43 results on '"Textor, Stephen C."'
Search Results
2. List of Contributors
- Author
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Abramovitz, Blaise, primary, Adu, Dwomoa, additional, Afshinnia, Farsad, additional, Agarwal, Anupam, additional, Andrews, Sarah C., additional, Appel, Gerald, additional, Bailey, James L., additional, Bakris, George L., additional, Bauer, Carolyn A., additional, Baxi, Pravir V., additional, Berns, Jeffrey S., additional, Birks, Peter, additional, Bomback, Andrew, additional, Bose, Anirban, additional, Brosius, Frank C., additional, Brown, Lee K., additional, Bushinsky, David A., additional, Busse, Laurence W., additional, Campbell, Ruth C., additional, Canney, Mark, additional, Cathro, Helen, additional, Chávez-Iñiguez, Jonathan, additional, Chawla, Lakhmir S., additional, Chen, Sheldon, additional, Chertow, Glenn M., additional, Chew, Emily Y., additional, Chonchol, Michel, additional, Clegg, Deborah J., additional, Clive, David M., additional, Clive, Pia H., additional, Cohen, Scott D., additional, Collins, Ashte' K., additional, Cooper, James E., additional, Correa-Rotter, Ricardo, additional, Cukor, Daniel, additional, Dalal, Monica, additional, Davenport, Andrew, additional, Davis, Scott, additional, Davison, Sara N., additional, Delanaye, Pierre, additional, de Zeeuw, Dick, additional, Dobre, Mirela A., additional, Drawz, Paul, additional, Ebert, Natalie, additional, Eggers, Paul, additional, Ferrè, Silvia, additional, Freedman, Barry I., additional, Furth, Susan L., additional, Gao, Bixia, additional, García-García, Guillermo, additional, Gashti, Casey N., additional, Germino, Gregory G., additional, Goldsmith, David, additional, Golestaneh, Ladan, additional, Goligorsky, Michael S., additional, Greenberg, Arthur, additional, Gregg, L. Parker, additional, Guay-Woodford, Lisa M., additional, Hamm, Lee, additional, Hart, Allyson, additional, Haselby, Danielle, additional, Hedayati, S. Susan, additional, Heerspink, Hiddo J.L., additional, Herzog, Charles A., additional, Hostetter, Thomas H., additional, House, Andrew A., additional, Hruska, Keith A., additional, Ishani, Areef, additional, Isom, Robert T., additional, James, Matthew T., additional, Jhaveri, Kenar D., additional, Johansen, Kirsten, additional, Johnson, Richard J., additional, Kang, Duk-Hee, additional, Kanno, Hiroko, additional, Kanno, Yoshihiko, additional, Karambelkar, Amrita D., additional, Karet Frankl, Fiona E., additional, Khoury, Charbel C., additional, Kimmel, Paul L., additional, Kopp, Jeffrey B., additional, Korbet, Stephen M., additional, Kruzel-Davila, Etty, additional, Kummer, Andrew, additional, LaFave, Laura, additional, Lakkis, Jay I., additional, Lerman, Lilach O., additional, Levin, Adeera, additional, Lew, Susie Q., additional, Luyckx, Valerie A., additional, Mattoo, Tej K., additional, Maynard, Sharon E., additional, McCullough, Peter A., additional, Mehrotra, Rajnish, additional, Meyer, Timothy W., additional, Mitch, William E., additional, Moe, Orson W., additional, Mohandes, Samer, additional, Moss, Alvin H., additional, Moxey-Mims, Marva, additional, Murugapandian, Sangeetha, additional, Nath, Karl A., additional, Neugarten, Joel, additional, Neyra, Javier A., additional, Nissenson, Allen R., additional, Nobakht, Ehsan, additional, Nolin, Thomas D., additional, Norris, Keith C., additional, Norton, Jenna M., additional, Nowak, Kristen L., additional, Ojo, Akinlolu O., additional, Pahl, Madeleine V., additional, Paller, Mark S., additional, Palmer, Biff F., additional, Palmer, Nicholette D., additional, Patel, Samir S., additional, Pecoits-Filho, Roberto, additional, Peitzman, Steven J., additional, Peixoto, Aldo J., additional, Pham, Phuong-Thu T., additional, Pham, Phuong-Chi T., additional, Piraino, Beth, additional, Pisoni, Roberto, additional, Rabelink, Ton, additional, Radhakrishnan, Jai, additional, Rahman, Mahboob, additional, Raj, Dominic S., additional, Ramírez-Sandoval, Juan C., additional, Rangaswami, Janani, additional, Reckelhoff, Jane F., additional, Regunathan-Shenk, Renu, additional, Reule, Scott, additional, Ronco, Claudio, additional, Rosenberg, Mark E., additional, Rosner, Mitchell H., additional, Rovin, Brad, additional, Roy-Chaudhury, Prabir, additional, Ruebner, Rebecca, additional, Rule, Andrew D., additional, Sands, Jeff M., additional, Schlanger, Lynn E., additional, Schrauben, Sarah J., additional, Seliger, Stephen, additional, Shah, Maulin, additional, Sterns, Richard H., additional, Stites, Erik, additional, Sugatani, Toshifumi, additional, Textor, Stephen C., additional, Thadhani, Ravi, additional, Thajudeen, Bijin, additional, Thakar, Surabhi, additional, Thomas, George, additional, Townsend, Raymond R., additional, Turner, Jeffrey, additional, Unruh, Mark L., additional, Urquhart, Bradley L., additional, Vassalotti, Joseph A., additional, Vaziri, Nosratola D., additional, Velasquez, Manuel T., additional, Ver Halen, Nisha, additional, Waddy, Salina P., additional, Wang, Jinwei, additional, Weber, Marc, additional, Weir, Matthew R., additional, White, Christine A., additional, Whittier, William L., additional, Williams, Matthew J., additional, Wiseman, Alexander C., additional, Wymer, David C., additional, Wymer, David T.G., additional, Yee, Jerry, additional, Zhang, Luxia, additional, Zhuang, Shougang, additional, and Ziyadeh, Fuad N., additional
- Published
- 2020
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3. Contributors
- Author
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Ali, Ailia W., primary, Alicic, Radica Z., additional, Amar, Laurence, additional, Anwaruddin, Saif, additional, Appel, Lawrence J., additional, August, Phyllis, additional, Azizi, Michel, additional, Bakris, George L., additional, Banegas, José R., additional, Bard, Robert L., additional, Barrett, Orit, additional, Benetos, Athanase, additional, Bernstein, Kenneth E., additional, Bhatt, Deepak L., additional, Biaggioni, Italo, additional, Blumenthal, Roger S., additional, Bobrie, Guillaume, additional, Brook, Robert D., additional, Byrd, J. Brian, additional, Carter, Barry L., additional, Cohen, Debbie L., additional, Cushman, William C., additional, De Leeuw, Peter Wilhelmus, additional, Ehret, Georg B., additional, Elliott, William J., additional, Ernst, Michael E., additional, Farooq, Muhammad U., additional, Faucon, Anne-Laure, additional, Fishbein, Lauren, additional, Flynn, Joseph T., additional, Fujita, Toshiro, additional, George, Mary G., additional, Gorelick, Philip B., additional, Gosmanova, Elvira O., additional, Grim, Carlene M., additional, Grim, Clarence E., additional, Gupta, Rajeev, additional, Hall, John E., additional, Hall, Michael E., additional, Hanevold, Coral D., additional, Harrison, David G., additional, Huang, Qi-Fang, additional, Hughes, Alun, additional, Joseph, Philip, additional, Kario, Kazuomi, additional, Karmali, Kunal N., additional, Kollias, Anastasios, additional, Laffin, Luke J., additional, Landsberg, Lewis, additional, Lloyd-Jones, Donald M., additional, Madjalian, Anne-Marie, additional, Malha, Line, additional, Mancia, Giuseppe, additional, McEvoy, John W., additional, Mensah, George A., additional, Milner, Ross, additional, Min, Jiangyong, additional, Ochoa, Juan Eugenio, additional, Ota, Takeyoshi, additional, Ott, Christian, additional, Parati, Gianfranco, additional, Pepine, Carl J., additional, Perkovic, Vlado, additional, Podymow, Tiina, additional, Rahimi, Kazem, additional, Ruilope, Luis Miguel, additional, Ruiz-Hurtado, Gema, additional, Schmieder, Roland E., additional, Shibata, Shigeru, additional, Smith, Steven M., additional, Sorrentino, Matthew J., additional, Stergiou, George S., additional, Sternlicht, Hillel, additional, Strollo, Patrick J., additional, Taler, Sandra J., additional, Tanaka, Akiko, additional, Textor, Stephen C., additional, Townsend, Raymond R., additional, Tuttle, Katherine R., additional, Wang, Ji-Guang, additional, Whelton, Seamus P., additional, White, William B., additional, Williams, Bryan, additional, Wolak, Talya, additional, Yamout, Hala, additional, Yancy, Clyde W., additional, Young, William F., additional, and Yusuf, Salim, additional
- Published
- 2018
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4. Renovascular Hypertension and Ischemic Nephropathy
- Author
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Textor, Stephen C., primary
- Published
- 2018
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5. List of Contributors
- Author
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Afshinnia, Farsad, primary, Agarwal, Anupam, additional, Appel, Gerald B., additional, Bagby, Susan P., additional, Bailey, James L., additional, Bakris, George L., additional, Barrett, Brendan J., additional, Bauer, Carolyn A., additional, Berl, Tomas, additional, Berns, Jeffrey S., additional, Bomback, Andrew, additional, Bose, Anirban, additional, Brosius, Frank C., additional, Brown, Lee K., additional, Bushinsky, David A., additional, Busse, Laurence W., additional, Campbell, Ruth C., additional, Cathro, Helen, additional, Chawla, Lakhmir S., additional, Chen, Sheldon, additional, Chertow, Glenn M., additional, Chew, Emily, additional, Chonchol, Michel, additional, Clive, David M., additional, Cohen, Debbie L., additional, Cohen, Lewis M., additional, Cohen, Scott D., additional, Collins, Ashte’ K., additional, Combs, Sara, additional, Correa-Rotter, Ricardo, additional, Cukor, Daniel, additional, Dalal, Monica, additional, Dancik, Tavis, additional, Davenport, Andrew, additional, Davison, Sara, additional, Zeeuw, Dick de, additional, Delanaye, Pierre, additional, Dharia, Sushma M., additional, Dobre, Mirela A., additional, Drawz, Paul, additional, Dreisbach, Albert W., additional, Emmett, Michael, additional, Fanton, John H., additional, Felsenfeld, Arnold J., additional, Fernandez, Hilda, additional, Flessner, Michael F., additional, Freedman, Barry I., additional, Fruchter, Yvette, additional, Furth, Susan L., additional, García-García, Guillermo, additional, Germain, Michael J., additional, Germino, Gregory G., additional, Goligorsky, Michael S., additional, Greenberg, Arthur, additional, Guay-Woodford, Lisa M., additional, Hawkins, Katrina, additional, Herzog, Charles A., additional, Holley, Jean L., additional, Hostetter, Thomas H., additional, House, Andrew A., additional, Hruska, Keith A., additional, Huan, Yonghong, additional, Ibrahim, Hassan N., additional, Imran, Nashat, additional, Iñiguez, Jonathan Chávez, additional, Isom, Robert T., additional, Jablonski, Kristen L., additional, Jhaveri, Kenar D., additional, Johansen, Kirsten, additional, Johnson, Richard J., additional, Junghare, Milind Y., additional, Kang, Duk-Hee, additional, Karadsheh, Feras F., additional, Kari, Jameela, additional, Kasiske, Bertram L., additional, Khoury, Charbel C., additional, Kimmel, Paul L., additional, Kopp, Jeffrey B., additional, Kummer, Andrew, additional, Heerspink, Hiddo J.Lambers, additional, Lerman, Lilach O., additional, Levin, Adeera, additional, Levine, Barton S., additional, Lew, Susie Q., additional, Mandayam, Sreedhar, additional, Mattoo, Tej K., additional, Maynard, Sharon E., additional, Meyer, Timothy W., additional, Mitch, William E., additional, Moss, Alvin H., additional, Moxey-Mims, Marva, additional, Muntner, Paul, additional, Murray, Anne M., additional, Nath, Karl A., additional, Neugarten, Joel, additional, No, Gloria, additional, Pahl, Madeleine V., additional, Paller, Mark S., additional, Palmer, Biff F., additional, Parfrey, Patrick S., additional, Patel, Samir S., additional, Pecoits-Filho, Roberto, additional, Peitzman, Steven J., additional, Peixoto, Aldo J., additional, Pham, Phuong-Chi T., additional, Pham, Phuong-Thu T., additional, Rabelink, Ton J., additional, Radhakrishnan, Jai, additional, Raed, Anas, additional, Raj, Dominic S., additional, Ramirez-Sandoval, Juan Carlos, additional, Reckelhoff, Jane F., additional, Ronco, Claudio, additional, Rosenberg, Mark E., additional, Rosner, Mitchell H., additional, Rovin, Brad, additional, Roy-Chaudhury, Prabir, additional, Ruebner, Rebecca, additional, Rule, Andrew D., additional, Sands, Jeff M., additional, Scheinman, Steven J., additional, Schlanger, Lynn E., additional, Seifert, Michael E., additional, Seliger, Stephen, additional, Singh, Ajay K., additional, Stendahl, John C., additional, Surendran, Kameswaran, additional, Textor, Stephen C., additional, Thadhani, Ravi I., additional, Townsend, Raymond R., additional, Unruh, Mark L., additional, Vassalotti, Joseph A., additional, Vaziri, Nosratola D., additional, Velasquez, Manuel T., additional, Ver Halen, Nisha, additional, Wang, Connie J., additional, Wanner, Christoph, additional, Weber, Marc, additional, Weir, Matthew R., additional, Wing, Maria R., additional, Winn, Michelle P., additional, Wymer, David C., additional, Yee, Jerry, additional, and Ziyadeh, Fuad N., additional
- Published
- 2015
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6. Approach to the Patient with Chronic Kidney Disease and Renovascular Disease
- Author
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Textor, Stephen C., primary and Lerman, Lilach O., additional
- Published
- 2015
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7. Pathophysiology of Renal Artery Disease
- Author
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Textor, Stephen C., primary
- Published
- 2013
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8. Contributors
- Author
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Alberts, Mark J., primary, Battinelli, Elisabeth M., additional, Beckman, Joshua A., additional, Belkin, Michael, additional, Blei, Francine, additional, Blume, Peter, additional, Brass, Eric P., additional, Brennan, Christina, additional, Carter-Monroe, Naima, additional, Chacko, Billy G., additional, Chadachan, Veerendra, additional, Chan, Stephen Y., additional, Cid, Maria C., additional, Coselli, Joseph S., additional, Creager, Mark A., additional, Criqui, Michael H., additional, Cronenwett, Jack L., additional, Dake, Michael D., additional, Danczyk, Rachel C., additional, Davis, Mark D.P., additional, Duran, Cihan, additional, Eagleton, Matthew J., additional, Eberhardt, Robert T., additional, Eikelboom, John W., additional, Fisher, Marc, additional, Freedman, Jane E., additional, Freischlag, Julie Ann, additional, Fulton, David R., additional, Garg, Nitin, additional, Gerhard-Herman, Marie, additional, Gloviczki, Peter, additional, Goldhaber, Samuel Z., additional, Goldstein, Larry B., additional, Gornik, Heather L., additional, Greif, Daniel M., additional, Griendling, Kathy K., additional, Habersberger, Jonathon, additional, Halperin, Jonathan L., additional, Hansen, Kimberley J., additional, Haqqani, Omar P., additional, Harrison, David G., additional, Harthun, Nancy, additional, Hiatt, William R., additional, Hilenski, Lula L., additional, Hoffman, Gary S., additional, Huh, Joseph, additional, Iafrati, Mark D., additional, Iyer, Sriram S., additional, Keegan, Kirk A., additional, Kwolek, Christopher J., additional, Landry, Gregory J., additional, Lau, Joe F., additional, LeMaire, Scott A., additional, Leopold, Jane A., additional, Libby, Peter, additional, Lichtman, Judith H., additional, Long, Chandler A., additional, Loscalzo, Joseph, additional, Luther, James M., additional, Machleder, Herbert I., additional, Madder, Ryan D., additional, Mahameed, Amjad Al, additional, Maksimowicz-McKinnon, Kathleen, additional, Maron, Bradley A., additional, McPhee, James T., additional, Menard, Matthew T., additional, Merkel, Peter A., additional, Moneta, Gregory L., additional, Moore, Wesley S., additional, Newburger, Jane W., additional, Newton, William B., additional, O'Gara, Patrick T., additional, Olin, Jeffrey W., additional, Önal, Mehmet Zülküf, additional, Pande, Reena L., additional, Penson, David F., additional, Perlstein, Todd S., additional, Piazza, Gregory, additional, Plummer, Mitchell M., additional, Raghow, Rajendra, additional, Rajagopalan, Sanjay, additional, Rathbun, Suman, additional, Rockson, Stanley G., additional, Rooke, Thom W., additional, Roubin, Gary, additional, Rybicki, Frank J., additional, Safian, Robert D., additional, Shepherd, Roger F.J., additional, Sobieszczyk, Piotr S., additional, Stone, David H., additional, Sumpio, Bauer E., additional, Tafur, Alfonso J., additional, Taylor, Allen J., additional, Textor, Stephen C., additional, Upchurch, Gilbert R., additional, Valentine, R. James, additional, Virmani, Renu, additional, Vitek, Jiri, additional, Walls, Michael C., additional, Watkins, Michael T., additional, Weitz, Jeffrey I., additional, White, Christopher J., additional, and Williams, Timothy K., additional
- Published
- 2013
- Full Text
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9. Contributors
- Author
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Advani, Andrew, primary, Allon, Michael, additional, Anderson, Amanda Hyre, additional, Appel, Gerald B., additional, Assady, Suheir, additional, Atala, Anthony, additional, Baigent, Colin, additional, Bakkaloglu, Sevcan A., additional, Barletta, Gina-Marie, additional, Becker, Gavin J., additional, Bellomo, Rinaldo, additional, Berns, Jeffrey S., additional, Bhalla, Vivek, additional, Biber, Jürg, additional, Bichet, Daniel G., additional, Bindels, René J.M., additional, Bleicher, Melissa B., additional, Blumenfeld, Jon D., additional, Bonnardeaux, Alain, additional, Bonventre, Joseph V., additional, Boswell, William D., additional, Bowden, Donald W., additional, Brenner, Barry M., additional, Breyer, Matthew D., additional, Breyer, Richard M., additional, Brown, Dennis, additional, Brugnara, Carlo, additional, Bunchman, Timothy E., additional, Bushinsky, David A., additional, Busque, Stéphan, additional, Carrero, Juan Jesús, additional, Cattran, Daniel, additional, Chan, James C., additional, Chandraker, Anil, additional, Chang, Ingrid J., additional, Choudhury, Devasmita, additional, Coe, Fredric L., additional, Collins, John F., additional, Cook, H. Terence, additional, Correa-Rotter, Ricardo, additional, Cowper, Shawn E., additional, Cravedi, Paolo, additional, Cueto-Manzano, Alfonso M., additional, D’Agati, Vivette D., additional, Davids, Mogomat Razeen, additional, Delacroix, Scott E., additional, Denker, Bradley M., additional, Depner, Thomas A., additional, DuBose, Thomas D., additional, Eckardt, Kai-Uwe, additional, Eldehni, Mohamed T., additional, Ellison, David H., additional, Emmett, Michael, additional, Falk, Ronald J., additional, Feldman, Harold I., additional, Fenton, Robert A., additional, Fenves, Andrew Z., additional, Finkel, Kevin W., additional, Fioretto, Paola, additional, Fogarty, Damian G., additional, Foringer, John R., additional, Fouque, Denis, additional, Freedman, Barry I., additional, Frøkiaer, Jørgen, additional, Funder, John W., additional, Game, David S., additional, Gilbert, Richard E., additional, Grantham, Jared J., additional, Halperin, Mitchell L., additional, Hand, Matthew, additional, Hanes, Donna S., additional, Harris, David C.H., additional, Harris, Raymond C., additional, Haynes, Richard, additional, Hoenderop, Joost G.J., additional, Hoorn, Ewout J., additional, Hostetter, Thomas H., additional, Hsu, Chi-yuan, additional, Hua-Lin, Shih, additional, Ibrahim, Hassan N., additional, Israni, Ajay K., additional, Jadvar, Jossein, additional, Jennette, J. Charles, additional, Jonasch, Eric, additional, Kamel, Kamel S., additional, Karumanchi, S. Ananth, additional, Kasiske, Bertram L., additional, Kellum, John A., additional, Kelly, Carolyn J., additional, Khanna, Ramesh, additional, Klassen, David K., additional, Ko, Christine J., additional, Kohli, Harbir Singh, additional, Kost, Curtis K., additional, Krane, L. Spencer, additional, Kreidberg, Jordan, additional, Kwon, Tae-Hwan, additional, Lahoti, Amit, additional, Landray, Martin J., additional, Laragh, John H., additional, Layton, Harold E., additional, Levi, Moshe, additional, Lindholm, Bengt, additional, Liu, Frank, additional, Luyckx, Valerie A., additional, Maddox, David A., additional, Maezawa, Yoshiro, additional, Matas, Arthur J., additional, Mauer, Michael, additional, Maya, Ivan D., additional, Maynard, Sharon E., additional, McDonough, Alicia A., additional, McIntyre, Christopher W., additional, Meyer, Timothy W., additional, Mitch, William E., additional, Moe, Orson W., additional, Moe, Sharon M., additional, Molitoris, Bruce A., additional, Moss, Alvin H., additional, Mount, David B., additional, Munger, Karen A., additional, Nachman, Patrick H., additional, Naicker, Saraladevi, additional, Nielsen, Søren, additional, Neilson, Eric G., additional, Nicolle, Lindsay E., additional, Ornt, Daniel B., additional, Palacín, Manuel, additional, Palevsky, Paul M., additional, Palmer, Suzanne L., additional, Parving, Hans-Henrik, additional, Patrakka, Jaakko, additional, Pearce, David, additional, Pecoits-Filho, Roberto, additional, Peralta, Carmen A., additional, Perico, Norberto, additional, Powe, Neil R., additional, Praditpornsilpa, Kearkiat, additional, Prætorius, Jeppe, additional, Quaggin, Susan E., additional, Quarles, L. Darryl, additional, Radhakrishnan, Jai, additional, Ramadan, Rawi, additional, Reggenenti, Piero, additional, Reich, Heather N., additional, Remuzzi, Andrea, additional, Remuzzi, Giuseppe, additional, Rich, Stephen S., additional, Riella, Miguel C., additional, Ritz, Eberhard, additional, Ronco, Claudio, additional, Rosenblum, Norman D., additional, Rossing, Peter, additional, Rubinger, Dvora, additional, Rude, Robert K., additional, Sabath, Ernesto, additional, Sabbisetti, Venkata, additional, Sakhuja, Vinay, additional, Salama, Alan D., additional, Sands, Jeff M., additional, Santos, Fernando, additional, Sayegh, Mohamed H., additional, Scandling, John D., additional, Schaefer, Franz, additional, Scheinman, Jon I., additional, Schwartz, John C., additional, Sharfuddin, Asif A., additional, Shaw, Susan, additional, Sitprija, Visith, additional, Skorecki, Karl L., additional, Slotki, Itzchak N., additional, Smith, James P., additional, Smogorzewski, Miroslaw J., additional, Sprague, Stuart M., additional, Stenvinkel, Peter, additional, Stokes, John B., additional, Taal, Maarten W., additional, Tamura, Manjula Kurella, additional, Tan, Jane C., additional, Textor, Stephen C., additional, Thadhani, Ravi, additional, Thomson, Scott C., additional, Torres, Vincente E., additional, Tryggvason, Karl, additional, Tuncel, Meryem, additional, Tungsanga, Kriang, additional, Verbalis, Joseph G., additional, Verlander, Jill W., additional, Wadee, Shoyab, additional, Weiner, I. David, additional, Weir, Matthew R., additional, Weisbord, Steven D., additional, Wheeler, David C., additional, Wilcox, Christopher S., additional, Wood, Christopher G., additional, Wright, Stephen H., additional, Yeun, Jane Y., additional, Yu, Alan S.L., additional, Zandi-Nejad, Kambiz, additional, and Zeidel, Mark L., additional
- Published
- 2012
- Full Text
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10. Renovascular Hypertension and Ischemic Nephropathy
- Author
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Textor, Stephen C., primary
- Published
- 2011
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11. Renovascular Hypertension and Ischemic Renal Disease
- Author
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Textor, Stephen C., primary and Greco, Barbara A., additional
- Published
- 2010
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12. Contributors
- Author
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Adler, Sharon, primary, Adrogué, Horacio J., additional, Aiyagari, Venkatesh, additional, Alpern, Robert J., additional, Alpers, Charles E., additional, Appel, Gerald B., additional, Arogundade, Fatiu A., additional, Ash, Stephen R., additional, Asif, Arif, additional, Aucouturier, Pierre, additional, August, Phyllis, additional, Bakris, George L., additional, Barlow, Adam D., additional, Barsoum, Rashad S., additional, Baylis, Chris, additional, Bello, Aminu, additional, Berl, Tomas, additional, Bhat, Suresh, additional, Bircher, Gemma, additional, Bonventre, Joseph V., additional, Bouchard, Josée, additional, Brook, Nicholas R., additional, Brown, Christopher, additional, Brown, Mark A., additional, Burdmann, Emmanuel A., additional, Bushinsky, David A., additional, Cattran, Daniel C., additional, Cervelli, Matthew J., additional, Chadban, Steven J., additional, Charlton, Karen E., additional, Chen, Yipu, additional, Cheng, Ignatius K.P., additional, Connolly, John O., additional, Couser, William G., additional, Cravedi, Paolo, additional, D’Agati, Vivette D., additional, Danovitch, Gabriel M., additional, Davies, Simon J., additional, Davison, John M., additional, Derman, Wayne, additional, DiBona, Gerald F., additional, Drüeke, Tilman B., additional, Dwyer, Jamie P., additional, Eckardt, Kai-Uwe, additional, Eckel, Jason, additional, Eitner, Frank, additional, Kossi, Mohsen El, additional, Elger, Marlies, additional, Elhassan, Elwaleed A., additional, Evenepoel, Pieter, additional, Fabian, June, additional, Falk, Ronald J., additional, Feehally, John, additional, Fischer, Evelyne A., additional, Fisher, Jonathan S., additional, Floege, Jürgen, additional, Fogazzi, Giovanni B., additional, Foreman, John W., additional, Fujita, Toshiro, additional, Gennari, F. John, additional, Gkougkousis, Evangelos G., additional, Glassock, Richard J., additional, Gorelick, Philip B., additional, Greco, Barbara A., additional, Gross, Peter, additional, Guay-Woodford, Lisa M., additional, Haddad, Nabil, additional, Harris, Kevin P.G., additional, Harris, Peter C., additional, Hebert, Lee A., additional, Heduschka, Peter, additional, Herzog, Charles A., additional, Hooton, Thomas, additional, Hörl, Walter H., additional, Hoyer, Peter F., additional, Hughes, Jeremy, additional, Hugo, Christian, additional, Imai, Enyu, additional, Irish, Ashley B., additional, Jaber, Bertrand L., additional, Jain, Sunjay, additional, Jayne, David, additional, Jefferson, J. Ashley, additional, Jennette, J. Charles, additional, Jha, Vivekanand, additional, Johnson, Richard J., additional, Kanagasundaram, Nigel S., additional, Kanellis, John, additional, Karumanchi, S. Ananth, additional, Kashtan, Clifford E., additional, Kauffman, Carol A., additional, Kawar, Bisher, additional, Kestenbaum, Bryan, additional, Ketteler, Markus, additional, Kopp, Jeffrey, additional, Kotanko, Peter, additional, Kriz, Wilhelm, additional, Kuhlmann, Martin K., additional, Kuypers, Dirk R., additional, Lakey, Jonathan R.T., additional, Lambert, Estelle V., additional, Lawton, William, additional, Levey, Andrew S., additional, Levin, Nathan W., additional, Levy, Jeremy, additional, Lewington, Andrew, additional, Lewis, Julia B., additional, Li, Felix F.K., additional, Linas, Stuart L., additional, Luft, Friedrich C., additional, Maaten, Jan C. ter, additional, Macdougall, Iain C., additional, Macedo, Etienne, additional, Madias, Nicolaos E., additional, Magee, Colm C., additional, Marsh, Christopher L., additional, Marshall, Mark R., additional, Martin, Kevin J., additional, Mason, Philip D., additional, Mathews, Ranjiv, additional, Mattoo, Tej K., additional, Mehta, Ravindra L., additional, Meier-Kriesche, Herwig-Ulf, additional, Mellon, J. Kilian, additional, Mirbolooki, M. Reza, additional, Monk, Rebeca D., additional, Moulin, Bruno, additional, Mulley, William R., additional, Nahas, Meguid El, additional, Naicker, Saraladevi, additional, Nangaku, Masaomi, additional, Neild, Guy H., additional, Nicholls, M. Gary, additional, Nicholson, Michael L., additional, O’Connell, Philip J., additional, O’Neill, W. Charles, additional, Palmer, Biff F., additional, Parikh, Chirag, additional, Pham, Phuong-Chi T., additional, Pham, Phuong-Thu T., additional, Pham, Son V., additional, Phelps, Richard G., additional, Pichler, Raimund, additional, Podymow, Tiina, additional, Pommer, Wolfgang, additional, Pusey, Charles D., additional, Rabb, Hamid, additional, Rayner, Brian, additional, Rayner, Hugh C., additional, Remuzzi, Giuseppe, additional, Richards, A. Mark, additional, Rippe, Bengt, additional, Ritz, Eberhard, additional, Robertson, R. Paul, additional, Rodriguez-Iturbe, Bernardo, additional, Ronco, Claudio, additional, Ronco, Pierre M., additional, Ross, Edward A., additional, Rossert, Jerome A., additional, Ruggenenti, Piero, additional, Ruland, Sean, additional, Russ, Graeme R., additional, Samuels, Martin A., additional, Sarafidis, Pantelis A., additional, Schena, F. Paolo, additional, Schold, Jesse D., additional, Schrier, Robert W., additional, Seabra, Victor F., additional, Segal, Mark S., additional, Seifter, Julian Lawrence, additional, Shastri, Shani, additional, Shirley, David G., additional, Sitprija, Visith, additional, Srinivas, Titte R., additional, Stenvinkel, Peter, additional, Stevens, Lesley A., additional, Textor, Stephen C., additional, Thurman, Joshua M., additional, Tong, Li-Li, additional, Topham, Peter S., additional, Tordoir, Jan H.M., additional, Torres, Vicente E., additional, Trence, Dace, additional, Turner, A. Neil, additional, Unwin, Robert J., additional, Vacher-Coponat, Henri, additional, Visweswaran, R. Kasi, additional, Wasse, Haimanot, additional, Wavamunno, Moses D., additional, Weiner, I. David, additional, Wheeler, David C., additional, Williams, Bryan, additional, Williams, John D., additional, Wingo, Charles S., additional, Winn, Michelle, additional, Wiseman, Alexander C., additional, Wolf, Gunter, additional, Womer, Karl, additional, Woodrow, Graham, additional, Wymer, David C., additional, Yang, Li, additional, and Yu, Xueqing, additional
- Published
- 2010
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13. Contributors
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Baril, Donald T., primary, Barthel, Ginger, additional, Timothy Baxter, B., additional, Beard, Jonathan D., additional, Becquemin, Jean-Pierre, additional, Belkin, Michael, additional, Bower, Thomas C., additional, Burnand, Kevin G., additional, Buth, Jaap, additional, Byrne, John, additional, Cambria, Richard P., additional, Carsten, Christopher G., additional, Cherry, Kenneth J., additional, Clouse, W. Darrin, additional, Coggia, Marc, additional, Corriere, Matthew A., additional, Cull, David L., additional, Cuypers, Philippe, additional, Dake, Michael D., additional, Davies, Alun H., additional, Donaldson, Magruder C., additional, Dubois, Josée, additional, Durán, Walter N, additional, Earnshaw, Jonothan J., additional, Edwards, James M., additional, Edwards, Matthew S., additional, Freischlag, Julie, additional, Giswold, Mary E., additional, Gloviczki, Peter, additional, GoËau-Brissonnière, Olivier, additional, Gohel, Manj S., additional, Gray, Bruce H., additional, Guimaraes, Marcelo, additional, Hamish, Maher, additional, Hansen, Kimberley J., additional, Harden, Paul N., additional, Hendriks, Johanna M., additional, Hertzer, Norman R., additional, Huda, Walter, additional, Hunter, Glenn C., additional, Ihnat, Daniel M., additional, Kalish, Jeffrey A., additional, Kalra, Manju, additional, Kieffer, Edouard, additional, Kyriakides, Constantinos, additional, Lederle, Frank A., additional, Leon, Luis R., additional, Lindsey, Benjamin, additional, London, Nick J.M., additional, Mackey, William C., additional, MacTaggart, Jason, additional, Markovic, Jovan N., additional, McGuinness, Catharine L., additional, Meissner, Mark H., additional, Menard, Matthew T., additional, Miller, Virginia M., additional, Mills, Joseph L., additional, Moneta, Gregory L., additional, Moss, Jonathan G., additional, Naoum, Joseph J., additional, Naylor, A. Ross, additional, Oderich, Gustavo S., additional, O'Hara, Patrick J., additional, Oliva, Vincent L., additional, Padberg, Frank, additional, Pascarella, Luigi, additional, Pomposelli, Frank B., additional, Quinn, Brendon, additional, Rasmussen, Todd E., additional, Rectenwald, John E., additional, Reed, Amy B., additional, Reilly, Linda M., additional, Rhee, Robert Y., additional, Rhodes, Jeffrey M., additional, Ricotta, Joseph J., additional, Rigberg, David, additional, Schönholz, Claudio, additional, Sharma, Paritosh, additional, Shepherd, Amanda, additional, Shortell, Cynthia, additional, Smith, Frank C.T., additional, Soulez, Gilles, additional, Stanley, James C., additional, Tan, Kong Teng, additional, Teso, Desarom, additional, Textor, Stephen C., additional, Thompson, Brad H., additional, Uflacker, Renan, additional, Upchurch, Gilbert R., additional, van Beek, Edwin J.R., additional, van Sambeek, Marc R.H.M., additional, Vandy, Frank C., additional, Vorwerk, Dierk, additional, Wakefield, Thomas W., additional, Wheeler, Nicole, additional, White, John V., additional, Wixon, Christopher L., additional, Woodburn, Kenneth R., additional, and Woodside, Kenneth J., additional
- Published
- 2009
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14. Pathophysiology and Evaluation of Renovascular Hypertension
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Textor, Stephen C., primary
- Published
- 2009
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15. Renovascular Hypertension and Ischemic Nephropathy: Angioplasty and Stenting
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Textor, Stephen C., primary and McKusick, Michael, additional
- Published
- 2008
- Full Text
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16. Contributors
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Akalin, Enver, primary, Appel, Alice Sue, additional, Appel, Gerald B., additional, Aslam, Shakil, additional, Atkins, Robert C., additional, Austin, Howard A., additional, Balow, James E., additional, Barratt, Jonathan, additional, Barrett, Brendan J., additional, Becker, Bryan N., additional, Berl, Tomas, additional, Blake, Catherine, additional, Blake, Peter G., additional, Blumberg, Emily A., additional, Bonventre, Joseph V., additional, Brater, D. Craig, additional, Braun, William E., additional, Bravo, Emmanuel L., additional, Brener, Zachary Z., additional, Briscoe, David M., additional, Bromberg, Jonathan, additional, Burkart, John, additional, Capasso, Giovambattista, additional, Cappuccio, Francesco P., additional, Carson, Culley C., additional, Chadban, Steven J., additional, Chapman, Arlene B., additional, Chen, Joline L.T., additional, Chesney, Russell W., additional, Cheung, Alfred K., additional, Cho, Monique E., additional, Cohen, Lewis M., additional, Conlin, Paul R., additional, Cruz, Dinna, additional, Cullis, Brett, additional, Curhan, Gary C., additional, Curtis, John J., additional, Cutie, Christopher J., additional, D-Amico, Giuseppe, additional, Davies, Simon J., additional, Davis, Connie L., additional, Davison, Sara N., additional, De Caterina, Raffaele, additional, Dember, Laura M., additional, Denton, Mark, additional, Depner, Thomas A., additional, Derksen, J. Eric, additional, Dharnidharka, Vikas R., additional, Dixon, Bradley S., additional, Dobbie, Hamish, additional, Druml, Wilfred, additional, DuBose, Thomas D., additional, Dworkin, Lance D., additional, Ellison, David H., additional, Fadem, Stephen Z., additional, Feehally, John, additional, Feinfeld, Donald A., additional, Fishbane, Steven, additional, Fitzpatrick, John M., additional, Ford, Daniel J., additional, Fornasieri, Alessandro, additional, Garnick, Marc B., additional, Gaston, Robert S., additional, Germain, Michael J., additional, Ginès, Pere, additional, Gonin, Joyce M., additional, Greene, Eddie L., additional, Grundy, Scott M., additional, Habli, Mounira, additional, Hall, Andrew, additional, Halperin, Mitchell L., additional, Harbord, Nikolas B., additional, Hewins, Peter, additional, Himmelfarb, Jonathan, additional, Hollenberg, Norman K., additional, Imai, Enyu, additional, Isaka, Yoshitaka, additional, Jang, Hye Ryoun, additional, Jayne, David, additional, Kaluvapalle, Jay R., additional, Kamel, Kamel S., additional, Kapa, Suraj, additional, Kaplan, Norman M., additional, Kist-van Holthe, Joana E., additional, Klotman, Mary E., additional, Klotman, Paul E., additional, Kopp, Jeffrey B., additional, Krakoff, Lawrence R., additional, Lentz, Aaron C., additional, Lerner, Susan M., additional, Levine, Jerrold S., additional, Levy, Jeremy B., additional, Lewis, Edmund J., additional, Lewis, Julia B., additional, Lin, Shih-Hua, additional, Llach, Francisco, additional, Luft, Friedrich C., additional, Mann, Samuel J., additional, Martin, Kevin J., additional, Masud, Tahsin, additional, Mathew, Roy O., additional, McDougal, W. Scott, additional, McKusick, Michael, additional, Mehta, Ravindra L., additional, Minetti, Luigi, additional, Mirot, Adam M., additional, Mitch, William E., additional, Moss, Alvin H., additional, Murphy, Barbara, additional, Nadim, Mitra K., additional, Neilson, Eric G., additional, Nora, Elizabeth H., additional, Noris, Marina, additional, Nouri, Pouneh, additional, Oh, Man S., additional, O-Meara, Yvonne M., additional, Palmer, Biff F., additional, Papademetriou, Vasilios, additional, Parfrey, Patrick S., additional, Patel, Manish P., additional, Pépin, Marie-Noëlle, additional, Plant, William D., additional, Pusey, Charles D., additional, Qazi, Rizwan A., additional, Rabb, Hamid, additional, Radbill, Brian D., additional, Rahbari-Oskoui, Frederic F., additional, Rees, Andrew J., additional, Remuzzi, Giuseppe, additional, Ricci, Zaccaria, additional, Ritz, Eberhard, additional, Rodig, Nancy M., additional, Ronco, Claudio, additional, Rubin, Robert H., additional, Rubin, Robert J., additional, Ruggenenti, Piero, additional, Salant, David J., additional, Sanders, Paul W., additional, Savage, Caroline O.S., additional, Sayegh, Mohamed H., additional, Schieppati, Arrigo, additional, Schröppel, Bernd, additional, Schulman, Gerald, additional, Shemin, Douglas G., additional, Sibai, Baha M., additional, Silva, Sandra, additional, Sims, Karen D., additional, Smith, James P., additional, Smith, Richard J.H., additional, Somers, Michael J.G., additional, Somers, Virend K., additional, Taal, Maarten W., additional, Takabatake, Yoshitsugu, additional, Taylor, Eric N., additional, Tessier, Edward G., additional, Textor, Stephen C., additional, Thurman, Joshua M., additional, Tolkoff-Rubin, Nina E., additional, Toto, Robert D., additional, Turner, A. Neil, additional, Unwin, Robert, additional, Vassalotti, Joseph A., additional, Vega, Gloria Lena, additional, Vella, John P., additional, Waldman, Meryl, additional, Wali, Ravinder K., additional, Wanner, Christoph, additional, Whittier, William L., additional, Wilcox, Christopher S., additional, Williams, John D., additional, Winchester, James F., additional, Wyatt, Christina M., additional, Yeun, Jane Y., additional, Yu, Alan S.L., additional, and Zoccali, Carmine, additional
- Published
- 2008
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17. Renal Artery Disease: Pathophysiology
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Textor, Stephen C., primary and Lerman, Lilach O., additional
- Published
- 2006
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18. CONTRIBUTORS
- Author
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AlMahameed, Amjad, primary, Ansell, Jack E., additional, Aquino, Melinda, additional, Aruny, John, additional, Ayerdi, Juan, additional, Beckman, Joshua A., additional, Belch, Jill J.F., additional, Belkin, Michael, additional, Berk, Bradford C., additional, Blei, Francine, additional, Blume, Peter, additional, Brass, Eric P., additional, Burke, Allen P., additional, Caplan, Louis R., additional, Cid, Maria C., additional, Coffman, Jay D., additional, Cooke, John P., additional, Creager, Mark A., additional, Criqui, Michael H., additional, Cronenwett, Jack L., additional, Davis, Mark D.P., additional, del Zoppo, Gregory J., additional, Donaldson, Magruder C., additional, Eagleton, Matthew J., additional, Edwards, Matthew S., additional, Fisher, Jonathan E.E., additional, Flohr, Thomas G., additional, Freedman, Jane E., additional, Freischlag, Julie A., additional, Fulton, David R., additional, Gerhard-Herman, Marie, additional, Giswold, Mary E., additional, Goldhaber, Samuel Z., additional, Goldstein, Irwin, additional, Gornik, Heather L., additional, Gram, Christopher H., additional, Gravereaux, Edwin C., additional, Halperin, Jonathan L., additional, Hansen, Kimberley J., additional, Hanzel, George, additional, Hiatt, William R., additional, Hobson, Robert W., additional, Hoffman, Gary S., additional, Iyer, Sriram S., additional, Kane, Laura B., additional, Kang, Andrew, additional, Kannel, William B., additional, Karamlou, Tara, additional, Kim, Noel N., additional, Klings, Elizabeth S., additional, Kronzon, Itzhak, additional, Kucher, Nils, additional, Lam, Everett Y., additional, Landry, Gregory J., additional, LeMaire, Scott A., additional, Lerman, Lilach O., additional, Libby, Peter, additional, Lipton, Martin J., additional, Loscalzo, Joseph, additional, Machleder, Herbert I., additional, Maksimowicz-McKinnon, Kathleen, additional, Mandel, Jess, additional, Menard, Matthew T., additional, Menzoian, James O., additional, Merkel, Peter A., additional, Miller, Virginia M., additional, Moneta, Gregory L., additional, Munarriz, Ricardo, additional, Newburger, Jane W., additional, Ninomiya, John, additional, O'Gara, Patrick, additional, Olin, Jeffrey W., additional, O'Rourke, Stephen T., additional, Ouriel, Kenneth, additional, Paszkowiak, Jacek, additional, Patterson, Dean, additional, Raffetto, Joseph D., additional, Raghow, Rajendra, additional, Rigberg, David A., additional, Rockson, Stanley G., additional, Rooke, Thom W., additional, Roubin, Gary S., additional, Ruberg, Frederick L., additional, Rzucidlo, Eva M., additional, Safian, Robert D., additional, Schoepf, U. Joseph, additional, Seyer, Jerome, additional, Sobieszczyk, Piotr, additional, Srivastava, Sunita D., additional, Stanton-Hicks, Michael, additional, Sumpio, Bauer E., additional, Taylor, Allen J., additional, Taylor, Lloyd M., additional, Textor, Stephen C., additional, Thompson, Robert W., additional, Topper, James N., additional, Traish, Abdul M., additional, Tunick, Paul A., additional, Upchurch, Gilbert R., additional, Valentine, R. James, additional, Vanhoutte, Paul M., additional, Virmani, Renu, additional, Vitek, Jiri J., additional, Wasserman, Scott M., additional, Weisz, Giora, additional, Welborn, M. Burress, additional, White, Christopher J., additional, Wilson, David B., additional, Wolf, Philip A., additional, and Yucel, E. Kent, additional
- Published
- 2006
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19. In a Phase 1a escalating clinical trial, autologous mesenchymal stem cell infusion for renovascular disease increases blood flow and the glomerular filtration rate while reducing inflammatory biomarkers and blood pressure.
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Abumoawad A, Saad A, Ferguson CM, Eirin A, Herrmann SM, Hickson LJ, Goksu BB, Bendel E, Misra S, Glockner J, Dietz AB, Lerman LO, and Textor SC
- Subjects
- Biomarkers, Blood Pressure, Glomerular Filtration Rate, Humans, Kidney, Renal Circulation, Mesenchymal Stem Cells, Renal Artery Obstruction therapy
- Abstract
Atherosclerotic renovascular disease (ARVD) reduces tissue perfusion and eventually leads to loss of kidney function with limited therapeutic options. Here we describe results of Phase 1a escalating dose clinical trial of autologous mesenchymal stem cell infusion for ARVD. Thirty-nine patients with ARVD were studied on two occasions separated by three months. Autologous adipose-derived mesenchymal stem cells were infused through the renal artery in 21 patients at three different dose levels (1, 2.5 and 5.0 × 10
5 cells/kg) in seven patients each. We measured renal blood flow, glomerular filtration rate (GFR) (iothalamate and estimated GFR), renal vein cytokine levels, blood pressure, and tissue oxygenation before and three months after stem cell delivery. These indices were compared to those of 18 patients with ARVD matched for age, kidney function and blood pressure receiving medical therapy alone that underwent an identical study protocol. Cultured mesenchymal stem cells were also studied in vitro. For the entire stem cell treated-cohort, mean renal blood flow in the treated stenotic kidney significantly increased after stem cell infusion from (164 to 190 ml/min). Hypoxia, renal vein inflammatory cytokines, and angiogenic biomarkers significantly decreased following stem cell infusion. Mean systolic blood pressure significantly fell (144 to 136 mmHg) and the mean two-kidney GFR (Iothalamate) modestly but significantly increased from (53 to 56 ml/min). Changes in GFR and blood pressure were largest in the high dose stem cell treated individuals. No such changes were observed in the cohort receiving medical treatment alone. Thus, our data demonstrate the potential for autologous mesenchymal stem cell to increase blood flow, GFR and attenuate inflammatory injury in post-stenotic kidneys. The observation that some effects are dose-dependent and related to in-vitro properties of mesenchymal stem cell may direct efforts to maximize potential therapeutic efficacy., (Copyright © 2019 International Society of Nephrology. Published by Elsevier Inc. All rights reserved.)- Published
- 2020
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20. Renovascular Hypertension.
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Herrmann SM and Textor SC
- Subjects
- Humans, Fibromuscular Dysplasia complications, Fibromuscular Dysplasia diagnosis, Fibromuscular Dysplasia physiopathology, Fibromuscular Dysplasia therapy, Hypertension, Renal diagnosis, Hypertension, Renal etiology, Hypertension, Renal physiopathology, Hypertension, Renal therapy, Hypertension, Renovascular diagnosis, Hypertension, Renovascular etiology, Hypertension, Renovascular physiopathology, Hypertension, Renovascular therapy, Nephritis diagnosis, Nephritis etiology, Nephritis physiopathology, Nephritis therapy, Renal Artery Obstruction complications, Renal Artery Obstruction diagnosis, Renal Artery Obstruction physiopathology, Renal Artery Obstruction therapy
- Abstract
Renovascular disease (RVD) is a major cause of secondary hypertension. Atherosclerotic renal artery stenosis is the most common type of RVD followed by fibromuscular dysplasia. It has long been recognized as the prototype of angiotensin-dependent hypertension. However, the mechanisms underlying the physiopathology of hypertensive occlusive vascular renal disease are complex and distinction between the different causes of RVD should be made. Recognition of these distinct types of RVD with different degrees of renal occlusive disease is important for management. The greatest challenge is to individualize and implement the best approach for each patient in the setting of widely different comorbidities., (Copyright © 2019 Elsevier Inc. All rights reserved.)
- Published
- 2019
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21. Medically Complex Living Kidney Donors: Where Are We Now?
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Textor SC
- Published
- 2019
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22. Tissue hypoxia, inflammation, and loss of glomerular filtration rate in human atherosclerotic renovascular disease.
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Abumoawad A, Saad A, Ferguson CM, Eirin A, Woollard JR, Herrmann SM, Hickson LJ, Bendel EC, Misra S, Glockner J, Lerman LO, and Textor SC
- Subjects
- Aged, Aged, 80 and over, Atherosclerosis physiopathology, Cell Hypoxia, Cross-Sectional Studies, Female, Humans, Inflammation etiology, Inflammation pathology, Kidney diagnostic imaging, Kidney physiopathology, Magnetic Resonance Imaging, Male, Middle Aged, Oxygen analysis, Oxygen blood, Oxygen Consumption, Renal Artery Obstruction etiology, Renal Artery Obstruction pathology, Renal Circulation, Atherosclerosis complications, Glomerular Filtration Rate, Inflammation physiopathology, Kidney pathology, Renal Artery Obstruction physiopathology
- Abstract
The relationships between renal blood flow (RBF), tissue oxygenation, and inflammatory injury in atherosclerotic renovascular disease (ARVD) are poorly understood. We sought to correlate RBF and tissue hypoxia with glomerular filtration rate (GFR) in 48 kidneys from patients with ARVD stratified by single kidney iothalamate GFR (sGFR). Oxygenation was assessed by blood oxygenation level dependent magnetic resonance imaging (BOLD MRI), which provides an index for the levels of deoxyhemoglobin within a defined volume of tissue (R2*). sGFR correlated with RBF and with the severity of vascular stenosis as estimated by duplex velocities. Higher cortical R2* and fractional hypoxia and higher levels of renal vein neutrophil-gelatinase-associated-lipocalin (NGAL) and monocyte-chemoattractant protein-1 (MCP-1) were observed at lower GFR, with an abrupt inflection below 20 ml/min. Renal vein MCP-1 levels correlated with cortical R2* and with fractional hypoxia. Correlations between cortical R2* and RBF in the highest sGFR stratum (mean sGFR 51 ± 12 ml/min; R = -0.8) were degraded in the lowest sGFR stratum (mean sGFR 8 ± 3 ml/min; R = -0.1). Changes in fractional hypoxia after furosemide were also absent in the lowest sGFR stratum. These data demonstrate relative stability of renal oxygenation with moderate reductions in RBF and GFR but identify a transition to overt hypoxia and inflammatory cytokine release with severely reduced GFR. Tissue oxygenation and RBF were less correlated in the setting of reduced sGFR, consistent with variable oxygen consumption or a shift to alternative mechanisms of tissue injury. Identifying transitions in tissue oxygenation may facilitate targeted therapy in ARVD., (Copyright © 2019 International Society of Nephrology. Published by Elsevier Inc. All rights reserved.)
- Published
- 2019
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23. Impact of aortic wall thrombus on late changes in renal function among patients treated by fenestrated-branched endografts.
- Author
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Sandri GA, Oderich GS, Tenorio ER, Ribeiro MS, Reis de Souza L, Cha SS, Macedo TA, and Textor SC
- Subjects
- Acute Kidney Injury mortality, Acute Kidney Injury physiopathology, Acute Kidney Injury therapy, Aged, Aged, 80 and over, Aortic Aneurysm, Abdominal complications, Aortic Aneurysm, Abdominal mortality, Aortic Aneurysm, Thoracic complications, Aortic Aneurysm, Thoracic mortality, Blood Vessel Prosthesis, Blood Vessel Prosthesis Implantation instrumentation, Blood Vessel Prosthesis Implantation mortality, Databases, Factual, Endovascular Procedures instrumentation, Endovascular Procedures mortality, Female, Humans, Male, Prosthesis Design, Retrospective Studies, Risk Factors, Thrombosis mortality, Time Factors, Treatment Outcome, Acute Kidney Injury etiology, Aortic Aneurysm, Abdominal surgery, Aortic Aneurysm, Thoracic surgery, Blood Vessel Prosthesis Implantation adverse effects, Endovascular Procedures adverse effects, Glomerular Filtration Rate, Kidney physiopathology, Thrombosis complications
- Abstract
Objective: Renal function deterioration is an important determinant of mortality in patients treated for complex aortic aneurysms. We have previously determined that catheter and guidewire manipulation in diseased aortas during fenestrated-branched endovascular aneurysm repair (F-BEVAR) is associated with risk of renal function deterioration. The aim of this study was to describe the impact of atherothrombotic aortic wall thrombus (AWT) on renal function deterioration among patients treated by F-BEVAR for pararenal and extent IV thoracoabdominal aortic aneurysms., Methods: Clinical data of 212 patients treated for complex aortic aneurysms with F-BEVAR were entered into a prospectively maintained database (2007-2015). AWT was evaluated by computed tomography angiography using volumetric measurements in nonaneurysmal aortic segments. AWT was classified as mild, moderate, or severe using objective assessment of the number of affected segments, thrombus type, thickness, area, and circumference. Acute kidney injury (AKI) was defined using Risk, Injury, Failure, Loss of kidney function, and End-stage renal disease (RIFLE) criteria, and renal function deterioration was defined by a decline in estimated glomerular filtration rate (eGFR) >30% from baseline. Patient survival and renal outcomes were assessed at dismissal, at 6 to 8 weeks, at 6 months, and annually, including AKI, serum creatinine concentration, eGFR, chronic kidney disease stage, need for renal replacement therapy, and presence of kidney infarction., Results: There were 169 male (80%) and 43 female (20%) patients with a mean age of 75 ± 7 years. Aneurysm extent was pararenal in 157 patients and extent IV thoracoabdominal aortic aneurysm in 55 patients. A total of 700 renal-mesenteric arteries were incorporated (3.1 ± 1 vessels/patient). AWT was classified as mild in 98 patients (46%), moderate in 75 (35%), and severe in 39 (19%). At 30 days, 45 patients (21%) developed AKI. Decline in eGFR and kidney infarction were associated with higher AWT volume index and severe AWT classification (P < .05). There was no association of AWT with 30-day mortality, which was 0.5% for the entire cohort. Mean follow-up was 29 ± 23 months. Freedom from renal function deterioration was 73% ± 6% for mild, 81% ± 6% for moderate, and 66% ± 8% for severe AWT patients at 3 years (P = .012) and 46% ± 9% and 82% ± 4% for those with or without AKI after the initial procedure (P < .001). Overall, 41 patients (19%) had progression of chronic kidney disease stage, but none of the patients required renal replacement therapy. Survival was 73% ± 5% for mild, 72% ± 6% for moderate, and 69% ± 10% for severe AWT patients at 3 years (P = .67)., Conclusions: AWT is a significant predictor of AKI and continued decline in renal function after the initial F-BEVAR procedure. Longer follow-up time is needed to determine the actual impact of AWT on survival., (Copyright © 2018 Society for Vascular Surgery. Published by Elsevier Inc. All rights reserved.)
- Published
- 2019
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24. Emerging evidence on renal denervation for the treatment of hypertension.
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Wyatt CM and Textor SC
- Subjects
- Denervation, Humans, Kidney, Single-Blind Method, Antihypertensive Agents, Hypertension
- Published
- 2018
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25. Intrarenal fat deposition does not interfere with the measurement of single-kidney perfusion in obese swine using multi-detector computed tomography.
- Author
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Ferguson CM, Eirin A, Michalak GJ, Hedayat AF, Abumoawad A, Saad A, Zhu X, Textor SC, McCollough CH, and Lerman LO
- Subjects
- Animals, Blood Flow Velocity, Contrast Media administration & dosage, Diet, High-Fat, Dietary Carbohydrates, Disease Models, Animal, Feasibility Studies, Iopamidol administration & dosage, Obesity etiology, Predictive Value of Tests, Renal Artery physiopathology, Sus scrofa, Time Factors, Adiposity, Kidney blood supply, Multidetector Computed Tomography, Obesity physiopathology, Perfusion Imaging methods, Renal Artery diagnostic imaging, Renal Circulation
- Abstract
Background: Altered vascular structure or function in several diseases may impair renal perfusion. Multi-detector computed tomography (MDCT) is a non-invasive tool to assess single-kidney perfusion and function based on dynamic changes in tissue attenuation during contrast media transit. However, changes in basal tissue attenuation might hamper these assessments, despite background subtraction. Evaluation of iodine concentration using the dual-energy (DECT) MDCT mode allows excluding effects of basal values on dynamic changes in tissue attenuation. We tested whether decreased basal kidney attenuation secondary to intrarenal fat deposition in swine obesity interferes with assessment of renal perfusion using MDCT., Methods: Domestic pigs were fed a standard (lean) or a high-cholesterol/carbohydrate (obese) diet (n = 5 each) for 16 weeks, and both kidneys were then imaged using MDCT/DECT after iodinated contrast injection. DECT images were post-processed to generate iodine and virtual-non-contrast (VNC) datasets, and the MDCT kidney/aorta CT number (following background subtraction) and DECT iodine ratios calculated during the peak vascular phase as surrogates of renal perfusion. Intrarenal fat was subsequently assessed with Oil-Red-O staining., Results: VNC maps in obese pigs revealed decreased basal cortical attenuation, and histology confirmed increased renal tissue fat deposition. Nevertheless, the kidney/aorta attenuation and iodine ratios remained similar, and unchanged compared to lean pigs., Conclusions: Despite decreased basal attenuation secondary to renal adiposity, background subtraction allows adequate assessment of kidney perfusion in obese pigs using MDCT. These observations support the feasibility of renal perfusion assessment in obese subjects using MDCT., (Copyright © 2018. Published by Elsevier Inc.)
- Published
- 2018
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26. The metabolic syndrome induces early changes in the swine renal medullary mitochondria.
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Eirin A, Woollard JR, Ferguson CM, Jordan KL, Tang H, Textor SC, Lerman A, and Lerman LO
- Subjects
- Animals, Cardiolipins metabolism, Diet adverse effects, Female, Glomerular Filtration Rate, Kidney Medulla diagnostic imaging, Kidney Medulla drug effects, Magnetic Resonance Imaging, Metabolic Syndrome drug therapy, Metabolic Syndrome etiology, Mitochondria drug effects, Oxidative Stress drug effects, Renal Circulation, Sus scrofa, Kidney Medulla pathology, Metabolic Syndrome physiopathology, Mitochondria pathology, Oligopeptides pharmacology
- Abstract
The metabolic syndrome (MetS) is associated with nutrient surplus and kidney hyperfiltration, accelerating chronic renal failure. Mitochondria can be overwhelmed by substrate excess, leading to inefficient energy production and thereby tissue hypoxia. Mitochondrial dysfunction is emerging as an important determinant of renal damage, but whether it contributes to MetS-induced renal injury remains unknown. We hypothesized that early MetS induces kidney mitochondrial abnormalities and dysfunction, which would be notable in the vulnerable renal medulla. Pigs were studied after 16 weeks of diet-induced MetS, MetS treated for the last 4 weeks with the mitochondria-targeted peptide elamipretide (0.1 mg/kg SC q.d), and Lean controls (n = 7 each). Single-kidney renal blood flow, glomerular filtration rate, and oxygenation were measured in-vivo, whereas cortical and medullary mitochondrial structure and function and renal injurious pathways were studied ex-vivo. Blood pressure was slightly elevated in MetS pigs, and their renal blood flow and glomerular filtration rate were elevated. Blood oxygen level-dependent magnetic resonance imaging demonstrated that this was associated with medullary hypoxia, whereas cortical oxygenation remained intact. MetS decreased renal content of the inner mitochondrial membrane cardiolipin, particularly the tetra-linoleoyl (C18:2) cardiolipin species, and altered mitochondrial morphology and function, particularly in the medullary thick ascending limb. MetS also increased renal cytochrome-c-induced apoptosis, oxidative stress, and tubular injury. Chronic mitoprotection restored mitochondrial structure, ATP synthesis, and antioxidant defenses and decreased mitochondrial oxidative stress, medullary hypoxia, and renal injury. These findings implicate medullary mitochondrial damage in renal injury in experimental MetS, and position the mitochondria as a therapeutic target., (Copyright © 2017 Elsevier Inc. All rights reserved.)
- Published
- 2017
- Full Text
- View/download PDF
27. Early atherosclerosis aggravates renal microvascular loss and fibrosis in swine renal artery stenosis.
- Author
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Sun D, Eirin A, Ebrahimi B, Textor SC, Lerman A, and Lerman LO
- Subjects
- Animals, Atherosclerosis pathology, Blood Pressure, Cholesterol blood, Disease Models, Animal, Female, Fibrosis, Glomerular Filtration Rate, Humans, Hypertension, Renovascular complications, Hypoxia etiology, Hypoxia physiopathology, Kidney diagnostic imaging, Lipoproteins, LDL blood, Oxidative Stress, Random Allocation, Renal Artery Obstruction complications, Renal Artery Obstruction diagnostic imaging, Sus scrofa, Vascular Remodeling, X-Ray Microtomography, Atherosclerosis complications, Hypertension, Renovascular pathology, Kidney blood supply, Kidney pathology, Microvessels pathology, Renal Artery Obstruction pathology, Renal Circulation
- Abstract
Renal function in patients with atherosclerosis and renal artery stenosis (ARAS) deteriorates more frequently than in nonatherosclerotic RAS. We hypothesized that ARAS aggravates stenotic-kidney micro vascular loss compared to RAS. Domestic pigs were randomized to normal, RAS, and ARAS (RAS fed a high-cholesterol diet) groups (n = 7 each). Ten weeks later stenotic-kidney oxygenation, renal blood flow, and glomerular filtration rate (GFR) were evaluated in vivo, and micro vascular density by micro-computed tomography. Blood pressure in both RAS and ARAS was elevated; and stenotic-kidney renal blood flow and GFR similarly decreased. RAS decreased the density of small-size cortical microvessels (<200 μm), whereas ARAS extended the decrease to medium-sized microvessels (200-300 μm). Cortical hypoxia and interstitial fibrosis increased in both RAS and ARAS but correlated inversely with micro vascular density only in RAS. Atherosclerosis aggravates loss of stenotic-kidney microvessels, yet additional determinants likely contribute to cortical hypoxia and fibrosis in swine ARAS., (Copyright © 2016 American Society of Hypertension. Published by Elsevier Inc. All rights reserved.)
- Published
- 2016
- Full Text
- View/download PDF
28. Secondary hypertension: renovascular hypertension.
- Author
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Textor SC
- Subjects
- Antihypertensive Agents therapeutic use, Glomerular Filtration Rate, Humans, Hydroxymethylglutaryl-CoA Reductase Inhibitors therapeutic use, Smoking Cessation, Stents, Hypertension, Renovascular diagnosis, Hypertension, Renovascular physiopathology, Hypertension, Renovascular therapy
- Published
- 2014
- Full Text
- View/download PDF
29. Increasing mortality by living kidney donation?: the devil is in the details.
- Author
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Amer H, Prieto M, Heimbach JK, Textor SC, and Taler SJ
- Subjects
- Female, Humans, Male, Kidney Transplantation adverse effects, Living Donors, Tissue and Organ Harvesting adverse effects
- Published
- 2014
- Full Text
- View/download PDF
30. Angiotensin receptor blockade has protective effects on the poststenotic porcine kidney.
- Author
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Zhang X, Eirin A, Li ZL, Crane JA, Krier JD, Ebrahimi B, Pawar AS, Zhu XY, Tang H, Jordan KL, Lerman A, Textor SC, and Lerman LO
- Subjects
- Acute Kidney Injury physiopathology, Angiotensin Receptor Antagonists pharmacology, Animals, Constriction, Pathologic etiology, Constriction, Pathologic physiopathology, Constriction, Pathologic prevention & control, Disease Models, Animal, Female, Glomerular Filtration Rate drug effects, Glomerular Filtration Rate physiology, Hemodynamics drug effects, Hemodynamics physiology, Kidney blood supply, Kidney pathology, Kidney physiopathology, Microcirculation drug effects, Oxidative Stress drug effects, Oxidative Stress physiology, Renal Artery Obstruction physiopathology, Swine, Tetrazoles pharmacology, Valine pharmacology, Valine therapeutic use, Valsartan, Acute Kidney Injury etiology, Acute Kidney Injury prevention & control, Angiotensin Receptor Antagonists therapeutic use, Receptors, Angiotensin drug effects, Renal Artery Obstruction complications, Tetrazoles therapeutic use, Valine analogs & derivatives
- Abstract
Angiotensin-converting enzyme inhibitors/angiotensin II receptor blockers (ARBs) may induce an acute decrease of glomerular filtration rate (GFR) in the stenotic kidney in renal artery stenosis, but most patients tolerate these drugs well. We hypothesized that angiotensin-converting enzyme inhibitors/ARBs stabilize stenotic kidney function during prolonged treatment by conferring protective effects. We tested this in control domestic pigs and pigs with renal artery stenosis untreated or treated with Valsartan, or triple therapy (seven pigs in each group) for 4 weeks starting 6 weeks after stenosis induction. Renal function, oxygenation, tubular function, and microcirculation were assessed by multi-detector computed tomography (CT), blood oxygen level-dependent magnetic-resonance imaging, and micro-CT. Valsartan and triple therapy decreased blood pressure similarly; however, Valsartan did not change the GFR of the stenotic kidney compared with renal artery stenosis and was similar to triple therapy. Both Valsartan and triple therapy stimulated microvascular density and improved tubular function. Valsartan also caused a greater increase of angiogenic factors and a decrease in oxidative stress, which were related to higher cortical perfusion and tubular response than triple therapy. Thus, Valsartan did not decrease stenotic kidney GFR, but improved cortical perfusion and microcirculation. These beneficial effects may partly offset the hemodynamic GFR reduction in renal artery stenosis and preserve kidney function.
- Published
- 2013
- Full Text
- View/download PDF
31. Percutaneous revascularization for ischemic nephropathy: the past, present, and future.
- Author
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Textor SC, Misra S, and Oderich GS
- Subjects
- Atherosclerosis surgery, Catheters, Humans, Hypertension, Renovascular etiology, Hypertension, Renovascular surgery, Ischemia complications, Kidney Diseases etiology, Renal Artery surgery, Renal Artery Obstruction etiology, Stents, Ischemia surgery, Kidney Diseases surgery, Renal Artery Obstruction surgery, Vascular Surgical Procedures methods, Vascular Surgical Procedures trends
- Abstract
Occlusion of the renal arteries can threaten the viability of the kidney when severe, in addition to accelerating hypertension and circulatory congestion. Renal artery stenting procedures have evolved from a treatment mainly for renovascular hypertension to a maneuver capable of recovering threatened renal function in patients with 'ischemic nephropathy' and improving management of congestive heart failure. Improved catheter design and techniques have reduced, but not eliminated, hazards associated with renovascular stenting. Expanded use of endovascular stent grafts to treat abdominal aortic aneurysms has introduced a new indication for renal artery stenting to protect the renal circulation when grafts cross the origins of the renal arteries. Although controversial, prospective randomized trials to evaluate the added benefit of revascularization to current medical therapy for atherosclerotic renal artery stenosis until now have failed to identify major benefits regarding either renal function or blood pressure control. These studies have been limited by selection bias and have been harshly criticized. While studies of tissue oxygenation using blood-oxygen-level-dependent (BOLD) magnetic resonance establish that kidneys can adapt to reduced blood flow to some degree, more severe occlusive disease leads to cortical hypoxia associated with microvascular rarefaction inflammatory injury, and fibrosis. Current research is directed toward identifying pathways of irreversible kidney injury due to vascular occlusion and to increase the potential for renal repair after restoring renal artery patency. The role of nephrologists likely will focus upon recognizing the limits of renal adaptation to vascular disease and identifying kidneys truly at risk for ischemic injury at a time point when renal revascularization can still be of benefit to recovering kidney function.
- Published
- 2013
- Full Text
- View/download PDF
32. Abnormal circadian blood pressure pattern 1-year after kidney transplantation is associated with subsequent lower glomerular filtration rate in recipients without rejection.
- Author
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Wadei HM, Amer H, Griffin MD, Taler SJ, Stegall MD, and Textor SC
- Subjects
- Adolescent, Adult, Aged, Albuminuria epidemiology, Female, Humans, Male, Middle Aged, Postoperative Period, Retrospective Studies, Young Adult, Blood Pressure physiology, Circadian Rhythm physiology, Glomerular Filtration Rate physiology, Kidney Transplantation physiology
- Abstract
Abnormal circadian blood pressure (BP) pattern is common after kidney transplantation but its relationship to long term allograft function is unclear. Of 119 kidney recipients who had ambulatory BP monitoring 1 year from transplantation, 36 patients without history of rejection were selected. Twenty-nine recipients were followed for 4 years and seven for 3 years. Iothalamate glomerular filtration rate (GFR) was obtained at 3 weeks then annually. Dippers (n = 10) had day-night systolic BP (SBP) drop (ΔSBP) of ≥10%, nondippers (n = 15) had ΔSBP 0%-9%, whereas reverse dippers (n = 11) had nocturnal rise in SBP. Compared with dippers, reverse and nondippers had a higher Banff cv score at 1 year (P = .03), lower GFR at last follow-up (73.7 ± 18.1, 55.7 ± 16.3, and 56.6 ± 21 mL/min/1.73 m(2) for dippers, non-, and reverse dippers, respectively, P = .05) and higher kidney function loss (8.0 ± 20, -9 ± 17, and 1 ± 14 mL/min/1.73 m(2) for dippers, non-, and reverse dippers, respectively, P = .02). GFR at 4 years and at last follow-up independently correlated with ΔSBP at 1 year (r = 0.46, P = .01; r = 0.34, P = .03). The current study indicates that abnormal circadian BP pattern at 1 year identifies a group of kidney recipients at risk for increased kidney function loss and lower GFR 3-4 years from transplantation., (Copyright © 2011 American Society of Hypertension. Published by Elsevier Inc. All rights reserved.)
- Published
- 2011
- Full Text
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33. Revascularization of swine renal artery stenosis improves renal function but not the changes in vascular structure.
- Author
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Favreau F, Zhu XY, Krier JD, Lin J, Warner L, Textor SC, and Lerman LO
- Subjects
- Animals, Apoptosis, Blood Pressure, Chronic Disease, Disease Models, Animal, Female, Fibrosis, Glomerular Filtration Rate, Hypertension, Renovascular pathology, Hypertension, Renovascular physiopathology, Kidney pathology, Kidney physiopathology, Microvessels pathology, Recovery of Function, Renal Artery pathology, Renal Artery Obstruction pathology, Renal Artery Obstruction physiopathology, Stents, Sus scrofa, Time Factors, Angioplasty, Balloon instrumentation, Hypertension, Renovascular therapy, Kidney blood supply, Microcirculation, Microvessels physiopathology, Renal Artery physiopathology, Renal Artery Obstruction therapy, Renal Circulation
- Abstract
Renal revascularization by percutaneous transluminal angioplasty improves blood pressure and stenotic kidney function in selected groups of patients, but the reversibility of intrarenal and microvascular remodeling remains unknown. Here, we tested the hypothesis that renal angioplasty improves the function and structure of renal microcirculation in experimental chronic renal artery stenosis. Stenotic kidney function, hemodynamics, and endothelial function were assessed in vivo in pigs after 10 weeks of unilateral renal artery stenosis. Renal microvascular remodeling, angiogenic pathways, and fibrosis were measured ex vivo. Angioplasty and stenting carried out 4 weeks before measurement decreased blood pressure, improved glomerular filtration rate, and improved microvascular endothelial function. It also promoted the expression of angiogenic factors and decreased renal apoptosis due to stenosis, compared with a sham intervention. The spatial density of renal microvessels, however, was partially improved after angioplasty. Renal blood flow was incompletely restored compared with the kidneys of sham-treated animals, as was interstitial fibrosis. Renal microvascular media-to-lumen ratio remained unchanged by angioplasty. Thus, our study shows that revascularization of a stenotic renal artery restores the glomerular filtration rate and renal endothelial function 4 weeks later. Renal hemodynamics and structure, however, are incompletely resolved.
- Published
- 2010
- Full Text
- View/download PDF
34. The uncertain value of renal artery interventions: where are we now?
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Textor SC, Lerman L, and McKusick M
- Subjects
- Arteriosclerosis mortality, Humans, Minnesota, Myocardial Revascularization, Renal Artery Obstruction mortality, Risk Assessment, Survival Analysis, United States, Arteriosclerosis therapy, Renal Artery, Renal Artery Obstruction therapy, Stents
- Abstract
Improved technology for detection of and endovascular procedures for renal artery stenosis due to atherosclerosis has been associated with increases in renal artery intervention. Hypertension with accelerated target organ injury, reduced kidney function, and episodic circulatory congestion in patients with renovascular disease predict reduced patient survival. Recent studies indicate that activation of pressor mechanisms depends upon hemodynamic gradients that are often overrated by visual estimates. Although activation of the renin-angiotensin system initiates renovascular hypertension, additional mechanisms perpetuate vascular remodeling and kidney injury that may not depend upon large vessel occlusion. Major advances in medical therapy have led to initiation of at least 4 major prospective trials comparing optimal medical therapy with or without stenting. Up to now, outcome data fail to support broad application of renal revascularization, including results from a recent large, prospective trial from the United Kingdom, despite small groups of patients that experience major clinical benefit. The ambiguity of these results partly reflect poor characterization of the severity of vascular lesions and competing risks within the population related to aging and pre-existing disease. Many patients currently undergoing renal artery interventions derive little net benefit and some are exposed to significant complications, including atheroembolic disease. Determining the appropriate role for renal artery interventions will depend on developing better methods for judging the role of large vessel occlusive disease regarding tissue oxygenation, activation of profibrotic pathways, and irreversible injury in the post-stenotic kidney.
- Published
- 2009
- Full Text
- View/download PDF
35. Living donor kidney and autologous stem cell transplantation for primary systemic amyloidosis (AL) with predominant renal involvement.
- Author
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Leung N, Griffin MD, Dispenzieri A, Haugen EN, Gloor JM, Schwab TR, Textor SC, Lacy MQ, Litzow MR, Cosio FG, Larson TS, Gertz MA, and Stegall MD
- Subjects
- Adolescent, Adult, Aged, Feasibility Studies, Female, Humans, Male, Middle Aged, Stem Cells, Tissue and Organ Harvesting, Transplantation, Autologous, Treatment Outcome, Amyloidosis surgery, Kidney Diseases surgery, Kidney Transplantation adverse effects, Living Donors, Stem Cell Transplantation
- Abstract
Primary systemic amyloidosis (AL) is characterized by multiorgan deposition of monoclonal immunoglobulin light chain. Renal involvement is common and impaired kidney function is associated with reduced median survival. Autologous stem cell transplantation (SCT) for AL achieves superior response rates compared to chemotherapy alone but patients with end-stage renal disease (ESRD) may be excluded from consideration. A treatment approach consisting of living donor kidney transplantation (LDKTx) followed by autologous SCT was developed for AL with ESRD. Eight patients underwent LDKTx with immediate graft function. Two suffered unanticipated complications post-KTx and died 10 and 3 months later. Two cases of subclinical acute cellular rejection (ACR) and one case of clinical ACR occurred--all reversible with corticosteroid. Six patients had successful stem cell harvests performed and five of these underwent SCT with satisfactory trilineage engraftment. Renal function remained stable following SCT in four and was reduced in one due to infectious and bleeding complications. One patient, who has thus far elected not to undergo SCT, has proteinuria and histologic evidence of recurrent renal amyloidosis. This experience supports the feasibility of sequential living donor KTx and autologous SCT for carefully selected patients with ESRD due to AL.
- Published
- 2005
- Full Text
- View/download PDF
36. New onset hyperglycemia and diabetes are associated with increased cardiovascular risk after kidney transplantation.
- Author
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Cosio FG, Kudva Y, van der Velde M, Larson TS, Textor SC, Griffin MD, and Stegall MD
- Subjects
- Adult, Aged, Female, Humans, Hyperglycemia etiology, Male, Middle Aged, Risk Factors, Cardiovascular Diseases etiology, Diabetes Complications etiology, Hyperglycemia complications, Kidney Transplantation adverse effects
- Abstract
Background: Post-transplant diabetes (PTDM) is a common and serious complication of kidney transplantation. The implications of developing hyperglycemia of lesser severity are not well understood., Methods: In this study we used American Diabetes Association (ADA) criteria to assess the incidence of abnormal glycemia post-transplant, the variables that relate to this complication, and the relationship between hyperglycemia and cardiovascular (CV) disease. Included in the study were 490 kidney recipients, transplanted from 1998 to 2003, without a history of diabetes, and with a pretransplant fasting glucose <126 mg/dL., Results: Within one week post-transplant, 45% of recipients had impaired fasting glycemia (IFG, glucose 100-125 mg/dL), and 21% PTDM (glucose > or =126). One year post-transplant, 33% of patients had IFG, and 13% PTDM. Risk factors for hyperglycemia at one year included: older recipient, male gender, higher BMI, higher pretransplant glucose, and higher glucose one week post-transplant (all P < 0.002 by multivariable analyses). During a follow-up period of 40 +/- 14 months, 12% of recipients had CV events (cardiac, CVA, and/or peripheral). Increasing fasting glucose levels at one, four, and/or 12 months post-transplant were significantly related to CV events. Furthermore, these relationships were independent of other CV risk factors, including: older age, CV events pretransplant, male gender, dyslipidemia, and transplant year. Fasting glucose levels >100 mg/dL were associated with higher incidence of post-transplant cardiac (P= 0.001) and peripheral vascular disease events (P= 0.003)., Conclusion: The incidence of post-transplant hyperglycemia and its CV impact have been underestimated. Pretransplant characteristics and, particularly, the glycemia during the first month post-transplant identified patients at risk of PTDM. Increasing glucose levels greater than 100 mg/dL, any time after the first month post-transplant, are associated with increasing CV risk. We postulate that aggressive detection and treatment of post-transplant hyperglycemia may significantly reduce CV morbidity and mortality after kidney transplantation.
- Published
- 2005
- Full Text
- View/download PDF
37. Obesity in living kidney donors: clinical characteristics and outcomes in the era of laparoscopic donor nephrectomy.
- Author
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Heimbach JK, Taler SJ, Prieto M, Cosio FG, Textor SC, Kudva YC, Chow GK, Ishitani MB, Larson TS, and Stegall MD
- Subjects
- Adult, Blood Pressure, Body Mass Index, Female, Follow-Up Studies, Glomerular Filtration Rate, Humans, Kidney pathology, Laparoscopy, Male, Middle Aged, Nephrectomy, Obesity, Postoperative Complications, Retrospective Studies, Smoking, Time Factors, Treatment Outcome, Wound Healing, Kidney Transplantation methods, Living Donors, Tissue Donors
- Abstract
Acceptance of obese individuals as living kidney donors is controversial related to possible increased risk for surgical complications and concern that obesity may contribute to long-term renal disease. We retrospectively examined 553 consecutive hand-assisted laparoscopic living kidney donations between October 1, 1999 and April 1, 2003. We stratified donors into quartiles by baseline body mass index (BMI) assessing perioperative complications and 6-12 months post-donation metabolic and renal function. Compared to BMI <25 kg/m(2), high BMI donors (> or =35 kg/m(2)) had slightly longer operative times (mean increase 19 min), more overall perioperative complications (mostly minor wound complications), yet the same low rate of major surgical complications (conversion to open and re-operation) and similar length-of-stay (2.3 vs. 2.4 days). At 6-12 months after donation (mean 11 months), renal function and microalbuminuria did not differ with BMI. These results suggest that laparoscopic donor nephrectomy is generally safe in selected obese donors and does not result in a high rate of major perioperative complications. Obese donors have higher baseline cardiovascular risk and warrant risk reduction for long-term health. While early results are encouraging, we advocate careful study of obese donors and do not support their widespread use until longer follow-up is available.
- Published
- 2005
- Full Text
- View/download PDF
38. Kidney allograft fibrosis and atrophy early after living donor transplantation.
- Author
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Cosio FG, Grande JP, Larson TS, Gloor JM, Velosa JA, Textor SC, Griffin MD, and Stegall MD
- Subjects
- Adult, Aged, Atrophy, Biopsy, Body Mass Index, Cadaver, Female, Fibrosis, Glomerular Filtration Rate, Graft Rejection, Graft Survival, Humans, Kidney Diseases pathology, Living Donors, Male, Middle Aged, Risk, Risk Factors, Time Factors, Treatment Outcome, Kidney pathology, Kidney Transplantation methods
- Abstract
Kidney allograft failure is most often caused by chronic allograft nephropathy, a process of interstitial fibrosis (GIF) and tubular atrophy (TA). We assessed the pathology of living donor (LD) grafts compared to deceased donor (DD). Included are 321 recipients (245 LD; 76 DD) with protocol biopsies the first 2 years of transplant. In LD, GIF was present in 7%, 31%, 61% and 71% of grafts at 0, 4, 12 and 24 months. TA progressed in parallel to GIF. Compared to LD, more DD grafts had GIF at time 0 (29%, p = 0.002); thereafter the incidence of GIF was similar. In LD, GIF was associated with lower glomerular filtration rate (GFR)(1 year) (no GIF, 62 +/- 16; GIF, 49 +/- 15 mL/min/m(2) iothalamate clearance, p = 0.001) and reduced graft survival (HR = 2.2, p = 0.009). GIF in LD related to acute rejection (HR = 2.6, p = 0.01), polyoma nephropathy (OR = 4.4, p = 0.02) and lower levels of GFR 3 weeks post-transplant (HR = 0.961; p = 0.03, multivariate). However, GIF also developed in 53% of recipients lacking these covariates. Thus, GIF/TA develops in the majority of LD grafts, it is often mild but is associated with reduced function and survival. GIF frequently develops in the absence of risk factors. Lower GFR post-transplant identify patients at highest risk of GIF.
- Published
- 2005
- Full Text
- View/download PDF
39. Surgical management of renal fibromuscular dysplasia: challenges in the endovascular era.
- Author
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Carmo M, Bower TC, Mozes G, Nachreiner RD, Textor SC, Hoskin TL, Kalra M, Noel AA, Panneton JM, Sullivan TM, and Gloviczki P
- Subjects
- Female, Follow-Up Studies, Graft Occlusion, Vascular, Humans, Hypertension, Renovascular etiology, Male, Middle Aged, Renal Veins surgery, Retrospective Studies, Saphenous Vein transplantation, Time Factors, Vascular Patency, Fibromuscular Dysplasia surgery, Hypertension, Renovascular surgery, Renal Artery surgery
- Abstract
Percutaneous transluminal renal angioplasty (PTRA) is the primary treatment for renal fibromuscular dysplasia (RFMD). Surgical revascularization is limited to patients who fail or are unsuitable for PTRA. All patients who were operated on with RFMD since the indications for renal PTRA were expanded in our institution were retrospectively reviewed. Outcome included patency, hypertension, and renal function. Twenty-six patients had reconstruction of 32 renal arteries between 1998 and 2004. The mean age was 47.1 +/- 14 years; the majority (81%) were female. Six patients had bilateral disease and three had a solitary kidney. Operations were done for hypertension in 25 patients, renal artery aneurysm in 8, and chronic dissection in 1, alone or in combination. Six patients had a failed PTRA and 20 were unsuitable for it. Aortorenal bypass was done most often (n = 28) and saphenous vein was the preferred conduit (n = 25). The distal anastomosis was to the main renal artery in 13 patients and to the branch arteries in 19. Ex vivo repair was needed in five patients. Five intraoperative revisions were done because of abnormalities on duplex scan. One patient died unexpectedly 42 days after operation from myocardial infarction. Extrarenal complications occurred in five patients. Median follow-up was 2.4 (range, 42 days to 6.3) years and was available in all but one patient (96%). Two bypasses occluded at 3 and 376 days, which resulted in loss of the kidneys. One graft stenosis was treated successfully with PTRA at 239 days. All failures occurred in men. One-year cumulative primary patency was 89 +/- 8% and was not adversely affected by prior PTRA or complex repair. Hypertension at 1 year was cured in 27% of the patients and improved in 60%. No patient developed acute or chronic renal failure. Surgical reconstruction for RFMD has excellent short-term patency. Failed PTRA or complex reconstructions did not adversely affect outcome.
- Published
- 2005
- Full Text
- View/download PDF
40. Patient and graft outcomes from older living kidney donors are similar to those from younger donors despite lower GFR.
- Author
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De La Vega LS, Torres A, Bohorquez HE, Heimbach JK, Gloor JM, Schwab TR, Taler SJ, Nyberg SL, Ishitani MB, Prieto M, Velosa JA, Larson TS, Stegall MD, Cosio FG, Textor SC, and Griffin MD
- Subjects
- Adolescent, Adult, Age Distribution, Aged, Aged, 80 and over, Female, Humans, Kidney Failure, Chronic surgery, Male, Middle Aged, Postoperative Complications mortality, Risk Factors, Graft Rejection mortality, Graft Survival, Kidney Failure, Chronic mortality, Kidney Transplantation mortality, Living Donors statistics & numerical data
- Abstract
Background: Donor age adversely affects deceased-donor kidney transplant outcomes, but its influence on living-donor transplantation is less well characterized., Methods: Living-donor kidney transplants at a single center between 1998 and 2000 were reviewed. Data were abstracted for 52 transplants from donors aged > or =50 years and for a matched group of 104 transplants from donors aged <50 years. Survival indices were compared during the first three years' post-transplantation. Functional indices, including serial iothalamate clearances, were compared at 1, 12, and 24 months., Results: Predonation glomerular filtration rate (GFR) was lower among older donors (94 +/- 12 vs. 108 +/- 17 mL/min/SA) but post-transplant compensatory hypertrophy was similar (11.7 +/- 26.3% vs. 7.7 +/- 31.4%). Recipients of older-donor grafts were older (52.8 +/- 16.5 vs. 46.1 +/- 15.1 years) and more frequently unrelated to the donor (54% vs. 39%). Trends toward higher frequency of slow graft function, cytomegalovirus (CMV) infection, and polyomavirus nephropathy were observed for older-donor grafts. Three-year recipient, graft, and death-censored graft survivals were > or =90% for both groups. At 1, 12, and 24 months, serum creatinine was higher and GFR was lower among recipients of older- compared with younger-donor grafts. Other functional indices (urine total protein, serum potassium and uric acid, hemoglobin, and number of antihypertensives) were not different. Donor age correlated with graft GFR at 1, 12, and 24 months for the entire study cohort by linear regression., Conclusion: Older donor age does not preclude excellent results from living-donor kidney transplantation but should be appreciated as being associated with relatively lower GFR.
- Published
- 2004
- Full Text
- View/download PDF
41. Histologic findings of antibody-mediated rejection in ABO blood-group-incompatible living-donor kidney transplantation.
- Author
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Fidler ME, Gloor JM, Lager DJ, Larson TS, Griffin MD, Textor SC, Schwab TR, Prieto M, Nyberg SL, Ishitani MB, Grande JP, Kay PA, and Stegall MD
- Subjects
- Adult, Aged, Biopsy, Blood Group Incompatibility, Glomerular Mesangium pathology, Graft Rejection, Graft Survival, Humans, Immunosuppressive Agents pharmacology, Kidney immunology, Living Donors, Middle Aged, Necrosis, Neutrophils immunology, Spleen pathology, Time Factors, Treatment Outcome, ABO Blood-Group System, Kidney Transplantation methods
- Abstract
The purpose of this study was to characterize the histology of antibody-mediated rejection (AMR) in ABO blood-group-incompatible (ABOI) kidney transplants as well as on protocol biopsies performed at the time of stable allograft function. Between 5/99 and 1/02, we performed 32 ABOI kidney transplants (13 A2, 19 non-A2 blood-group living donors). Nineteen biopsies were performed for allograft dysfunction, and 127 protocol biopsies were performed 0, 3, 7, 14, 28 days and 3 and 12 months post transplant. Twenty-five of 32 patients have functioning allografts (mean 585 days post transplant). Nine of 32 (28%) developed clinical AMR. Biopsy revealed glomerular thrombi (78%), mesangiolysis (78%), peritubular capillary C4d staining (56%) and neutrophil infiltration (67%), interstitial hemorrhage and necrosis (56%) and arteriolar thrombi (33%). Subclinical AMR was diagnosed by protocol biopsies in four patients. Findings consisted of glomerular thrombi (100%), mesangiolysis (25%), and C4d staining (100%). In late protocol biopsies performed 214-420 days post transplant, mild mesangiolysis was seen in 2/17 (11.7%), and C4d immunostaining was detected in 3/12 (25%). AMR is characterized by glomerular thrombi, mesangiolysis, peritubular capillary neutrophil infiltration interstitial hemorrhage, necrosis, and C4d deposition. Glomerular thrombi appear early in AMR and may appear prior to graft dysfunction.
- Published
- 2004
- Full Text
- View/download PDF
42. Overcoming a positive crossmatch in living-donor kidney transplantation.
- Author
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Gloor JM, DeGoey SR, Pineda AA, Moore SB, Prieto M, Nyberg SL, Larson TS, Griffin MD, Textor SC, Velosa JA, Schwab TR, Fix LA, and Stegall MD
- Subjects
- Adult, Antibodies administration & dosage, Antibody Specificity, Antigens, CD20 immunology, Female, Graft Survival, Humans, Immunoglobulins, Intravenous administration & dosage, Kidney Function Tests, Male, Middle Aged, Splenectomy, Kidney Transplantation, Living Donors
- Abstract
Many patients who have an otherwise acceptable living-kidney donor do not undergo transplantation because of the presence of antibodies against the donor cells resulting in a positive crossmatch. In the current study, 14 patients with a positive cytotoxic crossmatch (titer = 1 : 16) against their living donor underwent a regimen including pretransplant plasmapheresis, intravenous immunoglobulin, rituximab and splenectomy. Eleven of 14 grafts (79%) are functioning well 30-600 days after transplantation. Two grafts were lost to accelerated vasculopathy and one was lost to death with good function. No hyperacute or cellular rejections occurred. Antibody-mediated rejection occurred in six patients [two clinical (14%) and four subclinical (29%)] and was reversible with plasmapheresis and steroids. Our results suggest that selected crossmatch-positive patients can be transplanted successfully with living-donor kidney allografts, using a protocol of pretransplant plasmapheresis, intravenous immunoglobulin, rituximab and splenectomy. Longer follow-up will be needed, but the absence of anti-donor antibody and good early outcomes are encouraging.
- Published
- 2003
- Full Text
- View/download PDF
43. Renovascular hypertension: problems in evaluation and management.
- Author
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Kloner RA, Textor SC, and Tavel ME
- Subjects
- Humans, Male, Middle Aged, Radiography, Renal Artery diagnostic imaging, Renal Artery Obstruction therapy, Stents, Hypertension, Renovascular diagnosis, Hypertension, Renovascular diagnostic imaging, Hypertension, Renovascular drug therapy, Hypertension, Renovascular therapy
- Published
- 2002
- Full Text
- View/download PDF
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