bitzer, Markus, additional, Harned, Roger, additional, Ladd, Patricia, additional, Pyle, Laura, additional, Hodgin, Jeffrey B., additional, Brosius, Frank C., additional, Nelson, Robert G., additional, Kretzler, Matthias, additional, and Bjornstad, Petter, additional

Published
2022
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35. miR-21 mediates hematopoietic suppression in MDS by activating TGF-β signaling

Author

Bhagat, Tushar D., Zhou, Li, Sokol, Lubomir, Kessel, Rachel, Caceres, Gisela, Gundabolu, Krishna, Tamari, Roni, Gordon, Shanisha, Mantzaris, Ioannis, Jodlowski, Tomasz, Yu, Yiting, Jing, Xiaohong, Polineni, Rahul, Bhatia, Kavi, Pellagatti, Andrea, Boultwood, Jacqueline, Kambhampati, Suman, Steidl, Ulrich, Stein, Cy, Ju, Wenjun, Liu, Gang, Kenny, Paraic, List, Alan, Bitzer, Markus, and Verma, Amit

Published
2013
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39. Multi-scalar data integration links glomerular angiopoietin-tie signaling pathway activation with progression of diabetic kidney disease

Author

Liu, Jiahao, primary, Nair, Viji, additional, Zhao, Yi-yang, additional, Chang, Dong-yuan, additional, Eichinger, Felix, additional, Tanner, Emily, additional, Fermin, Damian, additional, Bellovich, Keith, additional, Steigerwalt, Susan, additional, Bhat, Zeenat, additional, Hawkins, Jennifer, additional, Subramanian, Lalita, additional, Rosas, Sylvia, additional, Sedor, John, additional, Vasquez, Miguel, additional, Waikar, Sushrut, additional, Bitzer, Markus, additional, Subramaniam, Pennathur, additional, Brosius, Frank, additional, Chen, Min, additional, Kretzler, Matthias, additional, and Ju, Wenjun, additional

Published
2021
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42. Multi-Scalar Data Integration Links Glomerular Angiopoietin-Tie Signaling Pathway Activation With Progression of Diabetic Kidney Disease.

Author

Liu, Jiahao, Nair, Viji, Zhao, Yi-yang, Chang, Dong-yuan, Limonte, Christine, Bansal, Nisha, Fermin, Damian, Eichinger, Felix, Tanner, Emily C., Bellovich, Keith A., Steigerwalt, Susan, Bhat, Zeenat, Hawkins, Jennifer J., Subramanian, Lalita, Rosas, Sylvia E., Sedor, John R., Vasquez, Miguel A., Waikar, Sushrut S., Bitzer, Markus, and Pennathur, Subramaniam

Subjects
EPITHELIAL cells, PROTEINS, RESEARCH funding, DIABETIC nephropathies, CELLULAR signal transduction, CHRONIC kidney failure, LONGITUDINAL method, DIABETES, DISEASE progression, CELL receptors, IMPACT of Event Scale
Abstract

Diabetic kidney disease (DKD) is the leading cause of end-stage kidney disease (ESKD). Prognostic biomarkers reflective of underlying molecular mechanisms are critically needed for effective management of DKD. A three-marker panel was derived from a proteomics analysis of plasma samples by an unbiased machine learning approach from participants (N = 58) in the Clinical Phenotyping and Resource Biobank study. In combination with standard clinical parameters, this panel improved prediction of the composite outcome of ESKD or a 40% decline in glomerular filtration rate. The panel was validated in an independent group (N = 68), who also had kidney transcriptomic profiles. One marker, plasma angiopoietin 2 (ANGPT2), was significantly associated with outcomes in cohorts from the Cardiovascular Health Study (N = 3,183) and the Chinese Cohort Study of Chronic Kidney Disease (N = 210). Glomerular transcriptional angiopoietin/Tie (ANG-TIE) pathway scores, derived from the expression of 154 ANG-TIE signaling mediators, correlated positively with plasma ANGPT2 levels and kidney outcomes. Higher receptor expression in glomeruli and higher ANG-TIE pathway scores in endothelial cells corroborated potential functional effects in the kidney from elevated plasma ANGPT2 levels. Our work suggests that ANGPT2 is a promising prognostic endothelial biomarker with likely functional impact on glomerular pathogenesis in DKD. [ABSTRACT FROM AUTHOR]

Published
2022
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44. Molecular Stratification of Chronic Kidney Disease

Author

Reznichenko, Anna, primary, Nair, Viji, additional, Eddy, Sean, additional, Tomilo, Mark, additional, Slidel, Timothy, additional, Ju, Wenjun, additional, Conway, James, additional, Badal, Shawn, additional, Wesley, Johnna, additional, Liles, John, additional, Moosmang, Sven, additional, Williams, Julie M, additional, Moreno Quinn, Carol, additional, Bitzer, Markus, additional, Karihaloo, Anil, additional, Breyer, Matthew, additional, Duffin, Kevin, additional, Patel, Uptal, additional, Magnone, Maria Chiara, additional, Bhat, Ratan, additional, and Kretzler, Matthias, additional

Published
2021
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46. Comprehensive Search for Novel Circulating miRNAs and Axon Guidance Pathway Proteins Associated with Risk of ESKD in Diabetes

Author

Satake, Eiichiro, primary, Saulnier, Pierre-Jean, additional, Kobayashi, Hiroki, additional, Gupta, Manoj K., additional, Looker, Helen C., additional, Wilson, Jonathan M., additional, Md Dom, Zaipul I., additional, Ihara, Katsuhito, additional, O’Neil, Kristina, additional, Krolewski, Bozena, additional, Pipino, Caterina, additional, Pavkov, Meda E., additional, Nair, Viji, additional, Bitzer, Markus, additional, Niewczas, Monika A., additional, Kretzler, Matthias, additional, Mauer, Michael, additional, Doria, Alessandro, additional, Najafian, Behzad, additional, Kulkarni, Rohit N., additional, Duffin, Kevin L., additional, Pezzolesi, Marcus G., additional, Kahn, C. Ronald, additional, Nelson, Robert G., additional, and Krolewski, Andrzej S., additional

Published
2021
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48. Continuous Renal Replacement Therapy among Patients with COVID-19 and Acute Kidney Injury.

Author

Sohaney, Ryann, Shaikhouni, Salma, Ludwig, John Travis, Tilea, Anca, Bitzer, Markus, Yessayan, Lenar, and Heung, Michael

Subjects
ACUTE kidney failure, COVID-19, RENAL replacement therapy, ADULT respiratory distress syndrome, POSITIVE end-expiratory pressure, KIDNEY diseases
Abstract

Background and Objectives: Acute kidney injury (AKI) is a common complication among patients with COVID-19 and acute respiratory distress syndrome. Reports suggest that COVID-19 confers a pro-thrombotic state, which presents challenges in maintaining hemofilter patency and delivering continuous renal replacement therapy (CRRT). We present our initial experience with CRRT in critically ill patients with COVID-19, emphasizing circuit patency and the association between fluid balance during CRRT and respiratory parameters. Design, Setting, Participants, and Measurements: Retrospective chart review of 32 consecutive patients with COVID-19 and AKI managed with continuous venovenous hemodiafiltration with regional citrate anticoagulation (CVVHDF-RCA) according to the University of Michigan protocol. Primary outcome was mean CRRT circuit life per patient during the first 7 days of CRRT. We used simple linear regression to assess the relationship between patient characteristics and filter life. We also explored the relationship between fluid balance on CRRT and respiratory parameters using repeated measures modeling. Results: Patients' mean age was 54.8 years and majority were Black (75%). Comorbidities included hypertension (90.6%), obesity (70.9%) diabetes (56.2%), and chronic kidney disease (40.6%). Median CRRT circuit life was 53.5 [interquartile range 39.1–77.6] hours. There was no association between circuit life and inflammatory or pro-thrombotic laboratory values (ferritin p = 0.92, C-reactive protein p = 0.29, D-dimer p = 0.24), or with systemic anticoagulation (p = 0.37). Net daily fluid removal during the first 7 days of CRRT was not associated with daily (closest recorded values to 20:00) PaO2/FIO2 ratio (p = 0.21) or positive end-expiratory pressure requirements (p = 0.47). Conclusions: We achieved adequate CRRT circuit life in COVID-19 patients using an established CVVHDF-RCA protocol. During the first 7 days of CRRT therapy, cumulative fluid balance was not associated with improvements in respiratory parameters, even after accounting for baseline fluid balance. [ABSTRACT FROM AUTHOR]

Published
2022
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49. The Michigan O'Brien Kidney Research Center: transforming translational kidney research through systems biology.

Author

Bitzer, Markus, Wenjun Ju, Subramanian, Lalita, Troost, Jonathan P., Tychewicz, Joseph, Steck, Becky, Wiggins, Roger C., Gipson, Debbie S., Gadegbeku, Crystal A., Brosius 3rd, Frank C., Kretzler, Matthias, and Pennathur, Subramaniam

Subjects
*SYSTEMS biology, *TRANSLATIONAL research, *RESEARCH institutes, *KIDNEYS, *BIG data
Abstract

Research on kidney diseases is being transformed by the rapid expansion and innovations in omics technologies. The analysis, integration, and interpretation of big data, however, have been an impediment to the growing interest in applying these technologies to understand kidney function and failure. Targeting this urgent need, the University of Michigan O'Brien Kidney Translational Core Center (MKTC) and its Administrative Core established the Applied Systems Biology Core. The Core provides need-based support for the global kidney community centered on enabling incorporation of systems biology approaches by creating web-based, user-friendly analytic and visualization tools, like Nephroseq and Nephrocell, guiding with experimental design, and processing, analysis, and integration of large data sets. The enrichment core supports systems biology education and dissemination through workshops, seminars, and individualized training sessions. Meanwhile, the Pilot and Feasibility Program of the MKTC provides pilot funding to both early-career and established investigators new to the field, to integrate a systems biology approach into their research projects. The relevance and value of the portfolio of training and services offered by MKTC are reflected in the expanding community of young investigators, collaborators, and users accessing resources and engaging in systems biology-based kidney research, thereby motivating MKTC to persevere in its mission to serve the kidney research community by enabling access to state-of-the-art data sets, tools, technologies, expertise, and learning opportunities for transformative basic, translational, and clinical studies that will usher in solutions to improve the lives of people impacted by kidney disease. [ABSTRACT FROM AUTHOR]

Published
2022
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50. Chloride channel accessory 1 integrates chloride channel activity and mTORC1 in aging‐related kidney injury

Author

Lee, Hak Joo, primary, Donati, Andrew, additional, Feliers, Denis, additional, Sun, Yuyang, additional, Ding, Yanli, additional, Madesh, Muniswamy, additional, Salmon, Adam B., additional, Ikeno, Yuji, additional, Ross, Corinna, additional, O'Connor, Christopher L., additional, Ju, Wenjun, additional, Bitzer, Markus, additional, Chen, Yidong, additional, Choudhury, Goutam Ghosh, additional, Singh, Brij B., additional, Sharma, Kumar, additional, and Kasinath, Balakuntalam S., additional

Published
2021
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