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2. The chromatin landscape of healthy and injured cell types in the human kidney

Author

Gisch, Debora L., Brennan, Michelle, Lake, Blue B., Basta, Jeannine, Keller, Mark S., Melo Ferreira, Ricardo, Akilesh, Shreeram, Ghag, Reetika, Lu, Charles, Cheng, Ying-Hua, Collins, Kimberly S., Parikh, Samir V., Rovin, Brad H., Robbins, Lynn, Stout, Lisa, Conklin, Kimberly Y., Diep, Dinh, Zhang, Bo, Knoten, Amanda, Barwinska, Daria, Asghari, Mahla, Sabo, Angela R., Ferkowicz, Michael J., Sutton, Timothy A., Kelly, Katherine J., De Boer, Ian H., Rosas, Sylvia E., Kiryluk, Krzysztof, Hodgin, Jeffrey B., Alakwaa, Fadhl, Winfree, Seth, Jefferson, Nichole, Türkmen, Aydın, Gaut, Joseph P., Gehlenborg, Nils, Phillips, Carrie L., El-Achkar, Tarek M., Dagher, Pierre C., Hato, Takashi, Zhang, Kun, Himmelfarb, Jonathan, Kretzler, Matthias, Mollah, Shamim, Jain, Sanjay, Rauchman, Michael, and Eadon, Michael T.

Published
2024
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4. A reference tissue atlas for the human kidney

Author

Hansen, Jens, Sealfon, Rachel, Menon, Rajasree, Eadon, Michael T, Lake, Blue B, Steck, Becky, Anjani, Kavya, Parikh, Samir, Sigdel, Tara K, Zhang, Guanshi, Velickovic, Dusan, Barwinska, Daria, Alexandrov, Theodore, Dobi, Dejan, Rashmi, Priyanka, Otto, Edgar A, Rivera, Miguel, Rose, Michael P, Anderton, Christopher R, Shapiro, John P, Pamreddy, Annapurna, Winfree, Seth, Xiong, Yuguang, He, Yongqun, de Boer, Ian H, Hodgin, Jeffrey B, Barisoni, Laura, Naik, Abhijit S, Sharma, Kumar, Sarwal, Minnie M, Zhang, Kun, Himmelfarb, Jonathan, Rovin, Brad, El-Achkar, Tarek M, Laszik, Zoltan, He, John Cijiang, Dagher, Pierre C, Valerius, M Todd, Jain, Sanjay, Satlin, Lisa M, Troyanskaya, Olga G, Kretzler, Matthias, Iyengar, Ravi, Azeloglu, Evren U, and Project, Kidney Precision Medicine

Subjects
Biotechnology, Genetics, Kidney Disease, Aetiology, 2.1 Biological and endogenous factors, Underpinning research, 1.1 Normal biological development and functioning, Generic health relevance, Renal and urogenital, Good Health and Well Being, Humans, Kidney, Kidney Diseases, Metabolomics, Proteomics, Transcriptome, Kidney Precision Medicine Project
Abstract

Kidney Precision Medicine Project (KPMP) is building a spatially specified human kidney tissue atlas in health and disease with single-cell resolution. Here, we describe the construction of an integrated reference map of cells, pathways, and genes using unaffected regions of nephrectomy tissues and undiseased human biopsies from 56 adult subjects. We use single-cell/nucleus transcriptomics, subsegmental laser microdissection transcriptomics and proteomics, near-single-cell proteomics, 3D and CODEX imaging, and spatial metabolomics to hierarchically identify genes, pathways, and cells. Integrated data from these different technologies coherently identify cell types/subtypes within different nephron segments and the interstitium. These profiles describe cell-level functional organization of the kidney following its physiological functions and link cell subtypes to genes, proteins, metabolites, and pathways. They further show that messenger RNA levels along the nephron are congruent with the subsegmental physiological activity. This reference atlas provides a framework for the classification of kidney disease when multiple molecular mechanisms underlie convergent clinical phenotypes.

Published
2022

5. 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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7. An atlas of healthy and injured cell states and niches in the human kidney

Author

Lake, Blue B., Menon, Rajasree, Winfree, Seth, Hu, Qiwen, Melo Ferreira, Ricardo, Kalhor, Kian, Barwinska, Daria, Otto, Edgar A., Ferkowicz, Michael, Diep, Dinh, Plongthongkum, Nongluk, Knoten, Amanda, Urata, Sarah, Mariani, Laura H., Naik, Abhijit S., Eddy, Sean, Zhang, Bo, Wu, Yan, Salamon, Diane, Williams, James C., Wang, Xin, Balderrama, Karol S., Hoover, Paul J., Murray, Evan, Marshall, Jamie L., Noel, Teia, Vijayan, Anitha, Hartman, Austin, Chen, Fei, Waikar, Sushrut S., Rosas, Sylvia E., Wilson, Francis P., Palevsky, Paul M., Kiryluk, Krzysztof, Sedor, John R., Toto, Robert D., Parikh, Chirag R., Kim, Eric H., Satija, Rahul, Greka, Anna, Macosko, Evan Z., Kharchenko, Peter V., Gaut, Joseph P., Hodgin, Jeffrey B., Eadon, Michael T., Dagher, Pierre C., El-Achkar, Tarek M., Zhang, Kun, Kretzler, Matthias, and Jain, Sanjay

Published
2023
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8. 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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9. Participant Experience with Protocol Research Kidney Biopsies in the Kidney Precision Medicine Project

Author

Victoria-Castro, Angela M., Corona-Villalobos, Celia P., Xu, Alan Y., Onul, Ingrid, Huynh, Courtney, Chen, Sarah W., Ugwuowo, Ugochukwu, Sarkisova, Natalya, Dighe, Ashveena L., Blank, Kristina N., Blanc, Victoria M., Rose, Michael P., Himmelfarb, Jonathan, de Boer, Ian H., Tuttle, Katherine R., Roberts, Glenda V., Alexandrov, Theodore, Alloway, Rita R., Alpers, Charles E., Amodu, Afolarin A., Anderton, Christopher R., Anjani, Kavya, Appelbaum, Paul, Ardayfio, Joseph, Arora, Tanima, Ascani, Heather, El-Achkar, Tarek M., Aulisio, Mark, Azeloglu, Evren U., Balderes, Olivia, Balis, Ulysses G.J., Bansal, Shweta, Barasch, Jonathan M., Bansal, Shweta, Barkell, Alex, Barwinska, Daria, Basit, Mujeeb, Basta, Jeanine, Bebiak, Jack, Beck, Laurence H., Bender, Filitsa, Berglund, Ashley, Bernard, Lauren, Berrouet, Cecilia, Berry, Brooke, Bjornstad, Petter M., Blanc, Victoria M., Blank, Kristina N., Bledsoe, Sharon, Boada, Patrick, Bogen, Steve, Bomback, Andrew S., Bonevich, Nikole, Borner, Katy, Brown, Keith, Bueckle, Andreas, Burg, Ashley R., Burgess, Adam, Bush, Lakeshia, Bush, William S., Campbell, Catherine E., Campbell, Taneisha, Canetta, Pietro A., Cantley, Lloyd G., Caprioli, Richard M., Carson, Jonas, Chen, Sarah, Chen, Yijiang M., Cheng, Yinghua, Cimino, Jim, Colona, Mia R., Conser, Ninive C., Cooperman, Leslie, Crawford, Dana C., DʼAgati, Vivette D., Dagher, Pierre C., Daniel, Stephen, Daratha, Kenn, de Boer, Ian H., Diettman, Sabine M., Dighe, Ashveena L., Donohoe, Isabel, Dowd, Frederick, Dunn, Kenneth W., Eadon, Michael T., Eddy, Sean, Elder, Michele M., Ferkowicz, Michael J., Frey, Renee, Gadegbeku, Crystal A., Gaut, Joseph P., Gilliam, Matthew, Ginley, Brandon, Gisch, Debora, Goltsev, Yury, Gonzalez-Vicente, Agustin, Greka, Anna, Grewenow, Stephanie M., Hacohen, Nir, Hall, Daniel E., Hansen, Jens, Hayashi, Lynda, He, Cijang, He, Yougqun, Hedayati, S. Susan, Henderson, Joel M., Hendricks, Allen H., Herlitz, Leal, Herr, Bruce W., Himmelfarb, Jonathan, Hodgin, Jeffrey B., Hoofnagle, Andrew N., Hoover, Paul J., Ilori, Titlayo, Iyengar, Ravi, Jain, Sanjay, Jain, Yashvardhan, Janowczyk, Andrew, Jefferson, Nichole, Johansen, Camille, Jolly, Stacey, Kakade, Vijaykumar R., Kellum, John A., Kelly, Katherine J., Kermani, Asra, Kiryluk, Krzysztof, Knight, Richard, Koewler, Robert, Kretzler, Matthias, Kudose, Satoru, Lake, Blue B., Larson, Brandon, Laszik, Zoltan G., Lecker, Stewart H., Lee, Paul J., Lee, Simon C., Lienczewski, Chrysta, Limonte, Christine, Lu, Christopher Y., Lucarelli, Nicholas, Lukowski, Jessica, Luo, Jinghui, Lutnick, Brendon, Ma, Shihong, Madabhushi, Anant, Madhavan, Sethu M., Maikhor, Shana, Mariani, Laura H., Marshall, Jamie L., McClelland, Robyn L., McMahon, Gearoid M., Mehl, Karla, Ferreira, Ricardo Melo, Menez, Steven, Menon, Rajasree, Miller, R. Tyler, Moe, Orson W., Moledina, Dennis, Montellano, Richard, Mooney, Sean D., Morales, Martha Catalina, Mukatash, Tariq, Murugan, Raghavan, Nam, Yunbi, Nguyen, Jane, Nolan, Garry, Oʼtoole, John, Oliver, George (Holt), Onul, Ingrid, Otto, Edgar, Palevsky, Paul M., Palmer, Ellen, Pamreddy, Annapurna, Parikh, Chirag R., Parikh, Samir, Park, Christopher, Park, Harold, Pasa-Tolic, Ljiljana, Patel, Jiten, Patterson, Nathan, Phuong, Jim, Pillai, Anil, Pinkeney, Roy, Poggio, Emilio, Pollack, Ari, Prasad, Pottumarthi, Pyle, Laura, Quardokus, Ellen M., Randhawa, Parmjeet, Rauchman, Michael I., Record, Elizabeth, Rennke, Helmut, Rezaei, Kasra, Rike, Adele, Rivera, Marcelino, Roberts, Glenda V., Rosas, Sylvia E., Rosenberg, Avi, Rosengart, Matthew, Rovin, Brad, Roy, Neil, Sabatello, Maya, Sambandam, Kamalanathan, Sarder, Pinaki, Sarkisova, Natalya, Sarwal, Minnie, Saul, John, Schaub, Jennifer, Schmidt, Insa, Sealfon, Rachel, Sedor, John, Sendrey, Dianna, Shang, Ning, Shankland, Stuart, Shapiro, John P., Sharma, Kumar, Sharman, Kavya, Shaw, Melissa M., Shi, Tiffany, Shpigel, Anna, Sigdel, Tara, Slade, Austen, Snyder, Jamie, Spates-Harden, Kassandra, Spraggins, Jeffrey M., Srivastava, Anand, Steck, Becky, Stillman, Isaac, Stutzke, Christy, Su, Jing, Sun, Jennifer, Sutton, Timothy A., Taliercio, Jonathan, Tan, Roderick, Torrealba, Jose, Toto, Robert D., Troyanskaya, Olga, Tublin, Mitchell, Tuttle, Katherine R., Ugwuowo, Ugochukwu, Valerius, M. Todd, Van de Plas, Raf, Varela, German, Vazquez, Miguel, Velickovic, Dusan, Venkatachalam, Manjeri, Verma, Ashish, Victoria-Castro, Angela M., Vijayan, Anitha, Corona-Villalobos, Celia P., Vinovskis, Carissa, Viswanathan, Vidya S., Vita, Tina, Waikar, Sushrut, Wang, Ashley, Wang, Ruikang, Wang, Nancy, Weins, Astrid, Wen, Natasha, Wen, Yumeng, Wilcox, Adam, Williams, James C., Jr., Kayleen Williams, Williams, Mark, Wilson, Francis P., Winfree, Seth, Winters, James, Wofford, Stephanie, Wong, Aaron, Woodle, E. Steve, Xiong, Yuguang, Xu, Alan, Yadati, Pranav, Ye, Hongping, Yu, Guanghao, Zhang, Dianbo, Zhang, Guanshi, and Zhang, Kun

Published
2024
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10. Efficacy of AAV9-mediated SGPL1 gene transfer in a mouse model of S1P lyase insufficiency syndrome.

Author

Zhao, Piming, Tassew, Gizachew B, Lee, Joanna Y, Oskouian, Babak, Muñoz, Denise P, Hodgin, Jeffrey B, Watson, Gordon L, Tang, Felicia, Wang, Jen-Yeu, Luo, Jinghui, Yang, Yingbao, King, Sarah, Krauss, Ronald M, Keller, Nancy, and Saba, Julie D

Subjects
Gene therapy, Genetic diseases, Metabolism, Therapeutics
Abstract

Sphingosine-1-phosphate lyase insufficiency syndrome (SPLIS) is a rare metabolic disorder caused by inactivating mutations in sphingosine-1-phosphate lyase 1 (SGPL1), which is required for the final step of sphingolipid metabolism. SPLIS features include steroid-resistant nephrotic syndrome and impairment of neurological, endocrine, and hematopoietic systems. Many affected individuals die within the first 2 years. No targeted therapy for SPLIS is available. We hypothesized that SGPL1 gene replacement would address the root cause of SPLIS, thereby serving as a universal treatment for the condition. As proof of concept, we evaluated the efficacy of adeno-associated virus 9-mediated transfer of human SGPL1 (AAV-SPL) given to newborn Sgpl1-KO mice that model SPLIS and die in the first weeks of life. Treatment dramatically prolonged survival and prevented nephrosis, neurodevelopmental delay, anemia, and hypercholesterolemia. STAT3 pathway activation and elevated proinflammatory and profibrogenic cytokines observed in KO kidneys were attenuated by treatment. Plasma and tissue sphingolipids were reduced in treated compared with untreated KO pups. SGPL1 expression and activity were measurable for at least 40 weeks. In summary, early AAV-SPL treatment prevents nephrosis, lipidosis, and neurological impairment in a mouse model of SPLIS. Our results suggest that SGPL1 gene replacement holds promise as a durable and universal targeted treatment for SPLIS.

Published
2021

11. Rationale and design of the Kidney Precision Medicine Project

Author

de Boer, Ian H, Alpers, Charles E, Azeloglu, Evren U, Balis, Ulysses GJ, Barasch, Jonathan M, Barisoni, Laura, Blank, Kristina N, Bomback, Andrew S, Brown, Keith, Dagher, Pierre C, Dighe, Ashveena L, Eadon, Michael T, El-Achkar, Tarek M, Gaut, Joseph P, Hacohen, Nir, He, Yongqun, Hodgin, Jeffrey B, Jain, Sanjay, Kellum, John A, Kiryluk, Krzysztof, Knight, Richard, Laszik, Zoltan G, Lienczewski, Chrysta, Mariani, Laura H, McClelland, Robyn L, Menez, Steven, Moledina, Dennis G, Mooney, Sean D, O’Toole, John F, Palevsky, Paul M, Parikh, Chirag R, Poggio, Emilio D, Rosas, Sylvia E, Rosengart, Matthew R, Sarwal, Minnie M, Schaub, Jennifer A, Sedor, John R, Sharma, Kumar, Steck, Becky, Toto, Robert D, Troyanskaya, Olga G, Tuttle, Katherine R, Vazquez, Miguel A, Waikar, Sushrut S, Williams, Kayleen, Wilson, Francis Perry, Zhang, Kun, Iyengar, Ravi, Kretzler, Matthias, Himmelfarb, Jonathan, Project, Kidney Precision Medicine, Lecker, Stewart, Stillman, Isaac, Waikar, Sushrut, Mcmahon, Gearoid, Weins, Astrid, Short, Samuel, Hoover, Paul, Aulisio, Mark, Cooperman, Leslie, Herlitz, Leal, O’Toole, John, Poggio, Emilio, Sedor, John, Jolly, Stacey, Appelbaum, Paul, Balderes, Olivia, Barasch, Jonathan, Bomback, Andrew, Canetta, Pietro A, d’Agati, Vivette D, Kudose, Satoru, Mehl, Karla, Radhakrishnan, Jai, Weng, Chenhua, Alexandrov, Theodore, Ashkar, Tarek, Barwinska, Daria, Dagher, Pierre, Dunn, Kenneth, Eadon, Michael, Ferkowicz, Michael, Kelly, Katherine, Sutton, Timothy, Winfree, Seth, Parikh, Chirag, Rosenberg, Avi, Villalobos, Pam, Malik, Rubab, Fine, Derek, Atta, Mohammed, Trujillo, Jose Manuel Monroy, Slack, Alison, Rosas, Sylvia, and Williams, Mark

Subjects
Clinical Research, Transplantation, Kidney Disease, Prevention, Renal and urogenital, Good Health and Well Being, Acute Kidney Injury, Adult, Humans, Kidney, Precision Medicine, Prospective Studies, Proteomics, Renal Insufficiency, Chronic, acute kidney injury, chronic kidney disease, diabetes, hypertension, precision medicine, Kidney Precision Medicine Project, Clinical Sciences, Urology & Nephrology
Abstract

Chronic kidney disease (CKD) and acute kidney injury (AKI) are common, heterogeneous, and morbid diseases. Mechanistic characterization of CKD and AKI in patients may facilitate a precision-medicine approach to prevention, diagnosis, and treatment. The Kidney Precision Medicine Project aims to ethically and safely obtain kidney biopsies from participants with CKD or AKI, create a reference kidney atlas, and characterize disease subgroups to stratify patients based on molecular features of disease, clinical characteristics, and associated outcomes. An additional aim is to identify critical cells, pathways, and targets for novel therapies and preventive strategies. This project is a multicenter prospective cohort study of adults with CKD or AKI who undergo a protocol kidney biopsy for research purposes. This investigation focuses on kidney diseases that are most prevalent and therefore substantially burden the public health, including CKD attributed to diabetes or hypertension and AKI attributed to ischemic and toxic injuries. Reference kidney tissues (for example, living-donor kidney biopsies) will also be evaluated. Traditional and digital pathology will be combined with transcriptomic, proteomic, and metabolomic analysis of the kidney tissue as well as deep clinical phenotyping for supervised and unsupervised subgroup analysis and systems biology analysis. Participants will be followed prospectively for 10 years to ascertain clinical outcomes. Cell types, locations, and functions will be characterized in health and disease in an open, searchable, online kidney tissue atlas. All data from the Kidney Precision Medicine Project will be made readily available for broad use by scientists, clinicians, and patients.

Published
2021

12. Precision nephrology identified tumor necrosis factor activation variability in minimal change disease and focal segmental glomerulosclerosis

Author

Mariani, Laura H., Eddy, Sean, AlAkwaa, Fadhl M., McCown, Phillip J., Harder, Jennifer L., Nair, Viji, Eichinger, Felix, Martini, Sebastian, Ademola, Adebowale D., Boima, Vincent, Reich, Heather N., El Saghir, Jamal, Godfrey, Bradley, Ju, Wenjun, Tanner, Emily C., Vega-Warner, Virginia, Wys, Noel L., Adler, Sharon G., Appel, Gerald B., Athavale, Ambarish, Atkinson, Meredith A., Bagnasco, Serena M., Barisoni, Laura, Brown, Elizabeth, Cattran, Daniel C., Coppock, Gaia M., Dell, Katherine M., Derebail, Vimal K., Fervenza, Fernando C., Fornoni, Alessia, Gadegbeku, Crystal A., Gibson, Keisha L., Greenbaum, Laurence A., Hingorani, Sangeeta R., Hladunewich, Michelle A., Hodgin, Jeffrey B., Hogan, Marie C., Holzman, Lawrence B., Jefferson, J. Ashley, Kaskel, Frederick J., Kopp, Jeffrey B., Lafayette, Richard A., Lemley, Kevin V., Lieske, John C., Lin, Jen-Jar, Menon, Rajarasee, Meyers, Kevin E., Nachman, Patrick H., Nast, Cynthia C., O’Shaughnessy, Michelle M., Otto, Edgar A., Reidy, Kimberly J., Sambandam, Kamalanathan K., Sedor, John R., Sethna, Christine B., Singer, Pamela, Srivastava, Tarak, Tran, Cheryl L., Tuttle, Katherine R., Vento, Suzanne M., Wang, Chia-shi, Ojo, Akinlolu O., Adu, Dwomoa, Gipson, Debbie S., Trachtman, Howard, and Kretzler, Matthias

Published
2023
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14. A Participant-Centered Approach to Understanding Risks and Benefits of Participation in Research Informed by the Kidney Precision Medicine Project

Author

Alexandrov, Theodore, Alpers, Charles E., Anderton, Christopher R., Ardayfio, Joseph, Arora, Tanima, El-Achkar, Tarek M., Azeloglu, Evren U., Balderes, Olivia, Balis, Ulysses G.J., Bansal, Shweta, Barasch, Jonathan M., Barwinska, Daria, Bebiak, Jack, Blanc, Victoria M., Blank, Kristina N., Bomback, Andrew S., Brown, Keith D., Bush, William S., Campbell, Taneisha, Canetta, Pietro A., Carson, Jonas, Cooperman, Leslie, Crawford, Dana C., D’Agati, Vivette D., Dagher, Pierre C., Daniel, Stephen, Dowd, Frederick, Dunn, Kenneth W., Eadon, Michael T., Eddy, Sean, Elder, Michele M., Ferkowicz, Michael J., Gaut, Joe P., Goltsev, Yury, Gonzalez-Vicente, Agustin, Hacohen, Nir, Hansen, Jens, Hayashi, Lynda, He, Oliver, He, Cijang, Hedayati, S. Susan, Herlitz, Leal, Hodgin, Jeffrey B., Hoofnagle, Andrew N., Hoover, Paul J., Iyengar, Ravi, Jain, Sanjay, Jefferson, Nichole, Jolly, Stacey, Kellum, John A., Kelly, Katherine J., Kermani, Asra, Kiryluk, Krzysztof, Koewler, Robert, Kretzler, Matthias, Lake, Blue B., Laszik, Zoltan G., Lecker, Stewart H., Lee, Simon C., Lienczewski, Chrysta, Lu, Christopher Y., Mariani, Laura H., McClelland, Robyn L., McMahon, Gearoid M., Menez, Steven, Menon, Rajasree, Miller, Tyler, Moe, Orson W., Moledina, Dennis, Mooney, Sean D., Nguyen, Jane, Nolan, Garry, Oliver, George, Otto, Edgar, Palevsky, Paul M., Palmer, Ellen, Pamreddy, Annapurna, Parikh, Chirag R., Parikh, Samir, Park, Christopher, Park, Harold, Pasa-Tolic, Ljiljana, Pinkeney, Roy, Poggio, Emilio, Randhawa, Parmjeet, Rennke, Helmut, Roberts, Glenda V., Rosenberg, Avi, Rosengart, Matthew, Rovin, Brad, Roy, Neil, Sambandam, Kamalanathan, Sarwal, Minnie, Saul, John, Schaub, Jennifer, Sealfon, Rachel, Shang, Ning, Shankland, Stuart, Sharma, Kumar, Shpigel, Anna, Sigdel, Tara, Steck, Becky, Stillman, Isaac, Stutzke, Edith Christine, Sutton, Timothy A., Torrealba, Jose, Toto, Robert D., Troyanskaya, Olga, Tublin, Mitchell, Ugwuowo, Ugochukwu, Vazquez, Miguel, Velickovic, Dusan, Venkatachalam, Manjeri, Vijayan, Anitha, Corona-Villalobos, Celia P., Wang, Nancy, Weins, Astrid, Wilcox, Adam, Williams, Kayleen, Williams, Mark, Wilson, Francis P., Winfree, Seth, Xiong, Yuguang, Zhang, Kun, Zhang, Guanshi, Butler, Catherine R., Appelbaum, Paul S., Ascani, Heather, Aulisio, Mark, Campbell, Catherine E., de Boer, Ian H., Dighe, Ashveena L., Hall, Daniel E., Himmelfarb, Jonathan, Knight, Richard, Mehl, Karla, Murugan, Raghavan, Rosas, Sylvia E., Sedor, John R., O’Toole, John F., Tuttle, Katherine R., Waikar, Sushrut S., and Freeman, Michael

Published
2022
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15. Quantification of Glomerular Structural Lesions: Associations With Clinical Outcomes and Transcriptomic Profiles in Nephrotic Syndrome

Author

Dell, K., Sedor, J., Schachere, M., Negrey, J., Lemley, K., Lim, E., Srivastava, T., Garrett, A., Sethna, C., Laurent, K., Canetta, P., Pradhan, A., Greenbaum, L., Wang, C., Kang, C., Adler, S., LaPage, J., Athavale, A., Itteera, M., Atkinson, M., Boynton, S., Fervenza, F., Hogan, M., Lieske, J., Chernitskiy, V., Kaskel, F., Ross, M., Flynn, P., Kopp, J., Blake, J., Trachtman, H., Zhdanova, O., Modersitzki, F., Vento, S., Bray, M., Kelton, M., Cooper, A., Lafayette, R., Mehta, K., Gadegbeku, C., Quinn-Boyle, S., Hladunewich, M., Reich, H., Ling, P., Romano, M., Fornoni, A., Bidot, C., Kretzler, M., Gipson, D., Williams, A., LaVigne, J., Derebail, V., Gibson, K., Cole, E., Ormond-Foster, J., Holzman, L., Meyers, K., Kallem, K., Swenson, A., Sambandam, K., Wang, Z., Rogers, M., Jefferson, A., Hingorani, S., Tuttle, K., Lin, J.J., Barisoni, L., Bixler, J., Desmond, H., Eddy, S., Fermin, D., Gillespie, B., Kurtz, V., Larkina, M., Lavigne, J., Li, S., Lienczewski, C.C., Liu, J., Mainieri, T., Mariani, L., Sampson, M., Smith, A., Zee, J., Avila-Casado, Carmen, Bagnasco, Serena, Gaut, Joseph, Hewitt, Stephen, Hodgin, Jeff, Lemley, Kevin, Mariani, Laura, Palmer, Matthew, Rosenberg, Avi, Royal, Virginie, Thomas, David, Zee, Jarcy, Barisoni, Laura, Nast, Cynthia, Hodgin, Jeffrey B., Mariani, Laura H., Liu, Qian, Smith, Abigail R., Eddy, Sean, Hartman, John, Hamidi, Habib, Gaut, Joseph P., Palmer, Matthew B., Nast, Cynthia C., Chang, Anthony, Gillespie, Brenda W., Kretzler, Matthias, and Holzman, Lawrence B.

Published
2022
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16. Endogenous adenine mediates kidney injury in diabetic models and predicts diabetic kidney disease in patients

Author

Sharma, Kumar, Zhang, Guanshi, Hansen, Jens, Bjornstad, Petter, Lee, Hak Joo, Menon, Rajasree, Hejazi, Leila, Liu, Jian-Jun, Franzone, Anthony, Looker, Helen C., Choi, Byeong Yeob, Fernandez, Roman, Venkatachalam, Manjeri A., Kugathasan, Luxcia, Sridhar, Vikas S., Natarajan, Loki, Zhang, Jing, Sharma, Varun S., Kwan, Brian, Waikar, Sushrut S., Himmelfarb, Jonathan, Tuttle, Katherine R., Kestenbaum, Bryan, Fuhrer, Tobias, Feldman, Harold I., de Boer, Ian H., Tucci, Fabio C., Sedor, John, Heerspink, Hiddo Lambers, Schaub, Jennifer, Otto, Edgar A., Hodgin, Jeffrey B., Kretzler, Matthias, Anderton, Christopher R., Alexandrov, Theodore, Cherney, David, Lim, Su Chi, Nelson, Robert G., Gelfond, Jonathan, and Iyengar, Ravi

Subjects
United States. National Center for Advancing Translational Sciences, Thermo Fisher Scientific Inc., Bayer AG, Boehringer Ingelheim GmbH, AstraZeneca PLC, Eli Lilly and Co., Novo Nordisk A/S, Sanofi S.A., Medical research -- Health aspects, Medicine, Experimental -- Health aspects, Scientific equipment and supplies industry -- Health aspects, Chronic kidney failure -- Health aspects, Medical colleges -- Health aspects, Type 2 diabetes -- Health aspects, Native Americans -- Health aspects, Pharmaceutical industry -- Health aspects, Purines -- Health aspects, Health care industry
Abstract

Diabetic kidney disease (DKD) can lead to end-stage kidney disease (ESKD) and mortality; however, few mechanistic biomarkers are available for high-risk patients, especially those without macroalbuminuria. Urine from participants with diabetes from the Chronic Renal Insufficiency Cohort (CRIC) study, the Singapore Study of Macro-angiopathy and Micro-vascular Reactivity in Type 2 Diabetes (SMART2D), and the American Indian Study determined whether urine adenine/creatinine ratio (UAdCR) could be a mechanistic biomarker for ESKD. ESKD and mortality were associated with the highest UAdCR tertile in the CRIC study and SMART2D. ESKD was associated with the highest UAdCR tertile in patients without macroalbuminuria in the CRIC study, SMART2D, and the American Indian study. Empagliflozin lowered UAdCR in nonmacroalbuminuric participants. Spatial metabolomics localized adenine to kidney pathology, and single-cell transcriptomics identified ribonucleoprotein biogenesis as a top pathway in proximal tubules of patients without macroalbuminuria, implicating mTOR. Adenine stimulated matrix in tubular cells via mTOR and stimulated mTOR in mouse kidneys. A specific inhibitor of adenine production was found to reduce kidney hypertrophy and kidney injury in diabetic mice. We propose that endogenous adenine may be a causative factor in DKD., Introduction Progression to organ failure is marked by fibrosis and loss of architecture in solid organs, such as the kidney. In almost all progressive chronic kidney diseases (CKDs), the features [...]

Published
2023
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18. 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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19. Cadherin-11, Sparc-related modular calcium binding protein-2, and Pigment epithelium-derived factor are promising non-invasive biomarkers of kidney fibrosis

Author

Knight, Richard, Lecker, Stewart H., Stillman, Isaac, Bogen, Steve, Amodu, Afolarin A., Ilori, Titlayo, Maikhor, Shana, Schmidt, Insa M., Beck, Laurence H., Henderson, Joel M., Onul, Ingrid, Verma, Ashish, McMahon, Gearoid M., Valerius, M. Todd, Waikar, Sushrut, Weins, Astrid, Colona, Mia R., Greka, Anna, Hacohen, Nir, Hoover, Paul J., Marshall, Jamie L., Aulisio, Mark, Chen, Yijiang M., Janowczyk, Andrew, Jayapandian, Catherine, Viswanathan, Vidya S., Bush, William S., Crawford, Dana C., Madabhushi, Anant, Bush, Lakeshia, Cooperman, Leslie, Gonzalez-Vicente, Agustin, Herlitz, Leal, Jolly, Stacey, Nguyen, Jane, O’toole, John, Palmer, Ellen, Poggio, Emilio, Sedor, John, Sendrey, Dianna, Spates-Harden, Kassandra, Taliercio, Jonathan, Bjornstad, Petter M., Pyle, Laura, Vinovskis, Carissa, Appelbaum, Paul, Balderes, Olivia, Barasch, Jonathan M., Bomback, Andrew S., Canetta, Pietro A., D’Agati, Vivette D., Kiryluk, Krzysztof, Kudose, Satoru, Mehl, Karla, Shang, Ning, Bansal, Shweta, Alexandrov, Theodore, Rennke, Helmut, El-Achkar, Tarek M., Barwinska, Daria, Bledso, Sharon, Borner, Katy, Bueckle, Andreas, Cheng, Yinghua, Dagher, Pierre C., Dunn, Kenneth W., Eadon, Michael T., Ferkowicz, Michael J., Herr, Bruce W., Kelly, Katherine J., Ferreira, Ricardo Melo, Quardokus, Ellen M., Record, Elizabeth, Rivera, Marcelino, Su, Jing, Sutton, Timothy A., Williams, James C., Jr., Winfree, Seth, Jain, Yashvardhan, Menez, Steven, Parikh, Chirag R., Rosenberg, Avi, Corona-Villalobos, Celia P., Wen, Yumeng, Johansen, Camille, Rosas, Sylvia E., Roy, Neil, Sun, Jennifer, Williams, Mark, Azeloglu, Evren U., Hansen, Jens, He, Cijang, Iyengar, Ravi, Xiong, Yuguang, Prasad, Pottumarthi, Srivastava, Anand, Madhavan, Sethu M., Parikh, Samir, Rovin, Brad, Shapiro, John P., Anderton, Christopher R., Lukowski, Jessica, Pasa-Tolic, Ljiljana, Velickovic, Dusan, Oliver, George (Holt), Ardayfio, Joseph, Bebiak, Jack, Brown, Keith, Campbell, Taneisha, Campbell, Catherine E., Hayashi, Lynda, Jefferson, Nichole, Roberts, Glenda V., Saul, John, Shpigel, Anna, Stutzke, Christy, Koewler, Robert, Pinkeney, Roy, Sealfon, Rachel, Troyanskaya, Olga, Wong, Aaron, Tuttle, Katherine R., Pollack, Ari, Goltsev, Yury, Ginley, Brandon, Lucarelli, Nicholas, Lutnick, Brendon, Sarder, Pinaki, Lake, Blue B., Zhang, Kun, Boada, Patrick, Laszik, Zoltan G., Nolan, Garry, Anjani, Kavya, Sarwal, Minnie, Mukatash, Tariq, Sigdel, Tara, Alloway, Rita R., Burg, Ashley R., Lee, Paul J., Rike, Adele, Shi, Tiffany, Woodle, E. Steve, Ascani, Heather, Balis, Ulysses G.J., Blanc, Victoria M., Conser, Ninive C., Eddy, Sean, Frey, Renee, He, Yougqun, Hodgin, Jeffrey B., Kretzler, Matthias, Lienczewski, Chrysta, Luo, Jinghui, Mariani, Laura H., Menon, Rajasree, Otto, Edgar, Schaub, Jennifer, Steck, Becky, Elder, Michele M., Gilliam, Matthew, Hall, Daniel E., Murugan, Raghavan, Palevsky, Paul M., Randhawa, Parmjeet, Rosengart, Matthew, Tublin, Mitchell, Vita, Tina, Winters, James, Kellum, John A., Alpers, Charles E., Berglund, Ashley, Berry, Brooke, Blank, Kristina N., Carson, Jonas, Daniel, Stephen, De Boer, Ian H., Dighe, Ashveena L., Dowd, Frederick, Grewenow, Stephanie M., Himmelfarb, Jonathan, Hoofnagle, Andrew N., Limonte, Christine, McClelland, Robyn L., Mooney, Sean D., Rezaei, Kasra, Shankland, Stuart, Snyder, Jamie, Wang, Ruikang, Wilcox, Adam, Williams, Kayleen, Park, Christopher, Montellano, Richard, Pamreddy, Annapurna, Sharma, Kumar, Venkatachalam, Manjeri, Ye, Hongping, Zhang, Guanshi, Basit, Mujeeb, Hedayati, S. Susan, Kermani, Asra, Lee, Simon C., Lu, Christopher Y., Miller, R. Tyler, Moe, Orson W., Patel, Jiten, Pillai, Anil, Sambandam, Kamalanathan, Torrealba, Jose, Toto, Robert D., Vazquez, Miguel, Wang, Nancy, Wen, Natasha, Zhang, Dianbo, Park, Harold, Caprioli, Richard M., Patterson, Nathan, Sharman, Kavya, Spraggins, Jeffrey M., Van de Plas, Raf, Basta, Jeanine, Diettman, Sabine M., Gaut, Joseph P., Jain, Sanjay, Rauchman, Michael I., Vijayan, Anitha, Cantley, Lloyd G., Kakade, Vijaykumar R., Moledina, Dennis, Shaw, Melissa M., Ugwuowo, Ugochukwu, Wilson, Francis P., Arora, Tanima, Kestenbaum, Bryan R., Alexopoulos, Leonidas G., Palsson, Ragnar, Liu, Jing, Stillman, Isaac E., Rennke, Helmut G., Vaidya, Vishal S., Wu, Haojia, Humphreys, Benjamin D., and Waikar, Sushrut S.

Published
2021
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20. APOL1 genotype-associated morphologic changes among patients with focal segmental glomerulosclerosis

Author

Zee, Jarcy, McNulty, Michelle T., Hodgin, Jeffrey B., Zhdanova, Olga, Hingorani, Sangeeta, Jefferson, Jonathan Ashley, and Gibson, Keisha L.

Subjects
Nephrotic syndrome -- Risk factors -- Care and treatment, Apolipoproteins -- Demographic aspects -- Risk factors, Health
Abstract

Background The G1 and G2 alleles of apolipoprotein L1 (APOL1) are common in the Black population and associated with increased risk of focal segmental glomerulosclerosis (FSGS). The molecular mechanisms linking APOL1 risk variants with FSGS are not clearly understood, and APOL1's natural absence in laboratory animals makes studying its pathobiology challenging. Methods In a cohort of 90 Black patients with either FSGS or minimal change disease (MCD) enrolled in the Nephrotic Syndrome Study Network (58% pediatric onset), we used kidney biopsy traits as an intermediate outcome to help illuminate tissue-based consequences of APOL1 risk variants and expression. We tested associations between APOL1 risk alleles or glomerular APOL1 mRNA expression and 83 light- or electron-microscopy traits measuring structural and cellular kidney changes. Results Under both recessive and dominant models in the FSGS patient subgroup (61%), APOL1 risk variants were significantly correlated (defined as FDR Conclusions While APOL1-associated FSGS is associated with two risk alleles, both one and two risk alleles are associated with cellular/tissue changes in this study of FSGS patients. Our lack of discovery of a large group of tissue differences in FSGS and no significant difference in MCD may be due to the lack of power but also supports investigating whether machine learning methods may more sensitively detect APOL1-associated changes., Author(s): Jarcy Zee [sup.1] , Michelle T. McNulty [sup.2] , Jeffrey B. Hodgin [sup.3] , Olga Zhdanova [sup.4] , Sangeeta Hingorani [sup.5] , Jonathan Ashley Jefferson [sup.6] , Keisha L. [...]

Published
2021
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21. Development and evaluation of deep learning–based segmentation of histologic structures in the kidney cortex with multiple histologic stains

Author

Sedor, J., Dell, K., Schachere, M., Negrey, J., Lemley, K., Lim, E., Srivastava, T., Garrett, A., Sethna, C., Laurent, K., Appel, G., Toledo, M., Barisoni, L., Greenbaum, L., Wang, C., Kang, C., Adler, S., Nast, C., LaPage, J., Stroger, John H., Jr., Athavale, A., Itteera, M., Neu, A., Boynton, S., Fervenza, F., Hogan, M., Lieske, J., Chernitskiy, V., Kaskel, F., Kumar, N., Flynn, P., Kopp, J., Blake, J., Trachtman, H., Zhdanova, O., Modersitzki, F., Vento, S., Lafayette, R., Mehta, K., Gadegbeku, C., Johnstone, D., Quinn-Boyle, S., Cattran, D., Hladunewich, M., Reich, H., Ling, P., Romano, M., Fornoni, A., Bidot, C., Kretzler, M., Gipson, D., Williams, A., LaVigne, J., Derebail, V., Gibson, K., Froment, A., Grubbs, S., Holzman, L., Meyers, K., Kallem, K., Lalli, J., Sambandam, K., Wang, Z., Rogers, M., Jefferson, A., Hingorani, S., Tuttle, K., Bray, M., Kelton, M., Cooper, A., Freedman, B., Lin, J.J., Jayapandian, Catherine P., Chen, Yijiang, Janowczyk, Andrew R., Palmer, Matthew B., Cassol, Clarissa A., Sekulic, Miroslav, Hodgin, Jeffrey B., Zee, Jarcy, Hewitt, Stephen M., O’Toole, John, Toro, Paula, Sedor, John R., Barisoni, Laura, and Madabhushi, Anant

Published
2021
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22. 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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23. SARS-CoV-2 receptor networks in diabetic and COVID-19–associated kidney disease

Author

Menon, Rajasree, Otto, Edgar A., Sealfon, Rachel, Nair, Viji, Wong, Aaron K., Theesfeld, Chandra L., Chen, Xi, Wang, Yuan, Boppana, Avinash S., Luo, Jinghui, Yang, Yingbao, Kasson, Peter M., Schaub, Jennifer A., Berthier, Celine C., Eddy, Sean, Lienczewski, Chrysta C., Godfrey, Bradley, Dagenais, Susan L., Sohaney, Ryann, Hartman, John, Fermin, Damian, Subramanian, Lalita, Looker, Helen C., Harder, Jennifer L., Mariani, Laura H., Hodgin, Jeffrey B., Sexton, Jonathan Z., Wobus, Christiane E., Naik, Abhijit S., Nelson, Robert G., Troyanskaya, Olga G., and Kretzler, Matthias

Published
2020
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25. Protein N-Glycans in Healthy and Sclerotic Glomeruli in Diabetic Kidney Disease

Author

Veličković, Dušan, Shapiro, John P., Parikh, Samir V., Rovin, Brad, Toto, Robert D., Vazquez, Miguel A., Poggio, Emilio D., O'Toole, John F., Sedor, John R., Alexandrov, Theodore, Jain, Sanjay, Bitzer, Markus, Hodgin, Jeffrey, Veličković, Marija, Sharma, Kumar, Anderton, Christopher R., Adeyi, Oyedele A., Alakwaa, Fadhl, Alexandrov, Theodore, Allen, Jamie L., Alpers, Charles E., Alvear, Alison Bunio, Ambekar, Akhil, Ancheta, Joed, Anderton, Christopher R., Angus, Sophia A., Anjani, Kavya, Appelbaum, Paul S., Ardayfio, Joseph, Arora, Tanima, Ascani, Heather K., Asghari, Mahla, El-Achkar, Tarek M., Athar, Humra, Atta, Mohamed G., Aulisio, Mark P., Aw, Stephanie J., Azeloglu, Evren U., Bagne, Cathy A., Balderes, Olivia, Balis, Ulysses G.J., Barasch, Jonathan, Barisoni, Laura, Barwinska, Daria, Basta, Jeannine, Bebiak, Jack, Beck, Laurence H., Berge, Jerica M., Berglund, Ashley C., Bernard, Lauren, Berry, Brooke, Beyda, David H., Bhanushali, Jini Ashok, Bitzer, Markus, Bjornstad, Petter, Blanc, Victoria M., Blank, Kristina N., Bledsoe, Sharon B., Bogen, Steve, Bomback, Andrew S., Bonevich, Nikole, Border, Samuel, Börner, Katy, Bowen, William S., Boys, Charlotte, Bracamonte, Erika R., Bream, Peter R., Brosius, Frank C., Brown, Keith D., Budiman, Tifanny, Bueckle, Andreas, Bui, J.T., James, T., Burg, Ashley R., Burgess, Adam, Bush, Lakeshia, Bush, William S., Cai, Qi, Calixte, Marie Florence, Cameron-Wheeler, Tashas, Campbell, Kirk N, Campbell, Taneisha, Campbell, Catherine, Campos, Baltazar, Canetta, Pietro A., Cantley, Lloyd G, Caramori, M. Luiza, Carmona-Powell, Eunice, Carson, Jonas M, Chan, Lili, Chen, Sarah W, Chen, Yijiang, Cheng, Ying-Hua, Bejarano, Maria Chilo, Choe, Kisurb, Cimino, James G., Coca, Steven G., Coleman, Alyson, Colley, Madeline E., Collie, Mary M., Colona, Mia R., Commander, Clayton W., Conlon, Kristine, Conser, Ninive, Cooperman, Leslie, Corona-Villalobos, Celia P., Crawford, Dana C., Creger, Nathan, Cuevas-Rios, Yarieli, D'Agati, Vivette ., Dagher, Pierre c., de Boer, Ian H., de Caestecker, M.P, de Cos, Marina, Gonçalves, Joana P., Dekker, Matthew, Demeke, Dawit, Dighe, Ashveena L, Ding, Yanli, Djambazova, Katerina V., Donohoe, Isabel, Dowd, Frederick, Drawz, P.E., Dufresne, Martin, Dull, Rachel, Dunn, Kenneth W., Duran, Daniel Damian, Eadon, Michael T, Eddy, Sean, Elder, Michele M, Fallegger, Robin, Farrow, Melissa A, Ferkowicz, Michael, Fine, Derek M., Flanagan, Siobhan M., Fogo, Agnes B., Fox, Monica L., Frey, Renee, Froment, Anne, Gaba, Ron C., Gadegbeku, Crystal A, Gaut, Joseph P., Gehlenborg, Nils, Geraghty, Molly C, Ghag, Reetika, Gilliam, Matthew, Ginley, Brandon, Gisch, Debora, Gordon, Ronald E., Gorman, Brittney L., Greka, Anna, Grewenow, Stephanie M., Gurung, Bhupendra Kumar, Guthrie, Leah, Hacohen, Nir, Haddad, Samuel, Hall, Daniel E., Hansen, Jens, Harindhanavudhi, Tasma, Hartman, John, Hayashi, Lynda, Haydak, Jonathan, He, John Cijiang, He, Yongqun, Hedayati, S. Susan, Henderson, Dori, Henderson, Joel M, Hendricks, Allen R, Henshaw, Asari, Herlitz, Leal, Hernandez, Jeanine, Herr, Bruce W., Himmelfarb, Jonathan, Hodgin, Jeffrey B., Hoofnagle, Andrew N, Horowitz, Carol R., Hsieh, E.W.Y., Huynh, Courtney, Iyengar, Ravi, Jain, Sanjay, Janowczyk, Andrew, Jeffers, Vivian, Jefferson, Nichole M., Jennette, J Charles, Johansen, Camille, Jolly, Stacey, Jones, Christopher J., Jones, Jennifer L., Jones, Kiasha, Joyeux, Cienn N., Ju, Wenjun, Judd, Audra M., Kakade, Vijayakumar R, Kakarla, Dhatri, Kaspari, Rachel R., Kaushal, Madhurima, Keefe, Nicole, Keller, Mark S., Kelley, Sara S., Kellum, John A., Kelly, K. J., Kelly, Tanika N., Kermani, Asra, Kiryluk, Krzysztof, Klett, Susan, Knight, Richard A., Knoten, Amanda, Koch, Gina, Koewler, Robert, Kretzler, Matthias, Kruse, Angela R.S., Küchenhoff, Leonie, Lake, Blue B., Lardenoije, Roy, Larson, Astrid, Larson, Brandon G, Lash, James P., Laszik, Zoltan G., Lecker, Stewart H., Lee, Simon C., Lee, Sora, Lefferts, Sean, Li, Xiang, Lienczewski, Chrysta C, Limonte, Christine P, Lucarelli, Nicholas, Lukowski, Jessica, Lutnick, Brendon, Ma, Shihong, Ma, Sisi, Madabhushi, Anant, Maikhor, Shana, Mao, Weiguang, Mariani, Laura H., Markovic, Marina, Marquez, Nicole, Marshall, Jamie L., McAdams, Meredith C, McClelland, Robyn L., McCown, Phillip J., McMahon, Gearoid Michael, McMurray, Amy, Mehl, Karla, Meliambro, Kristin, Ferreira, Ricardo Melo, Mendoza, Katherine, Menez, Steven, Menon, Rajasree, Meza, Natalie, Migas, Lukasz G., Miller, R. Tyler, Mimar, Sayat, Minor, Brittany C, Mody, Priya, Moeckel, Gilbert W., Moledina, D.G., Molina-Guzman, Jenny, Monroy-Trujillo, Jose M, Morales, Alexander, Moreno, Vanessa, Mottl, Amy K., Mukatash, Tariq, Munar, Dane, Murugan, Raghavan, Nachman, Patrick H., Nadkarni, Girish N, Naglah, Ahmed, Nair, Viji, Nam, Yunbi, Narasimhan, R., Nwanne, Gerald, O'Malley, Charles, O'Toole, John F., Toro, Fernanda Ochoa, Oliver, George (Holt), Onul, Ingrid F, Otto, Edgar A., Palevsky, Paul M., Palmer, Ellen, Pamreddy, Annapurna, Parikh, Chirag R., Parikh, Samir V, Park, Christopher, Park, Harold, Paša-Tolić, Ljiljana, Patel, Jiten, Patel, Marissa, Patlis, Boris S., Paul, Anindya S., Phuong, Jimmy, Pillai, Anil, Pinkeney, Roy, Plisiewicz, Alexa, Poggio, Emilio D, Pollack, Ari, Prasad, Pottumarthi V, Pyle, Laura, Quardokus, Ellen M., Quiroga, Arabela, Ragi, Nagarjunachary, Randhawa, Parmjeet, Randle, Teresa, Rao, Via, Rauchman, Michael, Rauwolf, Nicolas J, Reamy, Rebecca, Record, Elizabeth G., Redmond, Devona, Rennke, Helmut, Renteria, Amada, Rezaei, Kasra A, Rhodes, Rosamond, Ricardo, Ana C., Rice, Samuel, Rivera, Marcelino, Roberts, Glenda V., Rosas, R., Sylvia, E., Rose, Michael P., Rosen, Seymour, Rosenberg, Avi Z., Rosenberg, Michael S., Rosengart, Matthew R., Rovin, Brad H., Roy, Neil, Roy-Chaudhury, Prabir, Rubinsky, Melissa D., Sabo, Angela R., Saez-Rodriguez, Julio, Safadi, Sami, Samari, Imane H., Sanora, Ana Celina, Sarder, Pinaki, Sarkisova, Natalya, Sarwal, Minnie M, Saul, John, Saunders, Milda R., Schaub, Jennifer A., Schmidt, IM, Scott, Raymond, Scroggins, Aaron, Sealfon, Rachel S. G., Sedor, John R., Sendrey, Dianna, Setty, Suman, Shah, Sonya, Shariff, Saad Mohammed, Sharma, Kumar, Shaw, Melissa M., Sigdel, Tara K, Silva, Paolo S., Snyder, Jaime, Snyder, Michelle L., Spates-Harden, Kassandra, Sperati, C. John, Spraggins, Jeffrey M., Srivastava, Anand, Stashevsky, Jennifer, Steck, Becky, Stillman, Isaac E, Stutzke, Christy, Subramanian, Lalita, Sun, Jennifer K., Rajan, Sandhya Sundar, Sutton, Timothy A., Taliercio, Jonathan J, Tan, Roderick, Tanevski, Jovan, Thajudeen, Bijin, Thurman, Joshua M., Tokita, Joji, Torrealba, Jose R., Toto, Robert D, Tout, Haneen, Troyanskaya, Olga G, Tsosie, Rebecca, Turner, Jeffrey M, Tuttle, Katherine R., Ugwuowo, Ugochukwu, Upadhyay, Ashish, Valerius, M. Todd, Van de Plas, Raf, Varela, German, Vazquez, Miguel A., Velickovic, Dusan, Venkatachalam, Manjeri, Verdoes, Abraham, Verma, Ashish, Victoria-Castro, Angela M., Vijayan, Anitha, Villalobos, Alexander, Viloria, Noralinda B., Vinovskis, Carissa, Vita, Tina, Waikar, Sushrut S., Wang, Ashley R., Wang, Bangchen, Wang, Nancy, Wang, Ruikang, Wangperawong, Artit, Ward, Stephen C, Warfield, Curtis, Weins, Astrid, Wen, Natasha, Wen, Yumeng, Wilcox, Adam, Williams, James C., Williams, Kayleen, Williams, Mark E., Wilson, F. Perry, Winfree, Seth, Winters, James, Wofford, Stephanie, Wolf, Susan M., Wong, Aaron, Woodhead, Gregory, Wright, Devin M., Wright, Zach, Wright, Zoe, Wrobel, Julia, Xing, Fuyong, Xu, Alan, Yadati, Pranav, Ye, Hongping, Young, Bessie A., Yu, Guanghao, Mon-Wei Yu, Samuel, Zeinoun, Gabriel, Zeitler, Evan M., Zhang, Bo, Zhang, Guanshi, and Zhang, Yi

Published
2024
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26. Scaffold protein SH3BP2 signalosome is pivotal for immune activation in nephrotic syndrome

Author

Srivastava, Tarak, primary, Garola, Robert E., additional, Zhou, Jianping, additional, Boinpelly, Varun Chandra, additional, Rezaiekhaligh, Mohammad H., additional, Joshi, Trupti, additional, Jiang, Yuexu, additional, Ebadi, Diba, additional, Sharma, Siddarth, additional, Sethna, Christine, additional, Staggs, Vincent S., additional, Sharma, Ram, additional, Gipson, Debbie S., additional, Hao, Wei, additional, Wang, Yujie, additional, Mariani, Laura H., additional, Hodgin, Jeffrey B., additional, Rottapel, Robert, additional, Yoshitaka, Teruhito, additional, Ueki, Yasuyoshi, additional, and Sharma, Mukut, additional

Published
2023
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29. miRNA and mRNA Signatures in Human Acute Kidney Injury Tissue

Author

Janosevic, Danielle, primary, De Luca, Thomas, additional, Ferreira, Ricardo Melo, additional, Gisch, Debora L., additional, Hato, Takashi, additional, Luo, Jinghui, additional, Yang, Yingbao, additional, Hodgin, Jeffrey B., additional, Dagher, Pierre C., additional, and Eadon, Michael T., additional

Published
2023
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31. 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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34. Reproducibility and Feasibility of Strategies for Morphologic Assessment of Renal Biopsies Using the Nephrotic Syndrome Study Network Digital Pathology Scoring System

Author

Zee, Jarcy, Hodgin, Jeffrey B., Mariani, Laura H., Gaut, Joseph P., Palmer, Matthew B., Bagnasco, Serena M., Rosenberg, Avi Z., Hewitt, Stephen M., Holzman, Lawrence B., Gillespie, Brenda W., and Barisoni, Laura

Subjects
Nephrotic syndrome -- Diagnosis -- Care and treatment, Kidney biopsy -- Methods, Glomeruli -- Medical examination, Test reliability -- Evaluation, Health
Abstract

* Context.--Testing reproducibility is critical for the development of methodologies for morphologic assessment. Our previous study using the descriptor-based Nephrotic Syndrome Study Network Digital Pathology Scoring System (NDPSS) on glomerular images revealed variable reproducibility. Objective.--To test reproducibility and feasibility of alternative scoring strategies for digital morphologic assessment of glomeruli and explore use of alternative agreement statistics. Design.--The original NDPSS was modified (NDPSS1 and NDPSS2) to evaluate (1) independent scoring of each individual biopsy level, (2) use of continuous measures, (3) groupings of individual descriptors into classes and sub-classes prior to scoring, and (4) indication of pathologists' confidence/uncertainty for any given score. Three and 5 pathologists scored 157 and 79 glomeruli using the NDPSS1 and NDPSS2, respectively. Agreement was tested using conventional (Cohen [kappa]) and alternative (Gwet agreement coefficient 1 [[AC.sub.1]]) agreement statistics and compared with previously published data (original NDPSS). Results.--Overall, pathologists' uncertainty was low, favoring application of the Gwet [AC.sub.1]. Greater agreement was achieved using the Gwet [AC.sub.1] compared with the Cohen [kappa] across all scoring methodologies. Mean (standard deviation) differences in agreement estimates using the NDPSS1 and NDPSS2 compared with the single-level original NDPSS were -0.09 (0.17) and -0.17 (0.17), respectively. Using the Gwet [AC.sub.1], 79% of the original NDPSS descriptors had good or excellent agreement. Pathologist feedback indicated the NDPSS1 and NDPSS2 were time-consuming. Conclusions.--The NDPSS1 and NDPSS2 increased pathologists' scoring burden without improving reproducibility. Use of alternative agreement statistics was strongly supported. We suggest using the original NDPSS on whole slide images for glomerular morphology assessment and for guiding future automated technologies. (Arch Pathol Lab Med. 2018;142:613-625; doi: 10.5858/arpa.2017-0181-OA), In the setting of clinical trials and translational research, the morphologic evaluation of renal biopsies has progressively transitioned from use of conventional light microscopy to digital pathology on whole slide [...]

Published
2018
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36. Defining the molecular correlate of arteriolar hyalinosis in kidney disease progression by integration of single cell transcriptomic analysis and pathology scoring

Author

Menon, Rajasree, Otto, Edgar A., Barisoni, Laura, Ferreira, Ricardo Melo, Limonte, Christine P., Godfrey, Bradley, Eichinger, Felix, Nair, Viji, Naik, Abhijit S., Subramanian, Lalita, D’Agati, Vivette, Henderson, Joel M., Herlitz, Leal, Kiryluk, Krzysztof, Moledina, Dennis G., Moeckel, Gilbert W., Palevsky, Paul M., Parikh, Chirag R., Randhawa, Parmjeet, Rosas, Sylvia E., Rosenberg, Avi Z., Stillman, Isaac, Toto, Robert, Torrealba, Jose, Vazquez, Miguel A., Waikar, Sushrut, Alpers, Charles E., Nelson, Robert G., Eadon, Michael T., Kretzler, Matthias, and Hodgin, Jeffrey B.

Subjects
Article
Abstract

Arteriolar hyalinosis in kidneys is an independent predictor of cardiovascular disease, the main cause of mortality in chronic kidney disease (CKD). The underlying molecular mechanisms of protein accumulation in the subendothelial space are not well understood. Using single cell transcriptomic data and whole slide images from kidney biopsies of patients with CKD and acute kidney injury in the Kidney Precision Medicine Project, the molecular signals associated with arteriolar hyalinosis were evaluated. Co-expression network analysis of the endothelial genes yielded three gene set modules as significantly associated with arteriolar hyalinosis. Pathway analysis of these modules showed enrichment of transforming growth factor beta / Bone morphogenetic protein (TGFβ / BMP) and vascular endothelial growth factor (VEGF) signaling pathways in the endothelial cell signatures. Ligand-receptor analysis identified multiple integrins and cell adhesion receptors as over-expressed in arteriolar hyalinosis, suggesting a potential role of integrin-mediated TGFβ signaling in arteriolar hyalinosis. Further analysis of arteriolar hyalinosis associated endothelial module genes identified focal segmental glomerular sclerosis as an enriched term. On validation in gene expression profiles from the Nephrotic Syndrome Study Network cohort, one of the three modules was significantly associated with the composite endpoint (> 40% reduction in estimated glomerular filtration rate (eGFR) or kidney failure) independent of age, sex, race, and baseline eGFR, suggesting poor prognosis with elevated expression of genes in this module. Thus, integration of structural and single cell molecular features yielded biologically relevant gene sets, signaling pathways and ligand-receptor interactions, underlying arteriolar hyalinosis and putative targets for therapeutic intervention.

Published
2023

37. Role of endogenous adenine in kidney failure and mortality with diabetes

Author

Sharma, Kumar, Zhang, Guanshi, Hansen, Jens, Bjornstad, Petter, Lee, Hak Joo, Menon, Rajasree, Hejazi, Leila, Liu, Jian-Jun, Franzone, Anthony, Looker, Helen C., Choi, Byeong Yeob, Fernandez, Roman, Venkatachalam, Manjeri A., Kugathasan, Luxcia, Sridhar, Vikas S., Natarajan, Loki, Zhang, Jing, Sharma, Varun, Kwan, Brian, Waikar, Sushrut, Himmelfarb, Jonathan, Tuttle, Katherine, Kestenbaum, Bryan, Fuhrer, Tobias, Feldman, Harold, de Boer, Ian H., Tucci, Fabio C., Sedor, John, Heerspink, Hiddo Lambers, Schaub, Jennifer, Otto, Edgar, Hodgin, Jeffrey B., Kretzler, Matthias, Anderton, Christopher, Alexandrov, Theodore, Cherney, David, Lim, Su Chi, Nelson, Robert G., Gelfond, Jonathan, and Iyengar, Ravi

Subjects
Article
Abstract

Diabetic kidney disease (DKD) can lead to end-stage kidney disease (ESKD) and mortality, however, few mechanistic biomarkers are available for high risk patients, especially those without macroalbuminuria. Urine from participants with diabetes from Chronic Renal Insufficiency Cohort (CRIC), Singapore Study of Macro-Angiopathy and Reactivity in Type 2 Diabetes (SMART2D), and the Pima Indian Study determined if urine adenine/creatinine ratio (UAdCR) could be a mechanistic biomarker for ESKD. ESKD and mortality were associated with the highest UAdCR tertile in CRIC (HR 1.57, 1.18, 2.10) and SMART2D (HR 1.77, 1.00, 3.12). ESKD was associated with the highest UAdCR tertile in patients without macroalbuminuria in CRIC (HR 2.36, 1.26, 4.39), SMART2D (HR 2.39, 1.08, 5.29), and Pima Indian study (HR 4.57, CI 1.37-13.34). Empagliflozin lowered UAdCR in non-macroalbuminuric participants. Spatial metabolomics localized adenine to kidney pathology and transcriptomics identified ribonucleoprotein biogenesis as a top pathway in proximal tubules of patients without macroalbuminuria, implicating mammalian target of rapamycin (mTOR). Adenine stimulated matrix in tubular cells via mTOR and stimulated mTOR in mouse kidneys. A specific inhibitor of adenine production was found to reduce kidney hypertrophy and kidney injury in diabetic mice. We propose that endogenous adenine may be a causative factor in DKD.

Published
2023

38. 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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43. 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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44. Fn14 in podocytes and proteinuric kidney disease

Author

Sanchez-Niño, Maria Dolores, Poveda, Jonay, Sanz, Ana Belen, Mezzano, Sergio, Carrasco, Susana, Fernandez-Fernandez, Beatriz, Burkly, Linda C., Nair, Viji, Kretzler, Matthias, Hodgin, Jeffrey B., Ruiz-Ortega, Marta, Selgas, Rafael, Egido, Jesus, and Ortiz, Alberto

Published
2013
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48. Integrated single-cell sequencing and histopathological analyses reveal diverse injury and repair responses in a participant with acute kidney injury: a clinical-molecular-pathologic correlation

Author

Knight, Richard, Lecker, Stewart H., Stillman, Isaac, Bogen, Steve, Beck, Laurence H., Waikar, Sushrut, McMahon, Gearoid M., Weins, Astrid, Colona, Mia R., Hacohen, Nir, Hoover, Paul J., Aulisio, Mark, Bush, William S., Crawford, Dana C., O'toole, John, Poggio, Emilio, Sedor, John, Cooperman, Leslie, Jolly, Stacey, Herlitz, Leal, Nguyen, Jane, Gonzalez-Vicente, Agustin, Palmer, Ellen, Sendrey, Dianna, Vinovskis, Carissa, Bjornstad, Petter M., Appelbaum, Paul, Barasch, Jonathan M., Bomback, Andrew S., D'Agati, Vivette D., Kiryluk, Krzysztof, Mehl, Karla, Canetta, Pietro A., Shang, Ning, Balderes, Olivia, Kudose, Satoru, Bansal, Shweta, Alexandrov, Theodore, Rennke, Helmut, El-Achkar, Tarek M., Cheng, Yinghua, Dagher, Pierre C., Eadon, Michael T., Dunn, Kenneth W., Kelly, Katherine J., Sutton, Timothy A., Barwinska, Daria, Ferkowicz, Michael J., Winfree, Seth, Bledsoe, Sharon, Rivera, Marcelino, Williams, James C., Jr., Ferreira, Ricardo Melo, Parikh, Chirag R., Corona-Villalobos, Celia P., Menez, Steven, Rosenberg, Avi, Rosas, Sylvia E., Roy, Neil, Williams, Mark, Azeloglu, Evren U., He, Cijang, Iyengar, Ravi, Hansen, Jens, Xiong, Yuguang, Rovin, Brad, Parikh, Samir, Shapiro, John P., Anderton, Christopher R., Pasa-Tolic, Ljiljana, Velickovic, Dusan, Lukowski, Jessica, Oliver, George, Ardayfio, Joseph, Bebiak, Jack, Brown, Keith, Campbell, Catherine E., Saul, John, Shpigel, Anna, Stutzke, Christy, Koewler, Robert, Campbell, Taneisha, Hayashi, Lynda, Jefferson, Nichole, Roberts, Glenda V., Pinkeney, Roy, Troyanskaya, Olga, Sealfon, Rachel, Tuttle, Katherine R., Goltsev, Yury, Zhang, Kun, Lake, Blue B., Laszik, Zoltan G., Nolan, Garry, Boada, Patrick, Sarwal, Minnie, Sigdel, Tara, Lee, Paul J., Alloway, Rita R., Woodle, E. Steve, Ascani, Heather, Balis, Ulysses G.J., Hodgin, Jeffrey B., Kretzler, Matthias, Lienczewski, Chrysta, Mariani, Laura H., Menon, Rajasree, Steck, Becky, He, Yougqun, Otto, Edgar, Schaub, Jennifer, Blanc, Victoria M., Eddy, Sean, Conser, Ninive C., Luo, Jinghui, Palevsky, Paul M., Rosengart, Matthew, Kellum, John A., Hall, Daniel E., Randhawa, Parmjeet, Tublin, Mitchell, Murugan, Raghavan, Elder, Michele M., Winters, James, Alpers, Charles E., Blank, Kristina N., Carson, Jonas, De Boer, Ian H., Dighe, Ashveena L., Himmelfarb, Jonathan, Mooney, Sean D., Shankland, Stuart, Williams, Kayleen, Park, Christopher, Dowd, Frederick, McClelland, Robyn L., Daniel, Stephen, Hoofnagle, Andrew N., Wilcox, Adam, Grewenow, Stephanie M., Sharma, Kumar, Venkatachalam, Manjeri, Zhang, Guanshi, Pamreddy, Annapurna, Ye, Hongping, Montellano, Richard, Toto, Robert D., Vazquez, Miguel, Lee, Simon C., Miller, R. Tyler, Moe, Orson W., Torrealba, Jose, Wang, Nancy, Kermani, Asra, Sambandam, Kamalanathan, Park, Harold, Hedayati, S. Susan, Lu, Christopher Y., Jain, Sanjay, Vijayan, Anitha, Gaut, Joseph P., Moledina, Dennis, Wilson, Francis P., Ugwuowo, Ugochukwu, Arora, Tanima, and D’Agati, Vivette D.

Published
2022
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50. 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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