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1. Effects of empagliflozin on progression of chronic kidney disease: a prespecified secondary analysis from the empa-kidney trial

Author: Staplin, N, Haynes, R, Judge, PK, Wanner, C, Green, JB, Emberson, J, Preiss, D, Mayne, KJ, Ng, SYA, Sammons, E, Zhu, D, Hill, M, Stevens, W, Wallendszus, K, Brenner, S, Cheung, AK, Liu, ZH, Li, J, Hooi, LS, Liu, WJ, Kadowaki, T, Nangaku, M, Levin, A, Cherney, D, Maggioni, AP, Pontremoli, R, Deo, R, Goto, S, Rossello, X, Tuttle, KR, Steubl, D, Petrini, M, Seidi, S, Landray, MJ, Baigent, C, Herrington, WG, Abat, S, Abd Rahman, R, Abdul Cader, R, Abdul Hafidz, MI, Abdul Wahab, MZ, Abdullah, NK, Abdul-Samad, T, Abe, M, Abraham, N, Acheampong, S, Achiri, P, Acosta, JA, Adeleke, A, Adell, V, Adewuyi-Dalton, R, Adnan, N, Africano, A, Agharazii, M, Aguilar, F, Aguilera, A, Ahmad, M, Ahmad, MK, Ahmad, NA, Ahmad, NH, Ahmad, NI, Ahmad Miswan, N, Ahmad Rosdi, H, Ahmed, I, Ahmed, S, Aiello, J, Aitken, A, AitSadi, R, Aker, S, Akimoto, S, Akinfolarin, A, Akram, S, Alberici, F, Albert, C, Aldrich, L, Alegata, M, Alexander, L, Alfaress, S, Alhadj Ali, M, Ali, A, Alicic, R, Aliu, A, Almaraz, R, Almasarwah, R, Almeida, J, Aloisi, A, Al-Rabadi, L, Alscher, D, Alvarez, P, Al-Zeer, B, Amat, M, Ambrose, C, Ammar, H, An, Y, Andriaccio, L, Ansu, K, Apostolidi, A, Arai, N, Araki, H, Araki, S, Arbi, A, Arechiga, O, Armstrong, S, Arnold, T, Aronoff, S, Arriaga, W, Arroyo, J, Arteaga, D, Asahara, S, Asai, A, Asai, N, Asano, S, Asawa, M, Asmee, MF, Aucella, F, Augustin, M, Avery, A, Awad, A, Awang, IY, Awazawa, M, Axler, A, Ayub, W, Azhari, Z, Baccaro, R, Badin, C, Bagwell, B, Bahlmann-Kroll, E, Bahtar, AZ, Bains, D, Bajaj, H, Baker, R, Baldini, E, Banas, B, Banerjee, D, Banno, S, Bansal, S, Barberi, S, Barnes, S, Barnini, C, Barot, C, Barrett, K, Barrios, R, Bartolomei Mecatti, B, Barton, I, Barton, J, Basily, W, Bavanandan, S, Baxter, A, Becker, L, Beddhu, S, Beige, J, Beigh, S, Bell, S, Benck, U, Beneat, A, Bennett, A, Bennett, D, Benyon, S, Berdeprado, J, Bergler, T, Bergner, A, Berry, M, Bevilacqua, M, Bhairoo, J, Bhandari, S, Bhandary, N, Bhatt, A, Bhattarai, M, Bhavsar, M, Bian, W, Bianchini, F, Bianco, S, Bilous, R, Bilton, J, Bilucaglia, D, Bird, C, Birudaraju, D, Biscoveanu, M, Blake, C, Bleakley, N, Bocchicchia, K, Bodine, S, Bodington, R, Boedecker, S, Bolduc, M, Bolton, S, Bond, C, Boreky, F, Boren, K, Bouchi, R, Bough, L, Bovan, D, Bowler, C, Bowman, L, Brar, N, Braun, C, Breach, A, Breitenfeldt, M, Brettschneider, B, Brewer, A, Brewer, G, Brindle, V, Brioni, E, Brown, C, Brown, H, Brown, L, Brown, R, Brown, S, Browne, D, Bruce, K, Brueckmann, M, Brunskill, N, Bryant, M, Brzoska, M, Bu, Y, Buckman, C, Budoff, M, Bullen, M, Burke, A, Burnette, S, Burston, C, Busch, M, Bushnell, J, Butler, S, Büttner, C, Byrne, C, Caamano, A, Cadorna, J, Cafiero, C, Cagle, M, Cai, J, Calabrese, K, Calvi, C, Camilleri, B, Camp, S, Campbell, D, Campbell, R, Cao, H, Capelli, I, Caple, M, Caplin, B, Cardone, A, Carle, J, Carnall, V, Caroppo, M, Carr, S, Carraro, G, Carson, M, Casares, P, Castillo, C, Castro, C, Caudill, B, Cejka, V, Ceseri, M, Cham, L, Chamberlain, A, Chambers, J, Chan, CBT, Chan, JYM, Chan, YC, Chang, E, Chant, T, Chavagnon, T, Chellamuthu, P, Chen, F, Chen, J, Chen, P, Chen, TM, Chen, Y, Cheng, C, Cheng, H, Cheng, MC, Ching, CH, Chitalia, N, Choksi, R, Chukwu, C, Chung, K, Cianciolo, G, Cipressa, L, Clark, S, Clarke, H, Clarke, R, Clarke, S, Cleveland, B, Cole, E, Coles, H, Condurache, L, Connor, A, Convery, K, Cooper, A, Cooper, N, Cooper, Z, Cooperman, L, Cosgrove, L, Coutts, P, Cowley, A, Craik, R, Cui, G, Cummins, T, Dahl, N, Dai, H, Dajani, L, D'Amelio, A, Damian, E, Damianik, K, Danel, L, Daniels, C, Daniels, T, Darbeau, S, Darius, H, Dasgupta, T, Davies, J, Davies, L, Davis, A, Davis, J, Davis, L, Dayanandan, R, Dayi, S, Dayrell, R, De Nicola, L, Debnath, S, Deeb, W, Degenhardt, S, DeGoursey, K, Delaney, M, DeRaad, R, Derebail, V, Dev, D, Devaux, M, Dhall, P, Dhillon, G, Dienes, J, Dobre, M, Doctolero, E, Dodds, V, Domingo, D, Donaldson, D, Donaldson, P, Donhauser, C, Donley, V, Dorestin, S, Dorey, S, Doulton, T, Draganova, D, Draxlbauer, K, Driver, F, Du, H, Dube, F, Duck, T, Dugal, T, Dugas, J, Dukka, H, Dumann, H, Durham, W, Dursch, M, Dykas, R, Easow, R, Eckrich, E, Eden, G, Edmerson, E, Edwards, H, Ee, LW, Eguchi, J, Ehrl, Y, Eichstadt, K, Eid, W, Eilerman, B, Ejima, Y, Eldon, H, Ellam, T, Elliott, L, Ellison, R, Epp, R, Er, A, Espino-Obrero, M, Estcourt, S, Estienne, L, Evans, G, Evans, J, Evans, S, Fabbri, G, Fajardo-Moser, M, Falcone, C, Fani, F, Faria-Shayler, P, Farnia, F, Farrugia, D, Fechter, M, Fellowes, D, Feng, F, Fernandez, J, Ferraro, P, Field, A, Fikry, S, Finch, J, Finn, H, Fioretto, P, Fish, R, Fleischer, A, Fleming-Brown, D, Fletcher, L, Flora, R, Foellinger, C, Foligno, N, Forest, S, Forghani, Z, Forsyth, K, Fottrell-Gould, D, Fox, P, Frankel, A, Fraser, D, Frazier, R, Frederick, K, Freking, N, French, H, Froment, A, Fuchs, B, Fuessl, L, Fujii, H, Fujimoto, A, Fujita, A, Fujita, K, Fujita, Y, Fukagawa, M, Fukao, Y, Fukasawa, A, Fuller, T, Funayama, T, Fung, E, Furukawa, M, Furukawa, Y, Furusho, M, Gabel, S, Gaidu, J, Gaiser, S, Gallo, K, Galloway, C, Gambaro, G, Gan, CC, Gangemi, C, Gao, M, Garcia, K, Garcia, M, Garofalo, C, Garrity, M, Garza, A, Gasko, S, Gavrila, M, Gebeyehu, B, Geddes, A, Gentile, G, George, A, George, J, Gesualdo, L, Ghalli, F, Ghanem, A, Ghate, T, Ghavampour, S, Ghazi, A, Gherman, A, Giebeln-Hudnell, U, Gill, B, Gillham, S, Girakossyan, I, Girndt, M, Giuffrida, A, Glenwright, M, Glider, T, Gloria, R, Glowski, D, Goh, BL, Goh, CB, Gohda, T, Goldenberg, R, Goldfaden, R, Goldsmith, C, Golson, B, Gonce, V, Gong, Q, Goodenough, B, Goodwin, N, Goonasekera, M, Gordon, A, Gordon, J, Gore, A, Goto, H, Gowen, D, Grace, A, Graham, J, Grandaliano, G, Gray, M, Greene, T, Greenwood, G, Grewal, B, Grifa, R, Griffin, D, Griffin, S, Grimmer, P, Grobovaite, E, Grotjahn, S, Guerini, A, Guest, C, Gunda, S, Guo, B, Guo, Q, Haack, S, Haase, M, Haaser, K, Habuki, K, Hadley, A, Hagan, S, Hagge, S, Haller, H, Ham, S, Hamal, S, Hamamoto, Y, Hamano, N, Hamm, M, Hanburry, A, Haneda, M, Hanf, C, Hanif, W, Hansen, J, Hanson, L, Hantel, S, Haraguchi, T, Harding, E, Harding, T, Hardy, C, Hartner, C, Harun, Z, Harvill, L, Hasan, A, Hase, H, Hasegawa, F, Hasegawa, T, Hashimoto, A, Hashimoto, C, Hashimoto, M, Hashimoto, S, Haskett, S, Hauske, SJ, Hawfield, A, Hayami, T, Hayashi, M, Hayashi, S, Hazara, A, Healy, C, Hecktman, J, Heine, G, Henderson, H, Henschel, R, Hepditch, A, Herfurth, K, Hernandez, G, Hernandez Pena, A, Hernandez-Cassis, C, Herzog, C, Hewins, S, Hewitt, D, Hichkad, L, Higashi, S, Higuchi, C, Hill, C, Hill, L, Himeno, T, Hing, A, Hirakawa, Y, Hirata, K, Hirota, Y, Hisatake, T, Hitchcock, S, Hodakowski, A, Hodge, W, Hogan, R, Hohenstatt, U, Hohenstein, B, Hooi, L, Hope, S, Hopley, M, Horikawa, S, Hosein, D, Hosooka, T, Hou, L, Hou, W, Howie, L, Howson, A, Hozak, M, Htet, Z, Hu, X, Hu, Y, Huang, J, Huda, N, Hudig, L, Hudson, A, Hugo, C, Hull, R, Hume, L, Hundei, W, Hunt, N, Hunter, A, Hurley, S, Hurst, A, Hutchinson, C, Hyo, T, Ibrahim, FH, Ibrahim, S, Ihana, N, Ikeda, T, Imai, A, Imamine, R, Inamori, A, Inazawa, H, Ingell, J, Inomata, K, Inukai, Y, Ioka, M, Irtiza-Ali, A, Isakova, T, Isari, W, Iselt, M, Ishiguro, A, Ishihara, K, Ishikawa, T, Ishimoto, T, Ishizuka, K, Ismail, R, Itano, S, Ito, H, Ito, K, Ito, M, Ito, Y, Iwagaitsu, S, Iwaita, Y, Iwakura, T, Iwamoto, M, Iwasa, M, Iwasaki, H, Iwasaki, S, Izumi, K, Izumi, T, Jaafar, SM, Jackson, C, Jackson, Y, Jafari, G, Jahangiriesmaili, M, Jain, N, Jansson, K, Jasim, H, Jeffers, L, Jenkins, A, Jesky, M, Jesus-Silva, J, Jeyarajah, D, Jiang, Y, Jiao, X, Jimenez, G, Jin, B, Jin, Q, Jochims, J, Johns, B, Johnson, C, Johnson, T, Jolly, S, Jones, L, Jones, S, Jones, T, Jones, V, Joseph, M, Joshi, S, Judge, P, Junejo, N, Junus, S, Kachele, M, Kadoya, H, Kaga, H, Kai, H, Kajio, H, Kaluza-Schilling, W, Kamaruzaman, L, Kamarzarian, A, Kamimura, Y, Kamiya, H, Kamundi, C, Kan, T, Kanaguchi, Y, Kanazawa, A, Kanda, E, Kanegae, S, Kaneko, K, Kang, HY, Kano, T, Karim, M, Karounos, D, Karsan, W, Kasagi, R, Kashihara, N, Katagiri, H, Katanosaka, A, Katayama, A, Katayama, M, Katiman, E, Kato, K, Kato, M, Kato, N, Kato, S, Kato, T, Kato, Y, Katsuda, Y, Katsuno, T, Kaufeld, J, Kavak, Y, Kawai, I, Kawai, M, Kawase, A, Kawashima, S, Kazory, A, Kearney, J, Keith, B, Kellett, J, Kelley, S, Kershaw, M, Ketteler, M, Khai, Q, Khairullah, Q, Khandwala, H, Khoo, KKL, Khwaja, A, Kidokoro, K, Kielstein, J, Kihara, M, Kimber, C, Kimura, S, Kinashi, H, Kingston, H, Kinomura, M, Kinsella-Perks, E, Kitagawa, M, Kitajima, M, Kitamura, S, Kiyosue, A, Kiyota, M, Klauser, F, Klausmann, G, Kmietschak, W, Knapp, K, Knight, C, Knoppe, A, Knott, C, Kobayashi, M, Kobayashi, R, Kobayashi, T, Koch, M, Kodama, S, Kodani, N, Kogure, E, Koizumi, M, Kojima, H, Kojo, T, Kolhe, N, Komaba, H, Komiya, T, Komori, H, Kon, SP, Kondo, M, Kong, W, Konishi, M, Kono, K, Koshino, M, Kosugi, T, Kothapalli, B, Kozlowski, T, Kraemer, B, Kraemer-Guth, A, Krappe, J, Kraus, D, Kriatselis, C, Krieger, C, Krish, P, Kruger, B, Ku Md Razi, KR, Kuan, Y, Kubota, S, Kuhn, S, Kumar, P, Kume, S, Kummer, I, Kumuji, R, Küpper, A, Kuramae, T, Kurian, L, Kuribayashi, C, Kurien, R, Kuroda, E, Kurose, T, Kutschat, A, Kuwabara, N, Kuwata, H, La Manna, G, Lacey, M, Lafferty, K, LaFleur, P, Lai, V, Laity, E, Lambert, A, Langlois, M, Latif, F, Latore, E, Laundy, E, Laurienti, D, Lawson, A, Lay, M, Leal, I, Lee, AK, Lee, J, Lee, KQ, Lee, R, Lee, SA, Lee, YY, Lee-Barkey, Y, Leonard, N, Leoncini, G, Leong, CM, Lerario, S, Leslie, A, Lewington, A, Li, N, Li, X, Li, Y, Liberti, L, Liberti, ME, Liew, A, Liew, YF, Lilavivat, U, Lim, SK, Lim, YS, Limon, E, Lin, H, Lioudaki, E, Liu, H, Liu, J, Liu, L, Liu, Q, Liu, X, Liu, Z, Loader, D, Lochhead, H, Loh, CL, Lorimer, A, Loudermilk, L, Loutan, J, Low, CK, Low, CL, Low, YM, Lozon, Z, Lu, Y, Lucci, D, Ludwig, U, Luker, N, Lund, D, Lustig, R, Lyle, S, Macdonald, C, MacDougall, I, Machicado, R, MacLean, D, Macleod, P, Madera, A, Madore, F, Maeda, K, Maegawa, H, Maeno, S, Mafham, M, Magee, J, Mah, DY, Mahabadi, V, Maiguma, M, Makita, Y, Makos, G, Manco, L, Mangiacapra, R, Manley, J, Mann, P, Mano, S, Marcotte, G, Maris, J, Mark, P, Markau, S, Markovic, M, Marshall, C, Martin, M, Martinez, C, Martinez, S, Martins, G, Maruyama, K, Maruyama, S, Marx, K, Maselli, A, Masengu, A, Maskill, A, Masumoto, S, Masutani, K, Matsumoto, M, Matsunaga, T, Matsuoka, N, Matsushita, M, Matthews, M, Matthias, S, Matvienko, E, Maurer, M, Maxwell, P, Mazlan, N, Mazlan, SA, Mbuyisa, A, McCafferty, K, McCarroll, F, McCarthy, T, McClary-Wright, C, McCray, K, McDermott, P, McDonald, C, McDougall, R, McHaffie, E, McIntosh, K, McKinley, T, McLaughlin, S, McLean, N, McNeil, L, Measor, A, Meek, J, Mehta, A, Mehta, R, Melandri, M, Mené, P, Meng, T, Menne, J, Merritt, K, Merscher, S, Meshykhi, C, Messa, P, Messinger, L, Miftari, N, Miller, R, Miller, Y, Miller-Hodges, E, Minatoguchi, M, Miners, M, Minutolo, R, Mita, T, Miura, Y, Miyaji, M, Miyamoto, S, Miyatsuka, T, Miyazaki, M, Miyazawa, I, Mizumachi, R, Mizuno, M, Moffat, S, Mohamad Nor, FS, Mohamad Zaini, SN, Mohamed Affandi, FA, Mohandas, C, Mohd, R, Mohd Fauzi, NA, Mohd Sharif, NH, Mohd Yusoff, Y, Moist, L, Moncada, A, Montasser, M, Moon, A, Moran, C, Morgan, N, Moriarty, J, Morig, G, Morinaga, H, Morino, K, Morisaki, T, Morishita, Y, Morlok, S, Morris, A, Morris, F, Mostafa, S, Mostefai, Y, Motegi, M, Motherwell, N, Motta, D, Mottl, A, Moys, R, Mozaffari, S, Muir, J, Mulhern, J, Mulligan, S, Munakata, Y, Murakami, C, Murakoshi, M, Murawska, A, Murphy, K, Murphy, L, Murray, S, Murtagh, H, Musa, MA, Mushahar, L, Mustafa, R, Mustafar, R, Muto, M, Nadar, E, Nagano, R, Nagasawa, T, Nagashima, E, Nagasu, H, Nagelberg, S, Nair, H, Nakagawa, Y, Nakahara, M, Nakamura, J, Nakamura, R, Nakamura, T, Nakaoka, M, Nakashima, E, Nakata, J, Nakata, M, Nakatani, S, Nakatsuka, A, Nakayama, Y, Nakhoul, G, Naverrete, G, Navivala, A, Nazeer, I, Negrea, L, Nethaji, C, Newman, E, Ng, TJ, Ngu, LLS, Nimbkar, T, Nishi, H, Nishi, M, Nishi, S, Nishida, Y, Nishiyama, A, Niu, J, Niu, P, Nobili, G, Nohara, N, Nojima, I, Nolan, J, Nosseir, H, Nozawa, M, Nunn, M, Nunokawa, S, Oda, M, Oe, M, Oe, Y, Ogane, K, Ogawa, W, Ogihara, T, Oguchi, G, Ohsugi, M, Oishi, K, Okada, Y, Okajyo, J, Okamoto, S, Okamura, K, Olufuwa, O, Oluyombo, R, Omata, A, Omori, Y, Ong, LM, Ong, YC, Onyema, J, Oomatia, A, Oommen, A, Oremus, R, Orimo, Y, Ortalda, V, Osaki, Y, Osawa, Y, Osmond Foster, J, O'Sullivan, A, Otani, T, Othman, N, Otomo, S, O'Toole, J, Owen, L, Ozawa, T, Padiyar, A, Page, N, Pajak, S, Paliege, A, Pandey, A, Pandey, R, Pariani, H, Park, J, Parrigon, M, Passauer, J, Patecki, M, Patel, M, Patel, R, Patel, T, Patel, Z, Paul, R, Paulsen, L, Pavone, L, Peixoto, A, Peji, J, Peng, BC, Peng, K, Pennino, L, Pereira, E, Perez, E, Pergola, P, Pesce, F, Pessolano, G, Petchey, W, Petr, EJ, Pfab, T, Phelan, P, Phillips, R, Phillips, T, Phipps, M, Piccinni, G, Pickett, T, Pickworth, S, Piemontese, M, Pinto, D, Piper, J, Plummer-Morgan, J, Poehler, D, Polese, L, Poma, V, Postal, A, Pötz, C, Power, A, Pradhan, N, Pradhan, R, Preiss, E, Preston, K, Prib, N, Price, L, Provenzano, C, Pugay, C, Pulido, R, Putz, F, Qiao, Y, Quartagno, R, Quashie-Akponeware, M, Rabara, R, Rabasa-Lhoret, R, Radhakrishnan, D, Radley, M, Raff, R, Raguwaran, S, Rahbari-Oskoui, F, Rahman, M, Rahmat, K, Ramadoss, S, Ramanaidu, S, Ramasamy, S, Ramli, R, Ramli, S, Ramsey, T, Rankin, A, Rashidi, A, Raymond, L, Razali, WAFA, Read, K, Reiner, H, Reisler, A, Reith, C, Renner, J, Rettenmaier, B, Richmond, L, Rijos, D, Rivera, R, Rivers, V, Robinson, H, Rocco, M, Rodriguez-Bachiller, I, Rodriquez, R, Roesch, C, Roesch, J, Rogers, J, Rohnstock, M, Rolfsmeier, S, Roman, M, Romo, A, Rosati, A, Rosenberg, S, Ross, T, Roura, M, Roussel, M, Rovner, S, Roy, S, Rucker, S, Rump, L, Ruocco, M, Ruse, S, Russo, F, Russo, M, Ryder, M, Sabarai, A, Saccà, C, Sachson, R, Sadler, E, Safiee, NS, Sahani, M, Saillant, A, Saini, J, Saito, C, Saito, S, Sakaguchi, K, Sakai, M, Salim, H, Salviani, C, Sampson, A, Samson, F, Sandercock, P, Sanguila, S, Santorelli, G, Santoro, D, Sarabu, N, Saram, T, Sardell, R, Sasajima, H, Sasaki, T, Satko, S, Sato, A, Sato, D, Sato, H, Sato, J, Sato, T, Sato, Y, Satoh, M, Sawada, K, Schanz, M, Scheidemantel, F, Schemmelmann, M, Schettler, E, Schettler, V, Schlieper, GR, Schmidt, C, Schmidt, G, Schmidt, U, Schmidt-Gurtler, H, Schmude, M, Schneider, A, Schneider, I, Schneider-Danwitz, C, Schomig, M, Schramm, T, Schreiber, A, Schricker, S, Schroppel, B, Schulte-Kemna, L, Schulz, E, Schumacher, B, Schuster, A, Schwab, A, Scolari, F, Scott, A, Seeger, W, Segal, M, Seifert, L, Seifert, M, Sekiya, M, Sellars, R, Seman, MR, Shah, S, Shainberg, L, Shanmuganathan, M, Shao, F, Sharma, K, Sharpe, C, Sheikh-Ali, M, Sheldon, J, Shenton, C, Shepherd, A, Shepperd, M, Sheridan, R, Sheriff, Z, Shibata, Y, Shigehara, T, Shikata, K, Shimamura, K, Shimano, H, Shimizu, Y, Shimoda, H, Shin, K, Shivashankar, G, Shojima, N, Silva, R, Sim, CSB, Simmons, K, Sinha, S, Sitter, T, Sivanandam, S, Skipper, M, Sloan, K, Sloan, L, Smith, R, Smyth, J, Sobande, T, Sobata, M, Somalanka, S, Song, X, Sonntag, F, Sood, B, Sor, SY, Soufer, J, Sparks, H, Spatoliatore, G, Spinola, T, Squyres, S, Srivastava, A, Stanfield, J, Staylor, K, Steele, A, Steen, O, Steffl, D, Stegbauer, J, Stellbrink, C, Stellbrink, E, Stevenson, A, Stewart-Ray, V, Stickley, J, Stoffler, D, Stratmann, B, Streitenberger, S, Strutz, F, Stubbs, J, Stumpf, J, Suazo, N, Suchinda, P, Suckling, R, Sudin, A, Sugamori, K, Sugawara, H, Sugawara, K, Sugimoto, D, Sugiyama, H, Sugiyama, T, Sullivan, M, Sumi, M, Suresh, N, Sutton, D, Suzuki, H, Suzuki, R, Suzuki, Y, Swanson, E, Swift, P, Syed, S, Szerlip, H, Taal, M, Taddeo, M, Tailor, C, Tajima, K, Takagi, M, Takahashi, K, Takahashi, M, Takahashi, T, Takahira, E, Takai, T, Takaoka, M, Takeoka, J, Takesada, A, Takezawa, M, Talbot, M, Taliercio, J, Talsania, T, Tamori, Y, Tamura, R, Tamura, Y, Tan, CHH, Tan, EZZ, Tanabe, A, Tanabe, K, Tanaka, A, Tanaka, N, Tang, S, Tang, Z, Tanigaki, K, Tarlac, M, Tatsuzawa, A, Tay, JF, Tay, LL, Taylor, J, Taylor, K, Te, A, Tenbusch, L, Teng, KS, Terakawa, A, Terry, J, Tham, ZD, Tholl, S, Thomas, G, Thong, KM, Tietjen, D, Timadjer, A, Tindall, H, Tipper, S, Tobin, K, Toda, N, Tokuyama, A, Tolibas, M, Tomita, A, Tomita, T, Tomlinson, J, Tonks, L, Topf, J, Topping, S, Torp, A, Torres, A, Totaro, F, Toth, P, Toyonaga, Y, Tripodi, F, Trivedi, K, Tropman, E, Tschope, D, Tse, J, Tsuji, K, Tsunekawa, S, Tsunoda, R, Tucky, B, Tufail, S, Tuffaha, A, Turan, E, Turner, H, Turner, J, Turner, M, Tye, YL, Tyler, A, Tyler, J, Uchi, H, Uchida, H, Uchida, T, Udagawa, T, Ueda, S, Ueda, Y, Ueki, K, Ugni, S, Ugwu, E, Umeno, R, Unekawa, C, Uozumi, K, Urquia, K, Valleteau, A, Valletta, C, van Erp, R, Vanhoy, C, Varad, V, Varma, R, Varughese, A, Vasquez, P, Vasseur, A, Veelken, R, Velagapudi, C, Verdel, K, Vettoretti, S, Vezzoli, G, Vielhauer, V, Viera, R, Vilar, E, Villaruel, S, Vinall, L, Vinathan, 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Published: 2024
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2. Impact of primary kidney disease on the effects of empagliflozin in patients with chronic kidney disease: secondary analyses of the EMPA-KIDNEY trial

Author: Judge, PK, Staplin, N, Mayne, KJ, Wanner, C, Green, JB, Hauske, SJ, Emberson, JR, Preiss, D, Ng, SYA, Roddick, AJ, Sammons, E, Zhu, D, Hill, M, Stevens, W, Wallendszus, K, Brenner, S, Cheung, AK, Liu, ZH, Li, J, Hooi, LS, Liu, WJ, Kadowaki, T, Nangaku, M, Levin, A, Cherney, D, Maggioni, AP, Pontremoli, R, Deo, R, Goto, S, Rossello, X, Tuttle, KR, Steubl, D, Massey, D, Landray, MJ, Baigent, C, Haynes, R, Herrington, WG, Abat, S, Abd Rahman, R, Abdul Cader, R, Abdul Hafidz, MI, Abdul Wahab, MZ, Abdullah, NK, Abdul-Samad, T, Abe, M, Abraham, N, Acheampong, S, Achiri, P, Acosta, JA, Adeleke, A, Adell, V, Adewuyi-Dalton, R, Adnan, N, Africano, A, Agharazii, M, Aguilar, F, Aguilera, A, Ahmad, M, Ahmad, MK, Ahmad, NA, Ahmad, NH, Ahmad, NI, Ahmad Miswan, N, Ahmad Rosdi, H, Ahmed, I, Ahmed, S, Aiello, J, Aitken, A, AitSadi, R, Aker, S, Akimoto, S, Akinfolarin, A, Akram, S, Alberici, F, Albert, C, Aldrich, L, Alegata, M, Alexander, L, Alfaress, S, Alhadj Ali, M, Ali, A, Alicic, R, Aliu, 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Miyatsuka, T, Miyazaki, M, Miyazawa, I, Mizumachi, R, Mizuno, M, Moffat, S, Mohamad Nor, FS, Mohamad Zaini, SN, Mohamed Affandi, FA, Mohandas, C, Mohd, R, Mohd Fauzi, NA, Mohd Sharif, NH, Mohd Yusoff, Y, Moist, L, Moncada, A, Montasser, M, Moon, A, Moran, C, Morgan, N, Moriarty, J, Morig, G, Morinaga, H, Morino, K, Morisaki, T, Morishita, Y, Morlok, S, Morris, A, Morris, F, Mostafa, S, Mostefai, Y, Motegi, M, Motherwell, N, Motta, D, Mottl, A, Moys, R, Mozaffari, S, Muir, J, Mulhern, J, Mulligan, S, Munakata, Y, Murakami, C, Murakoshi, M, Murawska, A, Murphy, K, Murphy, L, Murray, S, Murtagh, H, Musa, MA, Mushahar, L, Mustafa, R, Mustafar, R, Muto, M, Nadar, E, Nagano, R, Nagasawa, T, Nagashima, E, Nagasu, H, Nagelberg, S, Nair, H, Nakagawa, Y, Nakahara, M, Nakamura, J, Nakamura, R, Nakamura, T, Nakaoka, M, Nakashima, E, Nakata, J, Nakata, M, Nakatani, S, Nakatsuka, A, Nakayama, Y, Nakhoul, G, Naverrete, G, Navivala, A, Nazeer, I, Negrea, L, Nethaji, C, Newman, E, Ng, TJ, Ngu, LLS, 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Piper, J, Plummer-Morgan, J, Poehler, D, Polese, L, Poma, V, Postal, A, Pötz, C, Power, A, Pradhan, N, Pradhan, R, Preiss, E, Preston, K, Prib, N, Price, L, Provenzano, C, Pugay, C, Pulido, R, Putz, F, Qiao, Y, Quartagno, R, Quashie-Akponeware, M, Rabara, R, Rabasa-Lhoret, R, Radhakrishnan, D, Radley, M, Raff, R, Raguwaran, S, Rahbari-Oskoui, F, Rahman, M, Rahmat, K, Ramadoss, S, Ramanaidu, S, Ramasamy, S, Ramli, R, Ramli, S, Ramsey, T, Rankin, A, Rashidi, A, Raymond, L, Razali, WAFA, Read, K, Reiner, H, Reisler, A, Reith, C, Renner, J, Rettenmaier, B, Richmond, L, Rijos, D, Rivera, R, Rivers, V, Robinson, H, Rocco, M, Rodriguez-Bachiller, I, Rodriquez, R, Roesch, C, Roesch, J, Rogers, J, Rohnstock, M, Rolfsmeier, S, Roman, M, Romo, A, Rosati, A, Rosenberg, S, Ross, T, Roura, M, Roussel, M, Rovner, S, Roy, S, Rucker, S, Rump, L, Ruocco, M, Ruse, S, Russo, F, Russo, M, Ryder, M, Sabarai, A, Saccà, C, Sachson, R, Sadler, E, Safiee, NS, Sahani, M, Saillant, A, Saini, J, Saito, C, Saito, S, Sakaguchi, K, Sakai, M, Salim, H, Salviani, C, Sampson, A, Samson, F, Sandercock, P, Sanguila, S, Santorelli, G, Santoro, D, Sarabu, N, Saram, T, Sardell, R, Sasajima, H, Sasaki, T, Satko, S, Sato, A, Sato, D, Sato, H, Sato, J, Sato, T, Sato, Y, Satoh, M, Sawada, K, Schanz, M, Scheidemantel, F, Schemmelmann, M, Schettler, E, Schettler, V, Schlieper, GR, Schmidt, C, Schmidt, G, Schmidt, U, Schmidt-Gurtler, H, Schmude, M, Schneider, A, Schneider, I, Schneider-Danwitz, C, Schomig, M, Schramm, T, Schreiber, A, Schricker, S, Schroppel, B, Schulte-Kemna, L, Schulz, E, Schumacher, B, Schuster, A, Schwab, A, Scolari, F, Scott, A, Seeger, W, Segal, M, Seifert, L, Seifert, M, Sekiya, M, Sellars, R, Seman, MR, Shah, S, Shainberg, L, Shanmuganathan, M, Shao, F, Sharma, K, Sharpe, C, Sheikh-Ali, M, Sheldon, J, Shenton, C, Shepherd, A, Shepperd, M, Sheridan, R, Sheriff, Z, Shibata, Y, Shigehara, T, Shikata, K, Shimamura, K, Shimano, H, Shimizu, Y, Shimoda, H, Shin, K, Shivashankar, G, Shojima, N, 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Tanabe, A, Tanabe, K, Tanaka, A, Tanaka, N, Tang, S, Tang, Z, Tanigaki, K, Tarlac, M, Tatsuzawa, A, Tay, JF, Tay, LL, Taylor, J, Taylor, K, Te, A, Tenbusch, L, Teng, KS, Terakawa, A, Terry, J, Tham, ZD, Tholl, S, Thomas, G, Thong, KM, Tietjen, D, Timadjer, A, Tindall, H, Tipper, S, Tobin, K, Toda, N, Tokuyama, A, Tolibas, M, Tomita, A, Tomita, T, Tomlinson, J, Tonks, L, Topf, J, Topping, S, Torp, A, Torres, A, Totaro, F, Toth, P, Toyonaga, Y, Tripodi, F, Trivedi, K, Tropman, E, Tschope, D, Tse, J, Tsuji, K, Tsunekawa, S, Tsunoda, R, Tucky, B, Tufail, S, Tuffaha, A, Turan, E, Turner, H, Turner, J, Turner, M, Tye, YL, Tyler, A, Tyler, J, Uchi, H, Uchida, H, Uchida, T, Udagawa, T, Ueda, S, Ueda, Y, Ueki, K, Ugni, S, Ugwu, E, Umeno, R, Unekawa, C, Uozumi, K, Urquia, K, Valleteau, A, Valletta, C, van Erp, R, Vanhoy, C, Varad, V, Varma, R, Varughese, A, Vasquez, P, Vasseur, A, Veelken, R, Velagapudi, C, Verdel, K, Vettoretti, S, Vezzoli, G, Vielhauer, V, Viera, R, Vilar, E, Villaruel, S, Vinall, L, Vinathan, J, Visnjic, M, Voigt, E, von-Eynatten, M, Vourvou, M, Wada, J, Wada, T, Wada, Y, Wakayama, K, Wakita, Y, Walters, T, Wan Mohamad, WH, Wang, L, Wang, W, Wang, X, Wang, Y, Wanninayake, S, Watada, H, Watanabe, K, Watanabe, M, Waterfall, H, Watkins, D, Watson, S, Weaving, L, Weber, B, Webley, Y, Webster, A, Webster, M, Weetman, M, Wei, W, Weihprecht, H, Weiland, L, Weinmann-Menke, J, Weinreich, T, Wendt, R, Weng, Y, Whalen, M, Whalley, G, Wheatley, R, Wheeler, A, Wheeler, J, Whelton, P, White, K, Whitmore, B, Whittaker, S, Wiebel, J, Wiley, J, Wilkinson, L, Willett, M, Williams, A, Williams, E, Williams, K, Williams, T, Wilson, A, Wilson, P, Wincott, L, Wines, E, Winkelmann, B, Winkler, M, Winter-Goodwin, B, Witczak, J, Wittes, J, Wittmann, M, Wolf, G, Wolf, L, Wolfling, R, Wong, C, Wong, E, Wong, HS, Wong, LW, Wong, YH, Wonnacott, A, Wood, A, Wood, L, Woodhouse, H, Wooding, N, Woodman, A, Wren, K, Wu, J, Wu, P, Xia, S, Xiao, H, Xiao, X, Xie, Y, Xu, C, Xu, Y, Xue, H, Yahaya, H, Yalamanchili, H, Yamada, A, Yamada, N, Yamagata, K, Yamaguchi, M, Yamaji, Y, Yamamoto, A, Yamamoto, S, Yamamoto, T, Yamanaka, A, Yamano, T, Yamanouchi, Y, Yamasaki, N, Yamasaki, Y, Yamashita, C, Yamauchi, T, Yan, Q, Yanagisawa, E, Yang, F, Yang, L, Yano, S, Yao, S, Yao, Y, Yarlagadda, S, Yasuda, Y, Yiu, V, Yokoyama, T, Yoshida, S, Yoshidome, E, Yoshikawa, H, Young, A, Young, T, Yousif, V, Yu, H, Yu, Y, Yuasa, K, Yusof, N, Zalunardo, N, Zander, B, Zani, R, Zappulo, F, Zayed, M, Zemann, B, Zettergren, P, Zhang, H, Zhang, L, Zhang, N, Zhang, X, Zhao, J, Zhao, L, Zhao, S, Zhao, Z, Zhong, H, Zhou, N, Zhou, S, Zhu, L, Zhu, S, Zietz, M, Zippo, M, Zirino, F, and Zulkipli, FH
Published: 2024
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3. Erratum to:Methods for evaluating medical tests and biomarkers

Author: Gopalakrishna, G, Langendam, M, Scholten, R, Bossuyt, P, Leeflang, M, Noel-Storr, A, Thomas, J, Marshall, I, Wallace, B, Whiting, P, Davenport, C, GopalaKrishna, G, De Salis, I, Mallett, S, Wolff, R, Riley, R, Westwood, M, Kleinen, J, Collins, G, Reitsma, H, Moons, K, Zapf, A, Hoyer, A, Kramer, K, Kuss, O, Ensor, J, Deeks, JJ, Martin, EC, Riley, RD, Rücker, G, Steinhauser, S, Schumacher, M, Snell, K, Willis, B, Debray, T, Deeks, J, Di Ruffano, LF, Taylor-Phillips, S, Hyde, C, Taylor, SA, Batnagar, G, STREAMLINE COLON Investigators, STREAMLINE LUNG Investigators, METRIC Investigators, Seedat, F, Clarke, A, Byron, S, Nixon, F, Albrow, R, Walker, T, Deakin, C, Zhelev, Z, Hunt, H, Yang, Y, Abel, L, Buchanan, J, Fanshawe, T, Shinkins, B, Wynants, L, Verbakel, J, Van Huffel, S, Timmerman, D, Van Calster, B, Zwinderman, A, Oke, J, O'Sullivan, J, Perera, R, Nicholson, B, Bromley, HL, Roberts, TE, Francis, A, Petrie, D, Mann, GB, Malottki, K, Smith, H, Billingham, L, Sitch, A, Gerke, O, Holm-Vilstrup, M, Segtnan, EA, Halekoh, U, Høilund-Carlsen, PF, Francq, BG, Dinnes, J, Parkes, J, Gregory, W, Hewison, J, Altman, D, Rosenberg, W, Selby, P, Asselineau, J, Perez, P, Paye, A, Bessede, E, Proust-Lima, C, Naaktgeboren, C, De Groot, J, Rutjes, A, Reitsma, J, Ogundimu, E, Cook, J, Le Manach, Y, Vergouwe, Y, Pajouheshnia, R, Groenwold, R, Peelen, L, Nieboer, D, De Cock, B, Pencina, MJ, Steyerberg, EW, Cooper, J, Parsons, N, Stinton, C, Smith, S, Dickens, A, Jordan, R, Enocson, A, Fitzmaurice, D, Adab, P, Boachie, C, Vidmar, G, Freeman, K, Connock, M, Court, R, Moons, C, Harris, J, Mumford, A, Plummer, Z, Lee, K, Reeves, B, Rogers, C, Verheyden, V, Angelini, GD, Murphy, GJ, Huddy, J, Ni, M, Good, K, Cooke, G, Hanna, G, Ma, J, Moons, KGMC, De Groot, JAH, Altman, DG, Reitsma, JB, Collins, GS, Moons, KGM, Kamarudin, AN, Kolamunnage-Dona, R, Cox, T, Borsci, S, Pérez, T, Pardo, MC, Candela-Toha, A, Muriel, A, Zamora, J, Sanghera, S, Mohiuddin, S, Martin, R, Donovan, J, Coast, J, Seo, MK, Cairns, J, Mitchell, E, Smith, A, Wright, J, Hall, P, Messenger, M, Calder, N, Wickramasekera, N, Vinall-Collier, K, Lewington, A, Damen, J, Cairns, D, Hutchinson, M, Sturgeon, C, Mitchel, L, Kift, R, Christakoudi, S, Rungall, M, Mobillo, P, Montero, R, Tsui, T-L, Kon, SP, Tucker, B, Sacks, S, Farmer, C, Strom, T, Chowdhury, P, Rebollo-Mesa, I, Hernandez-Fuentes, M, Damen, JAAG, Debray, TPA, Heus, P, Hooft, L, Scholten, RJPM, Schuit, E, Tzoulaki, I, Lassale, CM, Siontis, GCM, Chiocchia, V, Roberts, C, Schlüssel, MM, Gerry, S, Black, JA, Van der Schouw, YT, Peelen, LM, Spence, G, McCartney, D, Van den Bruel, A, Lasserson, D, Hayward, G, Vach, W, De Jong, A, Burggraaff, C, Hoekstra, O, Zijlstra, J, De Vet, H, Graziadio, S, Allen, J, Johnston, L, O'Leary, R, Power, M, Johnson, L, Waters, R, Simpson, J, Fanshawe, TR, Phillips, P, Plumb, A, Helbren, E, Halligan, S, Gale, A, Sekula, P, Sauerbrei, W, Forman, JR, Dutton, SJ, Takwoingi, Y, Hensor, EM, Nichols, TE, Kempf, E, Porcher, R, De Beyer, J, Hopewell, S, Dennis, J, Shields, B, Jones, A, Henley, W, Pearson, E, Hattersley, A, MASTERMIND consortium, Scheibler, F, Rummer, A, Sturtz, S, Großelfinger, R, Banister, K, Ramsay, C, Azuara-Blanco, A, Burr, J, Kumarasamy, M, Bourne, R, Uchegbu, I, Murphy, J, Carter, A, Marti, J, Eatock, J, Robotham, J, Dudareva, M, Gilchrist, M, Holmes, A, Monaghan, P, Lord, S, StJohn, A, Sandberg, S, Cobbaert, C, Lennartz, L, Verhagen-Kamerbeek, W, Ebert, C, Horvath, A, Test Evaluation Working Group of the European Federation of Clinical Chemistry and Laboratory Medicine, Jenniskens, K, Peters, J, Grigore, B, Ukoumunne, O, Levis, B, Benedetti, A, Levis, AW, Ioannidis, JPA, Shrier, I, Cuijpers, P, Gilbody, S, Kloda, LA, McMillan, D, Patten, SB, Steele, RJ, Ziegelstein, RC, Bombardier, CH, Osório, FDL, Fann, JR, Gjerdingen, D, Lamers, F, Lotrakul, M, Loureiro, SR, Löwe, B, Shaaban, J, Stafford, L, Van Weert, HCPM, Whooley, MA, Williams, LS, Wittkampf, KA, Yeung, AS, Thombs, BD, Cooper, C, Nieto, T, Smith, C, Tucker, O, Dretzke, J, Beggs, A, Rai, N, Bayliss, S, Stevens, S, Mallet, S, Sundar, S, Hall, E, Porta, N, Estelles, DL, De Bono, J, CTC-STOP protocol development group, and National Institute for Health Research
Subjects: medicine.medical_specialty, Astrophysics::High Energy Astrophysical Phenomena, MEDLINE, 030204 cardiovascular system & hematology, BTC (Bristol Trials Centre), MASTERMIND consortium, 03 medical and health sciences, 0302 clinical medicine, medicine, 030212 general & internal medicine, Intensive care medicine, CTC-STOP protocol development group, lcsh:R5-920, business.industry, Test Evaluation Working Group of the European Federation of Clinical Chemistry and Laboratory Medicine, Published Erratum, STREAMLINE COLON Investigators, 3. Good health, STREAMLINE LUNG Investigators, Centre for Surgical Research, Family medicine, METRIC Investigators, High Energy Physics::Experiment, Erratum, business, lcsh:Medicine (General)
Abstract: [This corrects the article DOI: 10.1186/s41512-016-0001-y.].
Published: 2017
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4. Erratum to: Methods for evaluating medical tests and biomarkers.

Author: Gopalakrishna, G, Langendam, M, Scholten, R, Bossuyt, P, Leeflang, M, Noel-Storr, A, Thomas, J, Marshall, I, Wallace, B, Whiting, P, Davenport, C, GopalaKrishna, G, de Salis, I, Mallett, S, Wolff, R, Riley, R, Westwood, M, Kleinen, J, Collins, G, Reitsma, H, Moons, K, Zapf, A, Hoyer, A, Kramer, K, Kuss, O, Ensor, J, Deeks, JJ, Martin, EC, Riley, RD, Rücker, G, Steinhauser, S, Schumacher, M, Snell, K, Willis, B, Debray, T, Deeks, J, di Ruffano, LF, Taylor-Phillips, S, Hyde, C, Taylor, SA, Batnagar, G, STREAMLINE COLON Investigators, STREAMLINE LUNG Investigators, METRIC Investigators, Di Ruffano, LF, Seedat, F, Clarke, A, Byron, S, Nixon, F, Albrow, R, Walker, T, Deakin, C, Zhelev, Z, Hunt, H, Yang, Y, Abel, L, Buchanan, J, Fanshawe, T, Shinkins, B, Wynants, L, Verbakel, J, Van Huffel, S, Timmerman, D, Van Calster, B, Zwinderman, A, Oke, J, O'Sullivan, J, Perera, R, Nicholson, B, Bromley, HL, Roberts, TE, Francis, A, Petrie, D, Mann, GB, Malottki, K, Smith, H, Billingham, L, Sitch, A, Gerke, O, Holm-Vilstrup, M, Segtnan, EA, Halekoh, U, Høilund-Carlsen, PF, Francq, BG, Dinnes, J, Parkes, J, Gregory, W, Hewison, J, Altman, D, Rosenberg, W, Selby, P, Asselineau, J, Perez, P, Paye, A, Bessede, E, Proust-Lima, C, Naaktgeboren, C, de Groot, J, Rutjes, A, Reitsma, J, Ogundimu, E, Cook, J, Le Manach, Y, Vergouwe, Y, Pajouheshnia, R, Groenwold, R, Peelen, L, Nieboer, D, De Cock, B, Pencina, MJ, Steyerberg, EW, Cooper, J, Parsons, N, Stinton, C, Smith, S, Dickens, A, Jordan, R, Enocson, A, Fitzmaurice, D, Adab, P, Boachie, C, Vidmar, G, Freeman, K, Connock, M, Court, R, Moons, C, Harris, J, Mumford, A, Plummer, Z, Lee, K, Reeves, B, Rogers, C, Verheyden, V, Angelini, GD, Murphy, GJ, Huddy, J, Ni, M, Good, K, Cooke, G, Hanna, G, Ma, J, Moons, KGMC, de Groot, JAH, Altman, DG, Reitsma, JB, Collins, GS, Moons, KGM, Kamarudin, AN, Kolamunnage-Dona, R, Cox, T, Borsci, S, Pérez, T, Pardo, MC, Candela-Toha, A, Muriel, A, Zamora, J, Sanghera, S, Mohiuddin, S, Martin, R, Donovan, J, Coast, J, Seo, MK, Cairns, J, Mitchell, E, Smith, A, Wright, J, Hall, P, Messenger, M, Calder, N, Wickramasekera, N, Vinall-Collier, K, Lewington, A, Damen, J, Cairns, D, Hutchinson, M, Sturgeon, C, Mitchel, L, Kift, R, Christakoudi, S, Rungall, M, Mobillo, P, Montero, R, Tsui, T-L, Kon, SP, Tucker, B, Sacks, S, Farmer, C, Strom, T, Chowdhury, P, Rebollo-Mesa, I, Hernandez-Fuentes, M, Damen, JAAG, Debray, TPA, Heus, P, Hooft, L, Scholten, RJPM, Schuit, E, Tzoulaki, I, Lassale, CM, Siontis, GCM, Chiocchia, V, Roberts, C, Schlüssel, MM, Gerry, S, Black, JA, van der Schouw, YT, Peelen, LM, Spence, G, McCartney, D, van den Bruel, A, Lasserson, D, Hayward, G, Vach, W, de Jong, A, Burggraaff, C, Hoekstra, O, Zijlstra, J, de Vet, H, Graziadio, S, Allen, J, Johnston, L, O'Leary, R, Power, M, Johnson, L, Waters, R, Simpson, J, Fanshawe, TR, Phillips, P, Plumb, A, Helbren, E, Halligan, S, Gale, A, Sekula, P, Sauerbrei, W, Forman, JR, Dutton, SJ, Takwoingi, Y, Hensor, EM, Nichols, TE, Kempf, E, Porcher, R, de Beyer, J, Hopewell, S, Dennis, J, Shields, B, Jones, A, Henley, W, Pearson, E, Hattersley, A, MASTERMIND consortium, Scheibler, F, Rummer, A, Sturtz, S, Großelfinger, R, Banister, K, Ramsay, C, Azuara-Blanco, A, Burr, J, Kumarasamy, M, Bourne, R, Uchegbu, I, Murphy, J, Carter, A, Marti, J, Eatock, J, Robotham, J, Dudareva, M, Gilchrist, M, Holmes, A, Monaghan, P, Lord, S, StJohn, A, Sandberg, S, Cobbaert, C, Lennartz, L, Verhagen-Kamerbeek, W, Ebert, C, Horvath, A, Test Evaluation Working Group of the European Federation of Clinical Chemistry and Laboratory Medicine, Jenniskens, K, Peters, J, Grigore, B, Ukoumunne, O, Levis, B, Benedetti, A, Levis, AW, Ioannidis, JPA, Shrier, I, Cuijpers, P, Gilbody, S, Kloda, LA, McMillan, D, Patten, SB, Steele, RJ, Ziegelstein, RC, Bombardier, CH, Osório, FDL, Fann, JR, Gjerdingen, D, Lamers, F, Lotrakul, M, Loureiro, SR, Löwe, B, Shaaban, J, Stafford, L, van Weert, HCPM, Whooley, MA, Williams, LS, Wittkampf, KA, Yeung, AS, Thombs, BD, Cooper, C, Nieto, T, Smith, C, Tucker, O, Dretzke, J, Beggs, A, Rai, N, Bayliss, S, Stevens, S, Mallet, S, Sundar, S, Hall, E, Porta, N, Estelles, DL, de Bono, J, CTC-STOP protocol development group, Gopalakrishna, G, Langendam, M, Scholten, R, Bossuyt, P, Leeflang, M, Noel-Storr, A, Thomas, J, Marshall, I, Wallace, B, Whiting, P, Davenport, C, GopalaKrishna, G, de Salis, I, Mallett, S, Wolff, R, Riley, R, Westwood, M, Kleinen, J, Collins, G, Reitsma, H, Moons, K, Zapf, A, Hoyer, A, Kramer, K, Kuss, O, Ensor, J, Deeks, JJ, Martin, EC, Riley, RD, Rücker, G, Steinhauser, S, Schumacher, M, Snell, K, Willis, B, Debray, T, Deeks, J, di Ruffano, LF, Taylor-Phillips, S, Hyde, C, Taylor, SA, Batnagar, G, STREAMLINE COLON Investigators, STREAMLINE LUNG Investigators, METRIC Investigators, Di Ruffano, LF, Seedat, F, Clarke, A, Byron, S, Nixon, F, Albrow, R, Walker, T, Deakin, C, Zhelev, Z, Hunt, H, Yang, Y, Abel, L, Buchanan, J, Fanshawe, T, Shinkins, B, Wynants, L, Verbakel, J, Van Huffel, S, Timmerman, D, Van Calster, B, Zwinderman, A, Oke, J, O'Sullivan, J, Perera, R, Nicholson, B, Bromley, HL, Roberts, TE, Francis, A, Petrie, D, Mann, GB, Malottki, K, Smith, H, Billingham, L, Sitch, A, Gerke, O, Holm-Vilstrup, M, Segtnan, EA, Halekoh, U, Høilund-Carlsen, PF, Francq, BG, Dinnes, J, Parkes, J, Gregory, W, Hewison, J, Altman, D, Rosenberg, W, Selby, P, Asselineau, J, Perez, P, Paye, A, Bessede, E, Proust-Lima, C, Naaktgeboren, C, de Groot, J, Rutjes, A, Reitsma, J, Ogundimu, E, Cook, J, Le Manach, Y, Vergouwe, Y, Pajouheshnia, R, Groenwold, R, Peelen, L, Nieboer, D, De Cock, B, Pencina, MJ, Steyerberg, EW, Cooper, J, Parsons, N, Stinton, C, Smith, S, Dickens, A, Jordan, R, Enocson, A, Fitzmaurice, D, Adab, P, Boachie, C, Vidmar, G, Freeman, K, Connock, M, Court, R, Moons, C, Harris, J, Mumford, A, Plummer, Z, Lee, K, Reeves, B, Rogers, C, Verheyden, V, Angelini, GD, Murphy, GJ, Huddy, J, Ni, M, Good, K, Cooke, G, Hanna, G, Ma, J, Moons, KGMC, de Groot, JAH, Altman, DG, Reitsma, JB, Collins, GS, Moons, KGM, Kamarudin, AN, Kolamunnage-Dona, R, Cox, T, Borsci, S, Pérez, T, Pardo, MC, Candela-Toha, A, Muriel, A, Zamora, J, Sanghera, S, Mohiuddin, S, Martin, R, Donovan, J, Coast, J, Seo, MK, Cairns, J, Mitchell, E, Smith, A, Wright, J, Hall, P, Messenger, M, Calder, N, Wickramasekera, N, Vinall-Collier, K, Lewington, A, Damen, J, Cairns, D, Hutchinson, M, Sturgeon, C, Mitchel, L, Kift, R, Christakoudi, S, Rungall, M, Mobillo, P, Montero, R, Tsui, T-L, Kon, SP, Tucker, B, Sacks, S, Farmer, C, Strom, T, Chowdhury, P, Rebollo-Mesa, I, Hernandez-Fuentes, M, Damen, JAAG, Debray, TPA, Heus, P, Hooft, L, Scholten, RJPM, Schuit, E, Tzoulaki, I, Lassale, CM, Siontis, GCM, Chiocchia, V, Roberts, C, Schlüssel, MM, Gerry, S, Black, JA, van der Schouw, YT, Peelen, LM, Spence, G, McCartney, D, van den Bruel, A, Lasserson, D, Hayward, G, Vach, W, de Jong, A, Burggraaff, C, Hoekstra, O, Zijlstra, J, de Vet, H, Graziadio, S, Allen, J, Johnston, L, O'Leary, R, Power, M, Johnson, L, Waters, R, Simpson, J, Fanshawe, TR, Phillips, P, Plumb, A, Helbren, E, Halligan, S, Gale, A, Sekula, P, Sauerbrei, W, Forman, JR, Dutton, SJ, Takwoingi, Y, Hensor, EM, Nichols, TE, Kempf, E, Porcher, R, de Beyer, J, Hopewell, S, Dennis, J, Shields, B, Jones, A, Henley, W, Pearson, E, Hattersley, A, MASTERMIND consortium, Scheibler, F, Rummer, A, Sturtz, S, Großelfinger, R, Banister, K, Ramsay, C, Azuara-Blanco, A, Burr, J, Kumarasamy, M, Bourne, R, Uchegbu, I, Murphy, J, Carter, A, Marti, J, Eatock, J, Robotham, J, Dudareva, M, Gilchrist, M, Holmes, A, Monaghan, P, Lord, S, StJohn, A, Sandberg, S, Cobbaert, C, Lennartz, L, Verhagen-Kamerbeek, W, Ebert, C, Horvath, A, Test Evaluation Working Group of the European Federation of Clinical Chemistry and Laboratory Medicine, Jenniskens, K, Peters, J, Grigore, B, Ukoumunne, O, Levis, B, Benedetti, A, Levis, AW, Ioannidis, JPA, Shrier, I, Cuijpers, P, Gilbody, S, Kloda, LA, McMillan, D, Patten, SB, Steele, RJ, Ziegelstein, RC, Bombardier, CH, Osório, FDL, Fann, JR, Gjerdingen, D, Lamers, F, Lotrakul, M, Loureiro, SR, Löwe, B, Shaaban, J, Stafford, L, van Weert, HCPM, Whooley, MA, Williams, LS, Wittkampf, KA, Yeung, AS, Thombs, BD, Cooper, C, Nieto, T, Smith, C, Tucker, O, Dretzke, J, Beggs, A, Rai, N, Bayliss, S, Stevens, S, Mallet, S, Sundar, S, Hall, E, Porta, N, Estelles, DL, de Bono, J, and CTC-STOP protocol development group
Abstract: [This corrects the article DOI: 10.1186/s41512-016-0001-y.].
Published: 2017

5. Rapid development of renal failure secondary to AA-type amyloidosis in a patient with polymyalgia rheumatica.

Author: Javaid MM, Kamalanathan M, and Kon SP
Abstract: Polymyalgia rheumatica (PMR) is a common chronic inflammatory disorder affecting patients over the age of 50. Renal involvement in PMR is extremely rare and very few cases of AA amyloidosis secondary to PMR have been described in literature. We present a case of a patient with history PMR who developed nephrotic range proteinuria and rapidly deteriorating renal function secondary to AA amyloidosis within 18 months of the onset of symptoms of PMR. This case reinforces the association of PMR with secondary AA amyloidosis and highlights the importance of monitoring renal function in patients with PMR. [ABSTRACT FROM AUTHOR]
Published: 2010
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6. Technical report. Increased plasma malondialdehyde levels in glomerular disease as determined by a fully validated HPLC method.

Author: Templar, J, Kon, SP, Milligan, TP, Newman, DJ, and Raftery, MJ
Abstract: Background.Reactive oxygen species and particularly free radical induced lipid peroxidative tissue damage have been implicated in the pathogenesis of various renal diseases. Lipid peroxidation is assessed indirectly by the measurement of secondary products, such as malondialdehyde (MDA), using the widely employed thiobarbituric acid reactive substances (TBARS) method. However, this method lacks sensitivity and specificity. We have therefore developed and validated an HPLC (high-performance liquid chromatography) method for measurement of MDA and applied this to a variety of plasma samples in renal patients. [ABSTRACT FROM PUBLISHER]
Published: 1999
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7. Influence of donor C3 allotype on late renal-transplantation outcome.

Author: Brown KM, Kondeatis E, Vaughan RW, Kon SP, Farmer CKT, Taylor JD, He X, Johnston A, Horsfield C, Janssen BJC, Gros P, Zhou W, Sacks SH, Sheerin NS, Brown, Katherine M, Kondeatis, Elli, Vaughan, Robert W, Kon, Sui P, Farmer, Christopher K T, and Taylor, John D
Abstract: Background: The complement system has a critical role in both the innate and the adaptive immune responses. In humans, C3 exists as two main allotypes, F (fast) and S (slow), which are known to affect the incidence of inflammatory disease. We conducted a study to address the influence of these alleles on late renal-graft outcome.Methods: We determined the C3 allotypes of 662 pairs of adult kidney donors and recipients from 1993 through 2002 and then related C3F/S polymorphism status to demographic and clinical outcome data. The median length of follow-up was 3.3 years.Results: Analysis of 513 pairs of white donors and recipients identified 113 C3S/S recipients of a C3S/F or a C3F/F kidney and 179 C3S/S recipients of a C3S/S kidney. Graft survival was significantly better with a C3F/F or C3F/S donor allotype than a C3S/S allotype (P=0.05). The hazard ratio for graft loss of C3S/S kidneys, as compared with C3F/F or C3F/S kidneys, was 2.21 (95 percent confidence interval, 1.04 to 4.72; P=0.04). The graft function of C3F/F or C3F/S donor kidneys was significantly better than that of C3S/S donor kidneys (P<0.001). The effect of the C3F allele was specific to recipients who did not themselves possess this allele. Multivariate analysis excluded effects of other factors known to influence graft outcome.Conclusions: Expression of C3 alleles by donor renal cells appears to have a differential effect on late graft outcome. Among white C3S/S recipients, receipt of a C3F/F or C3F/S donor kidney, rather than a C3S/S donor kidney, is associated with a significantly better long-term outcome. These findings suggest that the two alleles have functional differences. [ABSTRACT FROM AUTHOR]
Published: 2006

8. Development and validation of the first consensus gene-expression signature of operational tolerance in kidney transplantation, incorporating adjustment for immunosuppressive drug therapy.

Author: Christakoudi S, Runglall M, Mobillo P, Rebollo-Mesa I, Tsui TL, Nova-Lamperti E, Taube C, Norris S, Kamra Y, Hilton R, Augustine T, Bhandari S, Baker R, Berglund D, Carr S, Game D, Griffin S, Kalra PA, Lewis R, Mark PB, Marks SD, MacPhee I, McKane W, Mohaupt MG, Paz-Artal E, Kon SP, Serón D, Sinha MD, Tucker B, Viklický O, Stahl D, Lechler RI, Lord GM, and Hernandez-Fuentes MP
Subjects: Adult, Aged, Case-Control Studies, Consensus, Female, Graft Rejection genetics, Humans, Immunosuppressive Agents pharmacology, Kidney Transplantation adverse effects, Logistic Models, Male, Middle Aged, Real-Time Polymerase Chain Reaction, Gene Expression Profiling methods, Gene Regulatory Networks drug effects, Graft Rejection prevention & control, Immunosuppressive Agents therapeutic use, Transplantation Tolerance
Abstract: Background: Kidney transplant recipients (KTRs) with "operational tolerance" (OT) maintain a functioning graft without immunosuppressive (IS) drugs, thus avoiding treatment complications. Nevertheless, IS drugs can influence gene-expression signatures aiming to identify OT among treated KTRs., Methods: We compared five published signatures of OT in peripheral blood samples from 18 tolerant, 183 stable, and 34 chronic rejector KTRs, using gene-expression levels with and without adjustment for IS drugs and regularised logistic regression., Findings: IS drugs explained up to 50% of the variability in gene-expression and 20-30% of the variability in the probability of OT predicted by signatures without drug adjustment. We present a parsimonious consensus gene-set to identify OT, derived from joint analysis of IS-drug-adjusted expression of five published signature gene-sets. This signature, including CD40, CTLA4, HSD11B1, IGKV4-1, MZB1, NR3C2, and RAB40C genes, showed an area under the curve 0⋅92 (95% confidence interval 0⋅88-0⋅94) in cross-validation and 0⋅97 (0⋅93-1⋅00) in six months follow-up samples., Interpretation: We advocate including adjustment for IS drug therapy in the development stage of gene-expression signatures of OT to reduce the risk of capturing features of treatment, which could be lost following IS drug minimisation or withdrawal. Our signature, however, would require further validation in an independent dataset and a biomarker-led trial., Funding: FP7-HEALTH-2012-INNOVATION-1 [305147:BIO-DrIM] (SC,IR-M,PM,DSt); MRC [G0801537/ID:88245] (MPH-F); MRC [MR/J006742/1] (IR-M); Guy's&StThomas' Charity [R080530]&[R090782]; CONICYT-Bicentennial-Becas-Chile (EN-L); EU:FP7/2007-2013 [HEALTH-F5-2010-260687: The ONE Study] (MPH-F); Czech Ministry of Health [NV19-06-00031] (OV); NIHR-BRC Guy's&StThomas' NHS Foundation Trust and KCL (SC); UK Clinical Research Networks [portfolio:7521]., Competing Interests: Declaration of Competing Interest Dr. Christakoudi reports grants from FP7-HEALTH-2012-INNOVATION-1 (project number 305147: BIO-DrIM), grants from National Institute for Health Research (NIHR) Biomedical Research Centre based at Guy's and St Thomas' NHS Foundation Trust and King's College London, during the conduct of the study. Mr. Runglall has nothing to disclose. Dr. Mobillo reports grants from FP7-HEALTH-2012-INNOVATION-1 (project number 305147: BIO-DrIM), during the conduct of the study. Dr. Rebollo-Mesa reports grants from [MR/J006742/1] to MRC Centre for Transplantation, grants from FP7-HEALTH-2012-INNOVATION-1 (project number 305147: BIO-DrIM), during the conduct of the study; other from UCB Pharma SRL, outside the submitted work. Mr. Tsui has nothing to disclose. Dr. Nova-Lamperti reports grants from CONICYT Bicentennial-Becas-Chile scholarship, during the conduct of the study. Dr. Taube has nothing to disclose. Dr. Norris has nothing to disclose. Mr. Kamra has nothing to disclose. Dr. Hilton reports personal fees from Chiesi Ltd, outside the submitted work. Dr. Augustine has nothing to disclose. Dr. Bhandari has nothing to disclose. Dr. Baker has nothing to disclose. Dr. Berglund has nothing to disclose. Dr. Carr has nothing to disclose. Dr. Game reports personal fees from Advisory board Chiesi pharmaceuticals, personal fees from Advisory board Recordati Rare Diseases, personal fees from Advisory board Syneos Health, outside the submitted work. Dr. Griffin has nothing to disclose. Dr. Kalra has nothing to disclose. Dr. Lewis has nothing to disclose. Dr. Mark reports personal fees and non-financial support from Vifor, personal fees from Astrazeneca, grants from Boehringer Ingelheim, personal fees and non-financial support from Pharmacosmos, personal fees from Janssen, personal fees from Novartis, personal fees from Pfizer, personal fees from Bristol Myers Squibb, personal fees and non-financial support from Napp, outside the submitted work. Dr. Marks has nothing to disclose. Dr. MacPhee reports other from AstraZeneca, other from AstraZeneca, grants and personal fees from Chiesi, personal fees from Astellas, personal fees from Sandoz, outside the submitted work. Dr. McKane has nothing to disclose. Dr. Mohaupt has nothing to disclose. Dr. Paz-Artal has nothing to disclose. Dr. Kon has nothing to disclose. Dr. Seron has nothing to disclose. Dr. Sinha has nothing to disclose. Dr. Tucker has nothing to disclose. Prof. Viklicky reports grants from CZECH MINISTRY OF HEALTH, during the conduct of the study. Dr. Stahl reports grants from FP7-HEALTH-2012-INNOVATION-1 (project number 305147: BIO-DrIM), during the conduct of the study. Dr. Lechler has nothing to disclose. Dr. Lord has nothing to disclose. Dr. Hernandez-Fuentes reports grants from FP7-HEALTH-2012-INNOVATION-1 (project number 305147: BIO-DrIM), grants from Medical Research Council MRC grants to Maria P. Hernandez-Fuentes [G0801537/ID: 88245], grants from Guy's and St Thomas’ Charity [grants R080530 and R090782], grants from EU; FP7/2007–2013], under grant agreement [No HEALTH-F5–2010–260687: The ONE Study], grants and non-financial support from National Institute for Health Research (NIHR) Biomedical Research Centre based at Guy's and St Thomas' NHS Foundation Trust and King's College London, non-financial support from Clinical Research Networks [study portfolio number 7521], during the conduct of the study; other from UCB Celltech., outside the submitted work; ., (Copyright © 2020 The Authors. Published by Elsevier B.V. All rights reserved.)
Published: 2020
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9. Vaccine: friend or foe? Double seropositive vasculitis following influenza vaccination.

Author: Norton B, Kon SP, Perera R, and Hull R
Abstract: Administration of the influenza vaccine has been associated with development of several autoimmune phenomena. We describe the case of a 72-year-old male who developed double seropositive vasculitis following seasonal influenza vaccination. On presentation, he was positive for both myeloperoxidase anti-neutrophil cytoplasmic antibody and anti-glomerular basement membrane antibody. He had stage three acute kidney injury requiring dialysis and was treated with methylprednisolone, intravenous cyclophosphamide and plasma exchange. He was also noted to have an incidental seven centimetre abdominal aortic aneurysm. He achieved remission with recovery in renal function and became haemodialysis independent. We hypothesize that the temporal relationship between influenza vaccination and double seropositive vasculitis directly triggered a systemic immune response in a susceptible patient, although a causal relationship cannot be proved. To the best of our knowledge, this is the first case of double seropositive vasculitis occurring in close temporal association with seasonal influenza vaccination.
Published: 2019
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10. Steroid regulation: An overlooked aspect of tolerance and chronic rejection in kidney transplantation.

Author: Christakoudi S, Runglall M, Mobillo P, Rebollo-Mesa I, Tsui TL, Nova-Lamperti E, Norris S, Kamra Y, Hilton R, Bhandari S, Baker R, Berglund D, Carr S, Game D, Griffin S, Kalra PA, Lewis R, Mark PB, Marks SD, Macphee I, McKane W, Mohaupt MG, Pararajasingam R, Kon SP, Serón D, Sinha M, Tucker B, Viklický O, Lechler RI, Lord GM, Stahl D, and Hernandez-Fuentes MP
Subjects: Area Under Curve, Cell Count, Chronic Disease, Gene Expression Regulation drug effects, Graft Rejection genetics, Humans, Multivariate Analysis, Prednisolone administration & dosage, Prednisolone pharmacology, Probability, Protein Isoforms metabolism, Receptors, Glucocorticoid metabolism, Regression Analysis, Up-Regulation drug effects, Graft Rejection etiology, Graft Rejection immunology, Immune Tolerance drug effects, Immune Tolerance genetics, Kidney Transplantation adverse effects, Steroids pharmacology
Abstract: Steroid conversion (HSD11B1, HSD11B2, H6PD) and receptor genes (NR3C1, NR3C2) were examined in kidney-transplant recipients with "operational tolerance" and chronic rejection (CR), independently and within the context of 88 tolerance-associated genes. Associations with cellular types were explored. Peripheral whole-blood gene-expression levels (RT-qPCR-based) and cell counts were adjusted for immunosuppressant drug intake. Tolerant (n = 17), stable (n = 190) and CR patients (n = 37) were compared. Healthy controls (n = 14) were used as reference. The anti-inflammatory glucocorticoid receptor (NR3C1) and the cortisol-activating HSD11B1 and H6PD genes were up-regulated in CR and were lowest in tolerant patients. The pro-inflammatory mineralocorticoid gene (NR3C2) was downregulated in stable and CR patients. NR3C1 was associated with neutrophils and NR3C2 with T-cells. Steroid conversion and receptor genes, alone, enabled classification of tolerant patients and were major contributors to gene-expression signatures of both, tolerance and CR, alongside known tolerance-associated genes, revealing a key role of steroid regulation and response in kidney transplantation., (Copyright © 2018 Elsevier B.V. All rights reserved.)
Published: 2018
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11. Biomarkers of Tolerance in Kidney Transplantation: Are We Predicting Tolerance or Response to Immunosuppressive Treatment?

Author: Rebollo-Mesa I, Nova-Lamperti E, Mobillo P, Runglall M, Christakoudi S, Norris S, Smallcombe N, Kamra Y, Hilton R, Bhandari S, Baker R, Berglund D, Carr S, Game D, Griffin S, Kalra PA, Lewis R, Mark PB, Marks S, Macphee I, McKane W, Mohaupt MG, Pararajasingam R, Kon SP, Serón D, Sinha MD, Tucker B, Viklický O, Lechler RI, Lord GM, and Hernandez-Fuentes MP
Subjects: Adult, Aged, B-Lymphocytes drug effects, B-Lymphocytes immunology, B-Lymphocytes metabolism, Case-Control Studies, Female, Follow-Up Studies, Glomerular Filtration Rate, Graft Rejection drug therapy, Graft Rejection etiology, Graft Rejection metabolism, Graft Survival drug effects, Humans, Immune Tolerance drug effects, Kidney Failure, Chronic complications, Kidney Failure, Chronic surgery, Kidney Function Tests, Male, Middle Aged, Prognosis, Prospective Studies, Risk Factors, Biomarkers metabolism, Graft Rejection diagnosis, Graft Survival immunology, Immune Tolerance immunology, Immunosuppressive Agents therapeutic use, Kidney Transplantation adverse effects
Abstract: We and others have previously described signatures of tolerance in kidney transplantation showing the differential expression of B cell-related genes and the relative expansions of B cell subsets. However, in all of these studies, the index group-namely, the tolerant recipients-were not receiving immunosuppression (IS) treatment, unlike the rest of the comparator groups. We aimed to assess the confounding effect of these regimens and develop a novel IS-independent signature of tolerance. Analyzing gene expression in three independent kidney transplant patient cohorts (232 recipients and 14 tolerant patients), we have established that the expression of the previously reported signature was biased by IS regimens, which also influenced transitional B cells. We have defined and validated a new gene expression signature that is independent of drug effects and also differentiates tolerant patients from healthy controls (cross-validated area under the receiver operating characteristic curve [AUC] = 0.81). In a prospective cohort, we have demonstrated that the new signature remained stable before and after steroid withdrawal. In addition, we report on a validated and highly accurate gene expression signature that can be reliably used to identify patients suitable for IS reduction (approximately 12% of stable patients), irrespective of the IS drugs they are receiving. Only a similar approach will make the conduct of pilot clinical trials for IS minimization safe and hence allow critical improvements in kidney posttransplant management., (© 2016 The Authors. American Journal of Transplantation published by Wiley Periodicals, Inc. on behalf of American Society of Transplant Surgeons.)
Published: 2016
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12. Cardiorenal syndrome: review of our current understanding.

Author: Hadjiphilippou S and Kon SP
Subjects: Acute Disease, Humans, Cardio-Renal Syndrome classification, Cardio-Renal Syndrome physiopathology, Cardio-Renal Syndrome therapy
Abstract: Renal and cardiac diseases are both prevalent and carry significant morbidity and mortality. They share common vascular risk factors and are physiologically interlinked. Dysfunction in one organ affects the other. Concurrent renal and cardiac disease is associated with a poor prognosis. This close relationship is reflected through cardiorenal syndrome. A classification system has been proposed; however, the underlying process is complex and multifactorial. Management of this syndrome focuses on improving heart function, reducing volume overload, and managing heart failure and chronic kidney disease. This, however, is challenging, limited by paucity of evidence and may lead to suboptimal therapy. Increased recognition of this syndrome should raise awareness in providing early therapy and avoiding adverse outcomes due to under-treatment. In this article, we provide an overview of our current understanding of cardiorenal syndrome, as well as its pathophysiology and treatment options., (© The Royal Society of Medicine.)
Published: 2016
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13. Nephrotic and anti-phospholipid syndromes: multisystem conditions associated with acute myocardial infarction in young patients.

Author: Javaid MM, Grigoriou A, Katsianos D, and Kon SP
Subjects: Adult, Antiphospholipid Syndrome diagnosis, Coronary Angiography, Coronary Vessels pathology, Humans, Male, Nephrotic Syndrome diagnosis, Thrombophilia complications, Antiphospholipid Syndrome complications, Myocardial Infarction etiology, Nephrotic Syndrome complications
Abstract: Acute myocardial infarction is relatively uncommon in patients under the age of 40 years. Unlike the older patients where rupture of coronary artery atherosclerotic plaque is the main underlying pathology, the pathogenesis in younger patients can be varied and may require different diagnostic and therapeutic approaches. Hypercoagulable state associated with nephrotic syndrome and antiphospholipid syndrome can lead to the development of occlusive coronary artery thrombus in absence of atherosclerotic coronary artery disease. Acute myocardial infarction in such a setting can sometimes be the first manifestation of an underlying disease. We describe a case of myocardial infarction in a young man with both nephrotic and antiphospho-lipid syndromes and present a brief literature review., (© 2011 European Dialysis and Transplant Nurses Association/European Renal Care Association.)
Published: 2012
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14. Tumor lysis syndrome and acute renal failure--an increasing spectrum of presentations.

Author: Mukherjee E, Mukherji D, Jayawardene SA, and Kon SP
Subjects: Acute Kidney Injury diagnosis, Acute Kidney Injury therapy, Adult, Carcinoma, Hepatocellular drug therapy, Humans, Leukemia, Myeloid drug therapy, Liver Neoplasms drug therapy, Male, Middle Aged, Tumor Lysis Syndrome diagnosis, Tumor Lysis Syndrome therapy, Acute Kidney Injury etiology, Tumor Lysis Syndrome complications
Abstract: Tumor lysis syndrome has historically been associated with hyperuricemia and uric acid crystal deposition. We present three cases of tumor lysis syndrome resulting in renal failure in the context of normouricema, highlighting the spectrum of clinical presentations and mechanisms of renal damage. Two cases occurred following the treatment of hematological malignancies and were associated with hyperphosphatemia; the third resulted from ischemic necrosis following transarterial chemoembolization of a hepatic tumor. We also discuss the role of renal biopsy in the investigation of tumor lysis syndrome.
Published: 2007
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15. Nephrocalcinosis in a patient with secondary hyperoxaluria.

Author: Lim PB, Klebe B, and Kon SP
Subjects: Aged, Humans, Hyperoxaluria etiology, Kidney Failure, Chronic etiology, Kidney Failure, Chronic surgery, Kidney Transplantation pathology, Male, Radiography, Hyperoxaluria diagnostic imaging, Nephrocalcinosis diagnostic imaging
Published: 2004
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16. Increased plasma malondialdehyde levels in glomerular disease as determined by a fully validated HPLC method.

Author: Templar J, Kon SP, Milligan TP, Newman DJ, and Raftery MJ
Subjects: Chromatography, High Pressure Liquid methods, Humans, Sensitivity and Specificity, Glomerulonephritis blood, Malondialdehyde blood
Abstract: Background: Reactive oxygen species and particularly free radical induced lipid peroxidative tissue damage have been implicated in the pathogenesis of various renal diseases. Lipid peroxidation is assessed indirectly by the measurement of secondary products, such as malondialdehyde (MDA), using the widely employed thiobarbituric acid reactive substances (TBARS) method. However, this method lacks sensitivity and specificity. We have therefore developed and validated an HPLC (high-performance liquid chromatography) method for measurement of MDA and applied this to a variety of plasma samples in renal patients., Methods: The optimized method involves antioxidant treatment of the plasma sample, followed by a protein precipitation step using trichloroacetic acid, acid hydrolysis and formation of an MDA thiobarbituric acid complex. The MDA-(TBA)2 adduct is separated from other interfering compounds by C18 reverse-phase HPLC techniques, with visible detection at 532 nm., Results: The assay was linear over the ranges 0.25-1.0 microM MDA and the detection limit was 0.06 microM MDA. Within-run precision was <4.5% and between-run precision was <10.0%. MDA plasma concentrations (mean+/-SD) were higher in ESRF diabetic patients (0.32 +/- 0.14 microM, n=20), non-diabetic ESRF patients (0.32 +/- 0.09 microM, n=20), and CRF patients (0.14 +/- 0.06 microM, n=40) compared to healthy controls (0.11 +/- 0.03 microM, n=40), (P < 0.001, P < 0.001 and P = 0.008). Levels were similar in healthy controls with normal renal function and transplanted patients (0.12 +/- 0.03 microM MDA, n=40), (P=NS). No correlation was observed between MDA and creatinine levels (r2 = 0.05, n=80), which suggests that MDA does not correlate with the degree of renal impairment. We matched CRF patients with glomerular and non-glomerular causes of renal failure for creatinine levels and found that MDA levels were higher in patients with glomerulonephritis (0.16 +/- 0.06 microM) than in those with CRF from non-glomerular causes (0.12 +/- 0.04 microM, P = 0.002)., Conclusions: We have introduced a reliable and sensitive HPLC technique to enhance the specificity of MDA-(TBA)2 measurement, with a significant improvement in HPLC column life. Using this method, picomole quantities of MDA can be detected in plasma. We have shown that MDA levels are significantly raised in patients with CRF due to glomerulonephritis, regardless of serum creatinine, which suggests that there is oxidative injury independent of any possible MDA retention due to renal impairment.
Published: 1999
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17. Diagnostic contribution of renal allograft biopsies at various intervals after transplantation.

Author: Kon SP, Templar J, Dodd SM, Rudge CJ, and Raftery MJ
Subjects: Adolescent, Adult, Aged, Biopsy, Cyclosporine adverse effects, Cyclosporine blood, Female, Humans, Male, Middle Aged, Retrospective Studies, Transplantation, Homologous, Kidney pathology, Kidney Transplantation
Abstract: Renal allograft biopsy is the accepted gold standard for investigating episodes of graft dysfunction in the early posttransplant period. The situation is less clear in late transplant biopsies. Later renal biopsies performed for graft dysfunction or as part of a routine investigative protocol have not been subjected to detailed critical evaluation. Two hundred sixty-three consecutive renal allograft biopsies in a single center were evaluated. They were arbitrarily divided into three groups based on interval after transplantation: group 1, up to 3 months (n=117); group 2, 4-12 months (n=60); and group 3, greater than 12 months after transplantation (n=86). There were no significant differences in demographic factors among the groups. The mean interval after transplantation was 0.8+/-0.1 months in group 1, 6.1+/-0.3 months in group 2, and 40.1+/-3.4 months in group 3. There were six principal diagnostic categories: acute rejection (AR), chronic rejection (CR), cyclosporine (CsA) nephrotoxicity, acute tubular necrosis (ATN), normal, and others. A statistically significant decrease in the frequency of AR (P<0.001) was seen in group 3 (3%) compared with groups 1 (43%) and 2 (37%). In contrast, the frequency of CR was significantly higher (P<0.001) in group 3 (71%) compared with groups 1 (0) and 2 (10%). ATN was seen almost exclusively in group 1. All but one of the 37 patients with ATN were in this group. CsA nephrotoxicity remained an important cause of graft dysfunction in all three groups, with no significant difference in incidence among the three groups. The differences between groups with other histological types were not significant. Patient management was changed based on the biopsy report in 84 patients in group 1 (72%), 45 patients in group 2 (75%), and only 16 patients in group 3 (19%) (P<0.001). In only seven patients in group 3 did the change in management result in a significant change in serum creatinine. All of these seven patients had CsA nephrotoxicity on biopsy and also had a significantly higher level of CsA compared with those with AR or CR. Thus, the diagnosis might have been possible without the need for biopsy. We conclude that late renal allograft biopsies are only rarely helpful in patient management and as such should be an investigation of last resort.
Published: 1997
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18. Membranous nephropathy complicating adenolymphoma of the parotid (Warthin's tumour).

Author: Kon SP, Fan SL, Kwan JT, Dodd SM, and Raftery MJ
Subjects: Adenolymphoma pathology, Adenolymphoma surgery, Antineoplastic Agents, Alkylating adverse effects, Antineoplastic Agents, Alkylating therapeutic use, Antineoplastic Agents, Hormonal adverse effects, Antineoplastic Agents, Hormonal therapeutic use, Cyclophosphamide adverse effects, Cyclophosphamide therapeutic use, Glomerulonephritis, Membranous blood, Glomerulonephritis, Membranous pathology, Humans, Male, Middle Aged, Parotid Neoplasms pathology, Parotid Neoplasms surgery, Prednisolone adverse effects, Prednisolone therapeutic use, Adenolymphoma complications, Glomerulonephritis, Membranous complications, Parotid Neoplasms complications
Abstract: Membranous nephropathy has been described in association with many malignancies including various lymphomas. However, it has not been previously described as a complication of benign solid adenolymphoma of the parotid, also called Warthin's tumour. We describe a patient who presented with an adenolymphoma of the parotid, and developed a severe nephrotic syndrome due to membranous nephropathy 6 months after the parotid swelling. The nephrotic syndrome resolved following parotidectomy and a short course of immunosuppression with prednisolone and cyclophosphamide. The possible pathophysiologic mechanisms are discussed.
Published: 1996
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19. Urinary C5b-9 excretion and clinical course in idiopathic human membranous nephropathy.

Author: Kon SP, Coupes B, Short CD, Solomon LR, Raftery MJ, Mallick NP, and Brenchley PE
Subjects: Biopsy, Disease Progression, Enzyme-Linked Immunosorbent Assay, Female, Follow-Up Studies, Glomerulonephritis, Membranous drug therapy, Glomerulonephritis, Membranous pathology, Humans, Immunosuppressive Agents therapeutic use, Male, Middle Aged, Retrospective Studies, Complement Membrane Attack Complex urine, Glomerulonephritis, Membranous urine
Abstract: Recent reports suggested that the presence of terminal complement complex (C5b-9) in urine from patients with idiopathic membranous nephropathy (IMN) may indicate on-going immunological damage. This report documents the relationship between C5b-9 excretion and clinical outcome in 35 adult patients with biopsy-proven IMN and progressively declining renal function. There were two groups of patients. Group I received one of three treatment regimens: prednisolone alone, prednisolone and chlorambucil, or prednisolone and cyclophosphamide (N = 22). Group II received no immunosuppressive therapy (N = 17). Three of the 18 patients receiving immunosuppressive drugs had more than one treatment regimen as they experienced a clinical relapse during the study period; hence 22 treatments were available for analysis. Urine samples were collected regularly and urinary C5b-9 (uC5b-9) was determined by ELISA. Both groups were similar with respect to age, sex distribution, and the duration of follow-up. An improvement in proteinuria and creatinine clearance was noted in the immunosuppressed group. Thirty-five patients were excreting C5b-9 initially (18 from group I and 17 from group II); 17 patients continued to excrete C5b-9 at the end of the observation period. These 17 patients had a significantly worse clinical outcome when compared to the 18 patients whose C5b-9 excretion became negative, either spontaneously or with treatment (P < 0.005). These results indicate that continuing C5b-9 excretion is correlated with a poor clinical outcome. They also suggest that uC5b-9 is a dynamic marker of ongoing immunological injury, and therefore may be useful in the initial assessment and monitoring of patients with IMN and in identifying patients who may derive benefit from immunosuppressive therapy.
Published: 1995
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20. Reversible renal failure due to the antiphospholipid antibody syndrome, pre-eclampsia and renal thrombotic microangiopathy.

Author: Kon SP, Kwan JT, and Raftery MJ
Subjects: Acute Kidney Injury metabolism, Adult, Antibodies, Antiphospholipid metabolism, Antiphospholipid Syndrome metabolism, Female, Humans, Pre-Eclampsia complications, Pre-Eclampsia metabolism, Pregnancy, Acute Kidney Injury etiology, Antiphospholipid Syndrome complications, Kidney blood supply, Pregnancy Complications, Puerperal Disorders etiology, Thrombosis etiology
Abstract: A 27-year-old Caucasian female, with a past history of recurrent spontaneous abortions, was admitted with pre-eclampsia at 26 weeks' gestation during her sixth pregnancy. She was previously known to have antiphospholipid antibodies since her fifth abortion, but had no clinical or serological evidence of systemic lupus erythematosus. A small-for-dates infant was delivered by emergency Caesarean section at 27 weeks for poor placental blood flow and fetal distress. She was transferred to the renal unit on the sixth post partum day with pulmonary edema, hypertension, disseminated intravascular coagulation and acute renal failure. Renal biopsy showed lesions compatible with thrombotic microangiopathy with diffuse glomerular necrosis. She was plasma exchanged and remained dialysis dependent for 7 months. Antiphospholipid antibodies were present in high titres and were the presumed cause of her acute renal failure. The patient now has stable renal function with a creatinine clearance of 30 ml/min for over two years. The late recovery of renal function is unique in the above circumstances.
Published: 1995

21. Development of human T-cell lymphotropic virus type I-associated adult T-cell leukemia/lymphoma during immunosuppressive treatment following renal transplantation.

Author: Jenks PJ, Barrett WY, Raftery MJ, Kelsey SM, van der Walt JD, Kon SP, and Breuer J
Subjects: DNA, Viral analysis, Fatal Outcome, Human T-lymphotropic virus 1 isolation & purification, Humans, Immunosuppressive Agents administration & dosage, Kidney Transplantation immunology, Male, Middle Aged, Retrospective Studies, Immunosuppressive Agents adverse effects, Kidney Transplantation adverse effects, Leukemia-Lymphoma, Adult T-Cell etiology
Abstract: Although it is recognized that there is an increased incidence of lymphoproliferative disorders among patients who have received immunosuppressive therapy following transportation, there have been few reports of adult T-cell leukemia/lymphoma (ATLL) developing in previously asymptomatic carriers of human T-cell lymphotropic virus type I (HTLV-I) who have undergone transplantation. We describe the development of such a tumor in a man who was HTLV-I-positive and received immunosuppressive treatment following renal transplantation. As the number of individuals in ethnic groups at risk for organ transplantation increases, it would seem prudent to screen such individuals for carriage of HTLV-I before transplantation and to follow them prospectively to confirm if transplantation and immunosuppression predispose to the development of ATLL.
Published: 1995
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22. Renal ammonia in autosomal dominant polycystic kidney disease.

Author: Torres VE, Keith DS, Offord KP, Kon SP, and Wilson DM
Subjects: Acid-Base Equilibrium, Adult, Ammonium Chloride pharmacokinetics, Bicarbonates urine, Female, Glomerular Filtration Rate, Humans, Hydrogen-Ion Concentration, Kidney Tubules, Distal metabolism, Male, Polycystic Kidney, Autosomal Dominant physiopathology, Protons, Ammonia urine, Polycystic Kidney, Autosomal Dominant urine
Abstract: Recent studies have suggested that defective medullary trapping of ammonia underlies the acidosis associated with renal failure and sets in motion maladaptive compensatory mechanisms that contribute to the progression of renal disease. Since a renal concentrating defect is an early functional abnormality in autosomal dominant polycystic kidney disease (ADPKD), defective medullary trapping and urinary excretion of ammonia may also occur early and have important pathophysiological consequences. The urinary pH and excretions of ammonia, titratable acid, and bicarbonate, were measured during a 24-hour baseline period and following the administration of ammonium chloride (100 mg/kg body wt) in ADPKD patients with normal glomerular filtration rate and in age- and gender-matched healthy control subjects. The distal nephron hydrogen ion secretory capacity was assessed during a bicarbonate infusion. Ammonia, sodium, pH, C3dg, and C5b-9 were measured in cyst fluid samples. The excretion rates of ammonia during the 24-hour baseline period and following the administration of ammonium chloride were significantly lower, and the relationship of ammonia excretion to urinary pH was significantly shifted downward in ADPKD. No difference in the increment of urinary pCO2 (delta pCO2) or the peripheral blood-urine pCO2 gradient (U-B pCO2) between ADPKD patients and control subjects was detected during a sodium bicarbonate infusion. Calculated concentrations of free-base ammonia in cyst fluid samples exceeded those calculated from reported concentrations of ammonia in renal venous blood of normal subjects. C3dg and C5b-9 were detected in some cyst fluids. The urinary excretion of ammonia is reduced in ADPKD patients with normal glomerular filtration rate.(ABSTRACT TRUNCATED AT 250 WORDS)
Published: 1994
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23. The temporal relationship between urinary C5b-9 and C3dg and clinical parameters in human membranous nephropathy.

Author: Coupes BM, Kon SP, Brenchley PE, Short CD, and Mallick NP
Subjects: Complement Activation, Female, Glomerulonephritis, Membranous drug therapy, Glomerulonephritis, Membranous immunology, Humans, Male, Middle Aged, Complement C3b urine, Complement Membrane Attack Complex urine, Glomerulonephritis, Membranous urine, Peptide Fragments urine
Abstract: We have previously reported that urinary excretion of the complement activation products C3dg and C5b-9 in human membranous nephropathy (MN) correlated with clinical outcome in a cross-sectional analysis. We report here the results of a retrospective longitudinal study of the temporal relationship between urinary C3dg and C5b-9 excretion and clinical parameters. A group of 23 adult patients with biopsy-proven MN were studied over a mean time period per patient of 3.5 years. Freshly voided urine samples were collected regularly; C3dg and C5b-9 were measured by ELISA (mean number of samples per patient = 13). During the period of the study, nine patients with declining renal function (group A) were treated with a standard steroid regimen. Serum creatinine had improved or stabilized in seven of these patients at the end of treatment. All nine patients were excreting C3dg and C5b-9 before treatment. Six other patients with declining renal function (group B) were not treated with steroids because of clinical contraindications. Serum creatinine continued to increase during the study in four of these six patients. C3dg and C5b-9 were present in the urine samples of these six patients on the majority of dates tested. Eight patients maintained stable renal function during the study (group C), either normal (6 patients) or impaired (2 patients). Of these patients, six were consistently negative for urinary C3dg and C5b-9 despite persistent proteinuria, and one patient who was initially positive became negative within 15 months, and remained negative for the rest of the study period. One patient was positive on one of 12 occasions tested. These results suggest that urinary complement activation products indicate ongoing active glomerular damage and may prove to be important determinants for the introduction and monitoring of therapy.
Published: 1993

24. Once daily felodipine monotherapy in mild to moderate hypertension.

Author: Kon SP, Tan HW, Chua CT, Ong ML, Kamsiah J, Maheendran KK, Ponniah CA, Tariq AR, and Mahendran T
Subjects: Adult, Aged, Blood Pressure drug effects, Felodipine adverse effects, Felodipine pharmacology, Female, Heart Rate drug effects, Humans, Male, Middle Aged, Single-Blind Method, Felodipine therapeutic use, Hypertension drug therapy
Abstract: In a single-blind study conducted at our centres, 78 hypertensive patients were enrolled with 58 completing the study according to the protocol. Mean supine and standing blood pressures were significantly reduced after treatment with felodipine, reductions being 27/21 mmHg (p < 0.0001) and 25/19 mmHg (p < 0.0001) respectively. Of 46 patients given felodipine 5 mg, 44 (95.7%) achieved target blood pressure defined as a diastolic blood pressure of < 90 mmHg, while all 12 patients on felodipine 10 mg did so. The 2 patients who did not achieve target pressure at the final visit did so on previous visits. There were no differences in pre and post-treatment laboratory variables. Treatment was discontinued in 6 patients because of headaches. No adverse events of clinical significance were reported in the 58 patients who completed the study. In conclusion, we found felodipine given once daily to be effective in the treatment of mild to moderate hypertension.
Published: 1992

25. Oral pefloxacin in the treatment of CAPD peritonitis.

Author: Tan HW, Kon SP, Chua CT, and Ngeow NF
Subjects: Administration, Oral, Adult, Aged, Bacterial Infections etiology, Female, Hospitals, University, Humans, Male, Middle Aged, Pefloxacin administration & dosage, Peritonitis etiology, Bacterial Infections drug therapy, Pefloxacin therapeutic use, Peritoneal Dialysis, Continuous Ambulatory adverse effects, Peritonitis drug therapy
Abstract: Continuous ambulatory peritoneal dialysis (CAPD), a widely used replacement therapy for end stage renal failure, is frequently complicated by bacterial peritonitis. The infecting organisms are mainly staphylococci and gram negative aerobes. Pefloxacin is a fluorinated quinolone with good in-vitro activity against these pathogens. The objective of this open non comparative study is to determine the effectiveness and safety of oral pefloxacin mesylate as a single first line antimicrobial treatment of CAPD peritonitis. 28 episodes of CAPD peritonitis were treated with a stat dose of pefloxacin 800 mg. followed by 400 mg. 12 hourly for about 15-18 days. A pefloxacin sensitive organism was isolated in 17 episodes. 11 episodes were culture negative. Treatment results showed a cure in seventeen (60.7%), no treatment response in seven (25%), and relapses in four (14.2%). Side effects encountered were not serious except for one incident of a generalized seizure. We conclude that oral pefloxacin is convenient, safe and effective enough as a single first line antimicrobial treatment for CAPD peritonitis.
Published: 1992

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25 results on '"Kon, SP"'

1. Effects of empagliflozin on progression of chronic kidney disease: a prespecified secondary analysis from the empa-kidney trial

2. Impact of primary kidney disease on the effects of empagliflozin in patients with chronic kidney disease: secondary analyses of the EMPA-KIDNEY trial

3. Erratum to:Methods for evaluating medical tests and biomarkers

4. Erratum to: Methods for evaluating medical tests and biomarkers.

5. Rapid development of renal failure secondary to AA-type amyloidosis in a patient with polymyalgia rheumatica.

6. Technical report. Increased plasma malondialdehyde levels in glomerular disease as determined by a fully validated HPLC method.

7. Influence of donor C3 allotype on late renal-transplantation outcome.

8. Development and validation of the first consensus gene-expression signature of operational tolerance in kidney transplantation, incorporating adjustment for immunosuppressive drug therapy.

9. Vaccine: friend or foe? Double seropositive vasculitis following influenza vaccination.

10. Steroid regulation: An overlooked aspect of tolerance and chronic rejection in kidney transplantation.

11. Biomarkers of Tolerance in Kidney Transplantation: Are We Predicting Tolerance or Response to Immunosuppressive Treatment?

12. Cardiorenal syndrome: review of our current understanding.

13. Nephrotic and anti-phospholipid syndromes: multisystem conditions associated with acute myocardial infarction in young patients.

14. Tumor lysis syndrome and acute renal failure--an increasing spectrum of presentations.

15. Nephrocalcinosis in a patient with secondary hyperoxaluria.

16. Increased plasma malondialdehyde levels in glomerular disease as determined by a fully validated HPLC method.

17. Diagnostic contribution of renal allograft biopsies at various intervals after transplantation.

18. Membranous nephropathy complicating adenolymphoma of the parotid (Warthin's tumour).

19. Urinary C5b-9 excretion and clinical course in idiopathic human membranous nephropathy.

20. Reversible renal failure due to the antiphospholipid antibody syndrome, pre-eclampsia and renal thrombotic microangiopathy.

21. Development of human T-cell lymphotropic virus type I-associated adult T-cell leukemia/lymphoma during immunosuppressive treatment following renal transplantation.

22. Renal ammonia in autosomal dominant polycystic kidney disease.

23. The temporal relationship between urinary C5b-9 and C3dg and clinical parameters in human membranous nephropathy.

24. Once daily felodipine monotherapy in mild to moderate hypertension.

25. Oral pefloxacin in the treatment of CAPD peritonitis.

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