Author: "Grandaliano G" / Publication Year Range: Last 3 years - Searchworks@Jio Institute Digital Library Search Results

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31 results on '"Grandaliano G"'

1. Clinical and Economic Impact of Early Diagnosis of Chronic Kidney Disease in General Practice: The Endorse Study

Author: Pesce F, Bruno GM, Colombo GL, Di Matteo S, Maurizi AR, Mongelli V, Mele S, Narici L, Bianchi S, Bonomini M, Castellano G, De Nicola L, Gambaro G, Grandaliano G, La Manna G, Pani A, Ranghino A, and Gesualdo L
Subjects: egfr, uacr, awareness, chronic kidney disease, general practice, economic impact, training intervention, early diagnosis, Medicine (General), R5-920, Therapeutics. Pharmacology, RM1-950
Abstract: Francesco Pesce,1 Giacomo Matteo Bruno,2 Giorgio Lorenzo Colombo,2 Sergio Di Matteo,3 Anna Rita Maurizi,4 Valentina Mongelli,4 Silvia Mele,5 Lavinia Narici,5 Stefano Bianchi,6 Mario Bonomini,7 Giuseppe Castellano,8 Luca De Nicola,9 Giovanni Gambaro,10 Giuseppe Grandaliano,11 Gaetano La Manna,12 Antonello Pani,13 Andrea Ranghino,14 Loreto Gesualdo15 1Division of Renal Medicine, “Fatebenefratelli Isola Tiberina—Gemelli Isola”, Rome, 00186, Italy; 2Department of Drug Sciences, University of Pavia, Pavia, Italy; 3S.A.V.E. Studi Analisi Valutazioni Economiche, Milan, Italy; 4Cardiovascular, Renal and Metabolism Medical Affairs, AstraZeneca, Milan, Italy; 5Value & Access, AstraZeneca, Milan, Italy; 6Nephrology and Dialysis Unit, Department of Internal Medicine, ASL Toscana Nordovest, Regione Toscana, Livorno, Italy; 7Department of Medicine, Section of Nephrology and Dialysis, G. D’Annunzio University, Chieti, 66013, Italy; 8UOC of Nephrology, Dialysis, and Kidney Transplant, IRCCS Foundation Ca’ Granda Ospedale Maggiore Policlinico, Milan, Italy; 9Department of Advanced Medical and Surgical Sciences, Nephrology and Dialysis Unit, University Vanvitelli, Naples, Italy; 10Division of Nephrology and Dialysis, Department of Medicine, University of Verona, Verona, Italy; 11Department of Translational Medicine and Surgery, Università Cattolica Sacro Cuore, Rome, Italy; 12Nephrology Dialysis and Kidney Transplant Unit, IRCCS Azienda Ospedaliero-Universitaria Di Bologna, Bologna, Italy; 13Department of Nephrology and Dialysis, G. Brotzu Hospital, Cagliari, Italy; 14Nephrology, Dialysis and Kidney Transplant Unit, Ospedali Riuniti Ancona, Ancona, Italy; 15Nephrology, Dialysis and Transplantation Unit, Department of Precision and Regenerative Medicine and Ionian Area (Dimepre-J), University of Bari “aldo Moro”, Bari, ItalyCorrespondence: Giorgio Lorenzo Colombo, Email colombog@unipv.itIntroduction: The underdiagnosis of chronic kidney disease (CKD) remains a significant public health concern. The Early chroNic kiDney disease pOint of caRe Screening (ENDORSE) project aimed to evaluate the clinical and economic implications of a targeted training intervention for general practitioners (GPs) to enhance CKD awareness and early diagnosis.Methods: Data on estimated Glomerular Filtration Rate (eGFR) and Urinary Albumin-Creatinine Ratio (uACR) were collected by 53 Italian GPs from 112,178 patients at baseline and after six months. The intervention involved six months of hybrid training provided by 11 nephrologists, which included formal lectures, instant messaging support, and joint visits for complex cases.Results: The results demonstrated a substantial increase in the use of eGFR (+44.7%) and uACR (+95.2%) tests. This led to a 128.9% rise in the number of individuals screened for CKD using the KDIGO classification, resulting in a 62% increase in CKD diagnoses. The intervention’s impact was particularly notable in high-risk groups, including patients with type 2 diabetes, hypertension, and heart failure.Discussion: A budget impact analysis projected cumulative five-year savings of € 1.7 million for the study cohort. When these findings were extrapolated to the entire Italian CKD population, potential savings were estimated at € 106.6 million, highlighting significant cost savings for the national health service. The clinical simulation assumed that early diagnosed CKD patients would be treated according to current indications for dapagliflozin, which slows disease progression.Conclusion: The ENDORSE model demonstrated that targeted training for GPs can significantly improve early CKD detection, leading to better patient outcomes and considerable economic benefits. This approach shows promise for broader implementation to address the underdiagnosis of CKD on a national and potentially international scale. Keywords: eGFR, uACR, awareness, chronic kidney disease, general practice, economic impact, training intervention, early diagnosis
Published: 2024

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, 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, Emberson, J, 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, 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, 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Published: 2024
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3. 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, 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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, 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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4. Risk of end-stage kidney disease in kidney transplant recipients versus patients with native chronic kidney disease: multicentre unmatched and propensity-score matched analyses

Author: De Nicola, L., Serra, R., Provenzano, M., Minutolo, R., Michael, A., Ielapi, N., Federico, S., Carrano, R., Bellizzi, V., Garofalo, C., Iodice, C., Borrelli, S., Grandaliano, Giuseppe, Stallone, G., Gesualdo, L., Chiodini, P., Andreucci, M., Grandaliano G. (ORCID:0000-0003-1213-2177), De Nicola, L., Serra, R., Provenzano, M., Minutolo, R., Michael, A., Ielapi, N., Federico, S., Carrano, R., Bellizzi, V., Garofalo, C., Iodice, C., Borrelli, S., Grandaliano, Giuseppe, Stallone, G., Gesualdo, L., Chiodini, P., Andreucci, M., and Grandaliano G. (ORCID:0000-0003-1213-2177)
Abstract: Background: In kidney transplant recipients (KTR), the end-stage kidney disease (ESKD) risk dependent on the risk factors acting in native chronic kidney disease (CKD) remains undefined. Methods: We compared risk and determinants of ESKD between 757 adult KTR and 1940 patients with native CKD before and after propensity-score (PS) analysis matched for unmodifiable risk factors [(age, sex, diabetes, cardiovascular disease and estimated glomerular filtration rate (eGFR)]. Results: In unmatched cohorts, eGFR was lower in CKD versus KTR (45.9 ± 11.3 versus 59.2 ± 13.4 mL/min/1.73 m2, P < 0.001). During a median follow-up of 5.4 years, the unadjusted cumulative incidence of ESKD was consistently lower in unmatched KTR versus CKD. Conversely, in PS-matched analysis, the risk of ESKD in KTR was 78% lower versus CKD at 1 year of follow-up while progressively increased over time resulting similar to that of native CKD patients after 5 years and 2.3-fold higher than that observed in CKD at 10 years. R2 analysis in unmatched patients showed that the proportion of the outcome variance explained by traditional ESKD determinants was smaller in KTR versus native CKD (31% versus 70%). After PS matching, the risk of ESKD [hazard ratio (HR), 95% confidence interval (95% CI)] was significantly associated with systolic blood pressure (1.02, 1.01-1.02), phosphorus (1.31, 1.05-1.64), 24-h proteinuria (1.11, 1.05-1.17) and haemoglobin (0.85, 0.78-0.93) irrespective of KTR status. Similar data were obtained after matching also for modifiable risk factors. Conclusions: In KTR, when compared with matched native CKD patients, the risk of ESKD is lower in the first 5 years and higher later on. Traditional determinants of ESKD account for one-third of the variability of time-to-graft failure.
Published: 2023

5. Eradication of HCV by direct antiviral agents restores mitochondrial function and energy homeostasis in peripheral blood mononuclear cells

Author: Villani, R., Sangineto, M., Pontrelli, P., Bellanti, F., Bukke, V. N., Moola, A., Gesualdo, L., Vendemiale, G., Grandaliano, Giuseppe, Stallone, G., Serviddio, G., Grandaliano G. (ORCID:0000-0003-1213-2177), Villani, R., Sangineto, M., Pontrelli, P., Bellanti, F., Bukke, V. N., Moola, A., Gesualdo, L., Vendemiale, G., Grandaliano, Giuseppe, Stallone, G., Serviddio, G., and Grandaliano G. (ORCID:0000-0003-1213-2177)
Abstract: Hepatitis C virus (HCV) adopts several immune evasion mechanisms such as interfering with innate immunity or promoting T-cell exhaustion. However, the recent direct-antiviral agents (DAAs) rapidly eliminate the virus, and the repercussions in terms of immune system balance are unknown. Here we compared the PBMCs transcriptomic profile of patients with HCV chronic infection at baseline (T0) and 12 weeks after the end of the therapy (SVR12) with DAAs. 3862 genes were differently modulated, identifying oxidative phosphorylation as the top canonical pathway differentially activated. Therefore, we dissected PBMCs bioenergetic profile by analyzing mitochondrial respiration and glycolysis at 4 timepoints: T0, 4 weeks of therapy, end of therapy (EoT), and SVR12. Maximal and reserve respiratory capacity considerably increased at EoT, persisting until SVR12. Notably, over time a significant increase was observed in respiratory chain (RC) complexes protein levels and the enzymatic activity of complexes I, II, and IV. Mitochondrial-DNA integrity improved over time, and the expression of mitochondrial biogenesis key regulators such as TFAM, Nrf-1, and PPARGC1A significantly increased at SVR12; hence, RC complexes synthesis and mitochondrial respiration were supported after treatment. HCV clearance with DAAS profoundly changed PBMCs bioenergetic profile, suggesting the immunometabolism study as a new approach to the understanding of viral immune evasion mechanisms and host adaptations during infections and therapies.
Published: 2022

6. Increased Complement Gene Expression in Circulating B Cells From Kidney Transplant Recipients With Chronic Antibody-Mediated Rejection

Author: Cravedi, P., Bruschi, M., Pontrelli, P., Grandaliano, Giuseppe, Zaza, G., Fribourg, M., Grandaliano G. (ORCID:0000-0003-1213-2177), Cravedi, P., Bruschi, M., Pontrelli, P., Grandaliano, Giuseppe, Zaza, G., Fribourg, M., and Grandaliano G. (ORCID:0000-0003-1213-2177)
Abstract: N/A
Published: 2022

7. New-onset anemia and associated risk of ESKD and death in non-dialysis CKD patients: A multicohort observational study

Author: Minutolo, R., Provenzano, M., Chiodini, P., Borrelli, S., Garofalo, C., Andreucci, M., Liberti, M. E., Bellizzi, V., Conte, G., De Nicola, L., Zamboli, P., Iodice, F. C., Signoriello, S., Gallo, C., Cianciaruso, B., Pota, A., Nappi, F., Avella, F., Di Iorio, B. R., Cestaro, R., Martignetti, V., Morrone, L., Lupo, A., Abaterusso, C., Donadio, C., Bonomini, M., Sirolli, V., Casino, F., Lopez, T., Detomaso, F., Giannattasio, M., Virgilio, M., Tarantino, G., Cristofano, C., Tuccillo, S., Chimienti, S., Petrarulo, F., Giancaspro, V., Strippoli, M., Laraia, E., Gallucci, M., Gigante, B., Lodeserto, C., Santese, D., Montanaro, A., Giordano, R., Caglioti, A., Fuiano, G., Zoccali, C., Caridi, G., Postorino, M., Savica, V., Monardo, P., Bellinghieri, G., Santoro, D., Castellino, P., Rapisarda, F., Fatuzzo, P., Messina, A., Dal Canton, A., Esposito, V., Formica, M., Segoloni, G., Gallieni, M., Locatelli, F., Tarchini, R., Meneghel, G., Oldrizzi, L., Cossu, M., Di Giulio, S., Malaguti, M., Pizzarelli, F., Quintaliani, G., Pisani, A., Bonofiglio, R., Grandaliano, Giuseppe, Russo, D., Di Micco, L., Torraca, S., Sabbatini, M., Grandaliano G. (ORCID:0000-0003-1213-2177), Minutolo, R., Provenzano, M., Chiodini, P., Borrelli, S., Garofalo, C., Andreucci, M., Liberti, M. E., Bellizzi, V., Conte, G., De Nicola, L., Zamboli, P., Iodice, F. C., Signoriello, S., Gallo, C., Cianciaruso, B., Pota, A., Nappi, F., Avella, F., Di Iorio, B. R., Cestaro, R., Martignetti, V., Morrone, L., Lupo, A., Abaterusso, C., Donadio, C., Bonomini, M., Sirolli, V., Casino, F., Lopez, T., Detomaso, F., Giannattasio, M., Virgilio, M., Tarantino, G., Cristofano, C., Tuccillo, S., Chimienti, S., Petrarulo, F., Giancaspro, V., Strippoli, M., Laraia, E., Gallucci, M., Gigante, B., Lodeserto, C., Santese, D., Montanaro, A., Giordano, R., Caglioti, A., Fuiano, G., Zoccali, C., Caridi, G., Postorino, M., Savica, V., Monardo, P., Bellinghieri, G., Santoro, D., Castellino, P., Rapisarda, F., Fatuzzo, P., Messina, A., Dal Canton, A., Esposito, V., Formica, M., Segoloni, G., Gallieni, M., Locatelli, F., Tarchini, R., Meneghel, G., Oldrizzi, L., Cossu, M., Di Giulio, S., Malaguti, M., Pizzarelli, F., Quintaliani, G., Pisani, A., Bonofiglio, R., Grandaliano, Giuseppe, Russo, D., Di Micco, L., Torraca, S., Sabbatini, M., and Grandaliano G. (ORCID:0000-0003-1213-2177)
Abstract: Background: Anemia is a common complication of chronic kidney disease (CKD), but its incidence in nephrology settings is poorly investigated. Similarly, the risks of adverse outcomes associated with new-onset anemia are not known. Methods: We performed a pooled analysis of three observational cohort studies including 1031 non-anemic CKD patients with eGFR <60 mL/min/1.73 m2 regularly followed in renal clinics. We estimated the incidence of mild anemia (hemoglobin 11-12 g/dL in women and 11-13 g/dL in men) and severe anemia (hemoglobin <11 g/dL or use of erythropoiesis-stimulating agents) during a 3-year follow-up period. Thereafter we estimated the risk of end-stage kidney disease (ESKD) and all-cause death associated with new-onset mild and severe anemia. Results: The mean age was 63 ± 14 years, 60% were men and 20% had diabetes. The mean estimated glomerular filtration rate (eGFR) was 37 ± 13 mL/min/1.73 m2 and the median proteinuria was 0.4 g/day [interquartile range (IQR) 0.1-1.1]. The incidence of mild and severe anemia was 13.7/100 patients-year and 6.2/100 patients-year, respectively. Basal predictors of either mild or severe anemia were diabetes, lower hemoglobin, higher serum phosphate, eGFR <30 mL/min/1.73 m2 and proteinuria >0.50 g/day. Male sex, moderate CKD (eGFR 30-44 mL/min/1.73 m2) and moderate proteinuria (0.15-0.50 g/day) predicted only mild anemia. The incidence of anemia increased progressively with CKD stages (from 8.77 to 76.59/100 patients-year) and the proteinuria category (from 13.99 to 25.02/100 patients-year). During a median follow-up of 3.1 years, 232 patients reached ESKD and 135 died. Compared with non-anemic patients, mild anemia was associated with a higher adjusted risk of ESKD {hazard ratio [HR] 1.42 [95% confidence interval (CI) 1.02-1.98]} and all-cause death [HR 1.55 (95% CI 1.04-2.32)]. Severe anemia was associated with an even higher risk of ESKD [HR 1.73 (95% CI 1.20-2.51)] and death [HR 1.83 (95% CI 1.05-3.19)].
Published: 2022

8. Can SGLT2 inhibitors answer unmet therapeutic needs in chronic kidney disease?

Author: De Nicola, L, Cozzolino, M, Genovesi, S, Gesualdo, L, Grandaliano, G, Pontremoli, R, De Nicola, Luca, Cozzolino, Mario, Genovesi, Simonetta, Gesualdo, Loreto, Grandaliano, Giuseppe, Pontremoli, Roberto, De Nicola, L, Cozzolino, M, Genovesi, S, Gesualdo, L, Grandaliano, G, Pontremoli, R, De Nicola, Luca, Cozzolino, Mario, Genovesi, Simonetta, Gesualdo, Loreto, Grandaliano, Giuseppe, and Pontremoli, Roberto
Abstract: Chronic kidney disease (CKD) is a global health problem, affecting more than 850 million people worldwide. The number of patients receiving renal replacement therapy (dialysis or renal transplantation) has increased over the years, and it has been estimated that the number of people receiving renal replacement therapy will more than double from 2.618 million in 2010 to 5.439 million in 2030, with wide differences among countries. The main focus of CKD treatment has now become preserving renal function rather than replacing it. This is possible, at least to some extent, through the optimal use of multifactorial therapy aimed at preventing end-stage kidney disease and cardiovascular events. Sodium/glucose cotransporter 2 inhibitors (SGLT2i) reduce glomerular hypertension and albuminuria with beneficial effects on progression of renal damage in both diabetic and non-diabetic CKD. SGLT2 inhibitors also show great benefits in cardiovascular protection, irrespective of diabetes. Therefore, the use of these drugs will likely be extended to the whole CKD population as a new standard of care.
Published: 2022

9. Crystal-induced colitis

Author: Spasiano, Andrea, Castri, Federica, Giustiniani, Maria Cristina, Riccioni, Maria Elena, Naticchia, Alessandro, Grandaliano, Giuseppe, Panocchia, Nicola, Spasiano A., Castri F., Giustiniani M. C., Riccioni M. E. (ORCID:0000-0002-9239-4312), Naticchia A., Grandaliano G. (ORCID:0000-0003-1213-2177), Panocchia N., Spasiano, Andrea, Castri, Federica, Giustiniani, Maria Cristina, Riccioni, Maria Elena, Naticchia, Alessandro, Grandaliano, Giuseppe, Panocchia, Nicola, Spasiano A., Castri F., Giustiniani M. C., Riccioni M. E. (ORCID:0000-0002-9239-4312), Naticchia A., Grandaliano G. (ORCID:0000-0003-1213-2177), and Panocchia N.
Abstract: A 59-year-old man undergoing dialysis was admitted to our hospital with lower limb ischemia; he had a story of long-term use of phosphate and potassium chelator. Because of anemia and repeated episodes of bowel bleeding, he underwent colonoscopy with a biopsy of the ileocecal valve and ulcerative lesions of the proximal descending colon
Published: 2022

10. Can SGLT2 inhibitors answer unmet therapeutic needs in chronic kidney disease?

Author: Luca De Nicola, Mario Cozzolino, Simonetta Genovesi, Loreto Gesualdo, Giuseppe Grandaliano, Roberto Pontremoli, De Nicola, L, Cozzolino, M, Genovesi, S, Gesualdo, L, Grandaliano, G, Pontremoli, R, De Nicola, L., Cozzolino, M., Genovesi, S., Gesualdo, L., Grandaliano, G., and Pontremoli, R.
Subjects: Settore MED/14 - Nefrologia, CDK, Diabetes, ESKD, SGLT2i, Diabete, Kidney, Diabetes Mellitus, Type 2, Nephrology, Albuminuria, Humans, Renal Insufficiency, Chronic, Sodium-Glucose Transporter 2 Inhibitors
Abstract: Chronic kidney disease (CKD) is a global health problem, affecting more than 850 million people worldwide. The number of patients receiving renal replacement therapy (dialysis or renal transplantation) has increased over the years, and it has been estimated that the number of people receiving renal replacement therapy will more than double from 2.618 million in 2010 to 5.439 million in 2030, with wide differences among countries. The main focus of CKD treatment has now become preserving renal function rather than replacing it. This is possible, at least to some extent, through the optimal use of multifactorial therapy aimed at preventing end-stage kidney disease and cardiovascular events. Sodium/glucose cotransporter 2 inhibitors (SGLT2i) reduce glomerular hypertension and albuminuria with beneficial effects on progression of renal damage in both diabetic and non-diabetic CKD. SGLT2 inhibitors also show great benefits in cardiovascular protection, irrespective of diabetes. Therefore, the use of these drugs will likely be extended to the whole CKD population as a new standard of care. Graphical abstract
Published: 2022

11. Epitope Spreading in Immune-Mediated Glomerulonephritis: The Expanding Target.

Author: Strizzi CT, Ambrogio M, Zanoni F, Bonerba B, Bracaccia ME, Grandaliano G, and Pesce F
Subjects: Humans, Glomerulonephritis, Membranous immunology, Animals, Lupus Nephritis immunology, Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis immunology, Autoantibodies immunology, Receptors, Phospholipase A2 immunology, Autoimmune Diseases immunology, Glomerulonephritis immunology, Epitopes immunology
Abstract: Epitope spreading is a critical mechanism driving the progression of autoimmune glomerulonephritis. This phenomenon, where immune responses broaden from a single epitope to encompass additional targets, contributes to the complexity and severity of diseases such as membranous nephropathy (MN), lupus nephritis (LN), and ANCA-associated vasculitis (AAV). In MN, intramolecular spreading within the phospholipase A2 receptor correlates with a worse prognosis, while LN exemplifies both intra- and intermolecular spreading, exacerbating renal involvement. Similarly, ANCA reactivity in AAV highlights the destructive potential of epitope diversification. Understanding these immunological cascades reveals therapeutic opportunities-targeting early epitope spreading could curb disease progression. Despite promising insights, the clinical utility of epitope spreading as a prognostic tool remains debated. This review provides a complete overview of the current evidence, exploring the dual-edged nature of epitope spreading, the intricate immune mechanisms behind it, and its therapeutic implications. By elucidating these dynamics, we aim to pave the way for more precise, targeted interventions in autoimmune glomerular diseases.
Published: 2024
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12. Potential Add-On Benefits of Dietary Intervention in the Treatment of Autosomal Dominant Polycystic Kidney Disease.

Author: Rosati E, Condello G, Tacente C, Mariani I, Tommolini V, Calvaruso L, Fulignati P, Grandaliano G, and Pesce F
Subjects: Humans, Disease Progression, Signal Transduction, TOR Serine-Threonine Kinases metabolism, Polycystic Kidney, Autosomal Dominant diet therapy, Polycystic Kidney, Autosomal Dominant therapy, Diet, Ketogenic methods, Caloric Restriction methods
Abstract: Autosomal dominant polycystic kidney disease (ADPKD) is the most common inherited cause of renal failure. The pathogenesis of the disease encompasses several pathways and metabolic alterations, including the hyperactivation of mTOR and suppression of AMPK signaling pathways, as well as mitochondrial dysfunction. This metabolic reprogramming makes epithelial cyst-lining cells highly dependent on glucose for energy and unable to oxidize fatty acids. Evidence suggests that high-carbohydrate diets may worsen the progression of ADPKD, providing the rationale for treating ADPKD patients with calorie restriction and, in particular, with ketogenic dietary interventions, already used for other purposes such as in overweight/obese patients or in the treatment of refractory epilepsy in children. Preclinical studies have demonstrated that calorie restriction may prevent and/or slow disease progression by inducing ketosis, particularly through increased beta-hydroxybutyrate (BHB) levels, which may modulate the metabolic signaling pathways altered in ADKPK. In these patients, although limited, ketogenic intervention studies have shown promising beneficial effects. However, larger and longer randomized controlled trials are needed to confirm their tolerability and safety in long-term maintenance and their additive role in the therapy of polycystic kidney disease.
Published: 2024
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13. Updates on C3 Glomerulopathy in Kidney Transplantation: Pathogenesis and Treatment Options.

Author: Bartoli G, Dello Strologo A, Grandaliano G, and Pesce F
Subjects: Humans, Graft Rejection etiology, Glomerulonephritis etiology, Glomerulonephritis drug therapy, Glomerulonephritis therapy, Mycophenolic Acid therapeutic use, Kidney Transplantation adverse effects, Complement C3 metabolism
Abstract: C3 glomerulopathy is a rare disease, characterized by an abnormal activation of the complement's alternative pathway that leads to the accumulation of the C3 component in the kidney. The disease recurs in more than half of kidney transplant recipients, with a significant impact on graft survival. Recurrence of the primary disease represents the second cause of graft loss after organ rejection. In C3 glomerulopathy, there are several risk factors which can promote a recurrence during transplantation, such as delayed graft function, infection and monoclonal gammopathy. All these events can trigger the alternative complement pathway. In this review, we summarize the impact of C3 glomerulopathy on kidney grafts and present the latest treatment options. The most widely used treatments for the disease include corticosteroids and mycophenolate mofetil, which are already used chronically by kidney transplant recipients; thus, additional treatments for C3 glomerulopathy are required. Currently, several studies using anti-complement drugs (i.e., eculizumab, Ravalizumab, avacopan) for C3 glomerulopathy in kidney transplant patients are ongoing with encouraging results.
Published: 2024
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14. A novel scenario in the therapeutic management of anemia of chronic kidney disease: placement and use of roxadustat.

Author: Locatelli F, Ravera M, Esposito C, Grandaliano G, Gesualdo L, and Minutolo R
Subjects: Humans, Prolyl-Hydroxylase Inhibitors therapeutic use, Treatment Outcome, Hematinics therapeutic use, Renal Insufficiency, Chronic complications, Renal Insufficiency, Chronic drug therapy, Anemia drug therapy, Anemia etiology, Glycine analogs & derivatives, Glycine therapeutic use, Isoquinolines therapeutic use, Hypoxia-Inducible Factor-Proline Dioxygenases antagonists & inhibitors
Abstract: Anemia is a frequent and early chronic kidney disease (CKD) complication. Its management is currently based on oral or intravenous iron supplements, erythropoiesis-stimulating agents, and red blood cell transfusions, when the benefits of transfusion outweigh the risks. Anemia in CKD patients is underdiagnosed and undertreated. Current standard of care is associated with challenges and therefore new treatment approaches have been sought. Hypoxia-inducible factor-prolyl-hydroxylase enzyme inhibitors are a new class of orally administered drugs used to treat anemia associated with CKD. Small-molecule hypoxia-inducible factor-prolyl-hydroxylase inhibitors have a novel mechanism of action that activates the hypoxia-inducible factor (oxygen-sensing) pathway resulting in a coordinated erythropoietic response, leading to increased endogenous erythropoietin production, improved iron absorption and transport, and reduced hepcidin. Roxadustat is the first hypoxia-inducible factor-prolyl-hydroxylase inhibitor approved by the European Medicines Agency (EMA) and reimbursed in Italy by the Italian Medicines Agency (AIFA) for the treatment of adult patients with symptomatic CKD-related anemia. This authorization was based on the outcome of a globally-conducted phase 3 clinical trial program comprising eight pivotal multicenter randomized studies. In the absence of up-to-date guidelines, we performed a critical appraisal of the placement and use of roxadustat in this therapeutic context., (© 2024. The Author(s) under exclusive licence to Italian Society of Nephrology.)
Published: 2024
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15. Fragility Fractures in End-Stage Chronic Kidney Disease (CKD) Population: Patient-Related and CKD-Related Factor Analysis-A Single-Center Experience.

Author: De Mauro D, De Luca G, Marino S, Smakaj A, Rovere G, Liuzza F, Covino M, Fulignati P, Grandaliano G, and El Ezzo O
Abstract: Background: Chronic kidney disease (CKD) stands as a prevalent global health concern, and mineral and bone disease are among the most impactful consequences. A severe complication arising from mineral and bone disease is the occurrence of fragility fractures, which disproportionately affect individuals with CKD compared to the general population. The prevalence of these fractures impacts both survival rates and quality of life. The aims of this study are analyzing and identifying (i) patient-related risk factors and (ii) CKD-related risk factors to contribute to the development of preventive measures for fragility fractures for this population. Methods: A retrospective, single-center observational study was conducted, encompassing patient data from the years 2021 to 2023. Registry data were recorded, including patient-related and CKD-related data. Patients were interviewed about traumatological history, and their answers were recorded. Logistic regression analysis was employed to investigate the association between independent variables and dependent variables. Results: Eighty-four patients, with a mean age of 64.3 ± 15.2 years and a male percentage of 58.3%, were included in this study. Among them, 19.5% exhibited smoking habits. The mean Charlson Comorbidity Index was 3.06 ± 1.21. All patients were diagnosed with end-stage chronic kidney disease, with mean durations of 208 months from the diagnosis and 84.5 months from the beginning of dialysis. The logistic regression analysis, adjusted for age, sex, and CCI, revealed that smoking habits play a significant role as a risk factor for fragility fractures in lower limbs ( p: 0.011 *). The incidence of fragility fractures increases directly proportionally to the time since diagnosis ( p -value: 0.021 *) and the beginning of dialysis treatment ( p -value: 0.001 *). Conclusions: Among patient-related factors, smoking habits seem to significantly affect lower-limb fracture rates ( p < 0.05), whereas among CKD-related factors, time since CKD diagnosis and time since the beginning of dialysis treatment are directly related to higher risks of fragility fractures. No relevant correlations emerged in the studied treatments, except for a reduction in proximal femur fracture occurrence when patients underwent a combined treatment of a calcimimetic and a vitamin D analog.
Published: 2024
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16. Consensus commentary and position of the Italian Society of Nephrology on KDIGO controversies conference on novel anemia therapies in chronic kidney disease.

Author: Locatelli F, Del Vecchio L, Esposito C, Gesualdo L, Grandaliano G, Ravera M, and Minutolo R
Subjects: Humans, Consensus, Hematinics therapeutic use, Italy, Prolyl-Hydroxylase Inhibitors therapeutic use, Societies, Medical, Renal Insufficiency, Chronic complications, Anemia drug therapy, Anemia etiology, Nephrology standards, Hypoxia-Inducible Factor-Proline Dioxygenases antagonists & inhibitors
Abstract: Hypoxia-inducible factor prolyl hydroxylase inhibitors (HIF-PHIs) are new drugs developed for the treatment of anemia associated with chronic kidney disease (CKD). This class of drugs stimulates endogenous erythropoietin production and, at the same time, improves iron absorption and mobilization of iron stores (less evident with daprodustat, vadadustat and enarodustat). Several studies have been published in the last few years showing that these agents are not inferior to standard therapy in correcting anemia associated with CKD. The efficacy of HIF-PHIs is coupled with a safety profile comparable to that of standard erythropoiesis stimulating agent (ESA) treatment. However, studies with HIF-PHIs were not long enough to definitively exclude the impact of new drugs on adverse events, such as cancer, death and possibly cardiovascular events, that usually occur after a long follow-up period. Kidney Disease: Improving Global Outcomes (KDIGO) recently reported the conclusions of the Controversies Conference on HIF-PHIs held in 2021. The goal of the present position paper endorsed by the Italian Society of Nephrology is to better adapt the conclusions of the latest KDIGO Conference on HIF-PHIs to the Italian context by reviewing the efficacy and safety of HIF-PHIs as well as their use in subpopulations of interest as emerged from more recent publications not discussed during the KDIGO Conference., (© 2024. The Author(s).)
Published: 2024
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17. Assessment and management of heart failure in patients with chronic kidney disease.

Author: Guaricci AI, Sturdà F, Russo R, Basile P, Baggiano A, Mushtaq S, Fusini L, Fazzari F, Bertandino F, Monitillo F, Carella MC, Simonini M, Pontone G, Ciccone MM, Grandaliano G, Vezzoli G, and Pesce F
Subjects: Humans, Biomarkers, Heart Failure therapy, Heart Failure drug therapy, Renal Insufficiency, Chronic complications, Renal Insufficiency, Chronic epidemiology
Abstract: Heart failure (HF) and chronic kidney disease (CKD) are two pathological conditions with a high prevalence in the general population. When they coexist in the same patient, a strict interplay between them is observed, such that patients affected require a clinical multidisciplinary and personalized management. The diagnosis of HF and CKD relies on signs and symptoms of the patient but several additional tools, such as blood-based biomarkers and imaging techniques, are needed to clarify and discriminate the main characteristics of these diseases. Improved survival due to new recommended drugs in HF has increasingly challenged physicians to manage patients with multiple diseases, especially in case of CKD. However, the safe administration of these drugs in patients with HF and CKD is often challenging. Knowing up to which values of creatinine or renal clearance each drug can be administered is fundamental. With this review we sought to give an insight on this sizable and complex topic, in order to get clearer ideas and a more precise reference about the diagnostic assessment and therapeutic management of HF and CKD., (© 2023. The Author(s).)
Published: 2024
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18. Effects of low-sodium bread on dietary compliance and fecal cultivable bacteria in a randomized controlled pilot trial in hypertensive subjects.

Author: Cosola C, Pesce F, De Angelis M, Maranzano V, Zito A, Montemurno E, Dalfino G, Loiudice S, Creanza V, Pompa G, Ciccone MM, Grandaliano G, Stallone G, and Gesualdo L
Abstract: High salt intake and compliance to low-sodium (LS) diets are critical in hypertension. Salt reduction in processed foods can help to achieve the target sodium intake. To verify the hypothesis that an innovative LS formulation of a traditional bread could result in a reduction of sodium intake and blood pressure, we performed a 6-month randomized controlled pilot trial on hypertensive patients. We additionally explored the effects of sodium restriction on blood pressure and fecal cultivable bacteria.Fifty-seven patients were randomized in three groups. Group A (n = 19) followed a free diet using standard bread (750 mg Na/100 g), group B (n = 18) followed a LS diet (2300 mg Na/die) using standard bread, group C (n = 20) followed a LS diet (2300 mg Na/die) using LS bread (280 mg Na/100 g). We measured 24-h urinary sodium, blood pressure, routine parameters, fecal microbial counts (26 patients).After 6 months, as compared to group A, group C showed a reduction of 24-h urinary sodium excretion (-908 mg/24 h), diastolic pressure (-9 mmHg) and microbial counts of Bacteroides, Porphyromonas, Prevotella, Enterobacteriaceae, Staphylococcus, Micrococcus. These results suggest that LS bread could increase the adherence to a LS diet, reducing sodium excretion, diastolic pressure and abundance of some fecal cultivable bacteria.Trial registration Registration nr. NCT03127553, on 25/04/2017., (© 2024. The Author(s).)
Published: 2024
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19. Immunosuppressive therapy and oral anticoagulation in kidney transplant recipients: Direct oral anticoagulants versus vitamin-k antagonists.

Author: Santoro F, Casanova A, Simone S, Alfieri C, Falcone A, Dello Strologo A, Grandinetti V, Busutti M, Comai G, Marvulli TM, Zippo MG, Castellano G, La Manna G, Gesualdo L, Giuseppe G, and Pesce F
Subjects: Humans, Tacrolimus therapeutic use, Anticoagulants adverse effects, Fibrinolytic Agents therapeutic use, Vitamins therapeutic use, Administration, Oral, Vitamin K, Kidney Transplantation, Cyclosporins therapeutic use, Atrial Fibrillation drug therapy
Abstract: Background: direct oral anticoagulants (DOACs) are an alternative to conventional antagonist of vitamin-K (AVK). However, immune suppressive drugs (ISDs) may interfere with DOACs pharmacokinetic., Aim of This Study: evaluate safety and efficacy profile of DOACs compared to AVK in kidney transplant recipients (KTRs) treated with ISDs., Methods: a multi-center study from 4 Italian University hospitals enrolling consecutive KTRs on DOACs or AVK was carried out. Sixty-six patients on DOACs were compared with fifty patients on AVK with similar clinical features. Serial evaluation of renal function and serum levels of ISDs during 18 months follow-up (FU) was performed., Results: Mean age of DOACs patients was 67±9 and mean eGFR was 58,3± 30,4mL/min/1.73m 2 . ISDs included tacrolimus (n=47, 71%), cyclosporin (n=13, 20%), everolimus (n=10, 7%) and sirolimus (n=4, 6%). After 14 days of DOACs therapy initiation there was a slight increase of serum levels of tacrolimus (+0.19±0.67 p=0.80) and cyclosporine (+0.12±0.25 p=0.94) not statistically significant. Levels of Tacrolimus and cyclosporin were stable at serial evaluation during 18-months follow-up. There were no thromboembolic events among patients treated with DOACs or AVK and no differences in term of major bleeding (6% vs 4% p=0.69), at long-term follow-up. There was no difference in term of eGFR decline from start therapy to 18 months FU between DOACs vs AVK therapy (-3.9±1 vs -3.8±2 p=0.82)., Conclusion: DOACs have similar safety and efficacy than AVK among KTRs treated with ISDs. However, careful evaluation of potential drug interaction and ISDs serum levels is needed., Competing Interests: Declaration of Competing Interest The authors declare they have no conflict of interest. The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 European Federation of Internal Medicine. Published by Elsevier B.V. All rights reserved.)
Published: 2024
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20. COVID-19: The Dysregulated Response to Infection - Why Consider Polymethylmethacrylate Membrane in Hemodialysis Patients?

Author: Spasiano A, De Luca G, Bartoli G, Dello Strologo A, Arena M, and Grandaliano G
Subjects: Humans, SARS-CoV-2, Polymethyl Methacrylate, Renal Dialysis, Cytokines, COVID-19 complications, COVID-19 therapy, Respiratory Distress Syndrome etiology, Respiratory Distress Syndrome therapy
Abstract: Since SARS-CoV-2 spread through China at the end of 2019, COVID-19 has been probably the most difficult challenge in the last decades for healthcare systems all around the world, still representing a danger for fragile patients with different comorbidities. Chronic dialysis patients affected by COVID-19 experienced severe disease with a higher mortality rate compared to the general population. Morbidity and mortality of this severe acute respiratory syndrome depend on both acute respiratory failure and systemic immunological involvement with consequent inflammation-mediated injury. Indeed, the most important determining factor of COVID-19 severity is the strength of the so-called "cytokine storm" associated with SARS-CoV-2 infection. Therefore, this severe infection varies clinically from an asymptomatic condition to a generalized and violent inflammatory response and acute respiratory distress syndrome, with consequent pulmonary interstitial edema and a high risk of multi-organ failure. The use of extracorporeal therapies targeting cytokine clearance to improve patients' outcomes has been widely debated, especially in end-stage kidney disease's patients on maintenance dialysis or in individuals affected by acute kidney injury admitted to intensive care units. Different studies were conducted to demonstrate how specific dialyzers could decrease the COVID-19 inflammatory state. The aim of this narrative review was to summarize main studies about this topic, focusing primarily on the role of polymethylmethacrylate dialyzer and underlining pros and cons of this sorbent., (© 2023 S. Karger AG, Basel.)
Published: 2024
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21. Underlying Genetics of aHUS: Which Connection with Outcome and Treatment Discontinuation?

Author: Spasiano A, Palazzetti D, Dimartino L, Bruno F, Baccaro R, Pesce F, and Grandaliano G
Subjects: Humans, Mutation, Atypical Hemolytic Uremic Syndrome genetics, Thrombotic Microangiopathies complications, Kidney Failure, Chronic complications, Acute Kidney Injury complications
Abstract: Atypical hemolytic uremic syndrome (aHUS) is a rare disease caused by a genetic dysregulation of the alternative complement pathway, characterized by thrombocytopenia, hemolytic anemia, and acute kidney injury, and included in the group of thrombotic microangiopathies. With the introduction of humanized monoclonal antibodies that inhibit C5 activation, the natural history of aHUS completely changed, with a better prognosis, a quick recovery of renal function, and a significant reduction of end-stage renal disease incidence. Nowadays, there is an increasing interest in the molecular and genetic bases of this severe disease. The aim of this narrative review is to provide readers with a practical guide about different possible involved genes, elucidating the specific role of each transcribed protein in the pathogenesis of aHUS. Moreover, we analyzed the main current evidence about the relationship among genetic mutations, outcomes, and the risk of recurrence of this manifold disease.
Published: 2023
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22. Prevalence, incidence, and treatment of anaemia in patients with non-dialysis-dependent chronic kidney disease: findings from a retrospective real-world study in Italy.

Author: Minutolo R, Grandaliano G, Di Rienzo P, Snijder R, Degli Esposti L, Perrone V, and Todorova L
Subjects: Adult, Humans, Retrospective Studies, Prevalence, Incidence, Hemoglobins, Iron therapeutic use, Italy epidemiology, Anemia diagnosis, Anemia epidemiology, Anemia therapy, Renal Insufficiency, Chronic complications, Renal Insufficiency, Chronic epidemiology, Renal Insufficiency, Chronic therapy, Hematinics therapeutic use
Abstract: Background: Limited data are available on the epidemiology and clinical management of anaemia in patients with non-dialysis-dependent chronic kidney disease (NDD-CKD)., Methods: This retrospective observational study was based on records from databases of five Local Health Units across Italy. Adults with reported NDD-CKD stage 3a-5 between 1 January 2014 and 31 December 2016 were identified. Annual prevalence and incidence of anaemia (age- and sex-standardised) and clinical management (erythropoiesis-stimulating agents [ESAs], intravenous [IV] iron, and blood transfusions) were evaluated. Eligibility for ESAs was defined by ≥ 2 records of Hb < 10 g/dL, or < 11 g/dL over 6 months., Results: Overall, 101,143 individuals with NDD-CKD (3a-5) recorded between 2014 and 2016 were identified, of whom 40,020 (39.6%) were anaemic. Prevalence of anaemia was 33.8% in 2016 and incidence of anaemia was stable (11.4-12.4%) from 2014 to 2016. Prevalence and incidence of anaemia increased with CKD stage. Among eligible patients, 12.8% with Hb < 11 g/dL and 15.5% with Hb < 10 g/dL received ESAs, and the proportion treated increased with CKD stage. Among ESA-treated patients with at least 2 years of follow up, 18.4% and 19.3% received IV iron in the Hb < 11 and < 10 g/dL groups, respectively, and 16.5% and 19.4% received blood transfusions. Corresponding proportions for the overall anaemic cohort were 9.0% and 11.3%, respectively., Conclusions: Anaemia is a significant issue in patients with NDD-CKD. Low rates of ESA treatment indicate a potential treatment gap and suggest that anaemia may not be adequately controlled in many patients., (© 2022. The Author(s).)
Published: 2023
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23. Risk of end-stage kidney disease in kidney transplant recipients versus patients with native chronic kidney disease: multicentre unmatched and propensity-score matched analyses.

Author: De Nicola L, Serra R, Provenzano M, Minutolo R, Michael A, Ielapi N, Federico S, Carrano R, Bellizzi V, Garofalo C, Iodice C, Borrelli S, Grandaliano G, Stallone G, Gesualdo L, Chiodini P, and Andreucci M
Subjects: Adult, Humans, Disease Progression, Glomerular Filtration Rate, Kidney Transplantation adverse effects, Kidney Failure, Chronic etiology, Renal Insufficiency, Chronic complications, Renal Insufficiency, Chronic epidemiology, Diabetes Mellitus
Abstract: Background: In kidney transplant recipients (KTR), the end-stage kidney disease (ESKD) risk dependent on the risk factors acting in native chronic kidney disease (CKD) remains undefined., Methods: We compared risk and determinants of ESKD between 757 adult KTR and 1940 patients with native CKD before and after propensity-score (PS) analysis matched for unmodifiable risk factors [(age, sex, diabetes, cardiovascular disease and estimated glomerular filtration rate (eGFR)]., Results: In unmatched cohorts, eGFR was lower in CKD versus KTR (45.9 ± 11.3 versus 59.2 ± 13.4 mL/min/1.73 m2, P < 0.001). During a median follow-up of 5.4 years, the unadjusted cumulative incidence of ESKD was consistently lower in unmatched KTR versus CKD. Conversely, in PS-matched analysis, the risk of ESKD in KTR was 78% lower versus CKD at 1 year of follow-up while progressively increased over time resulting similar to that of native CKD patients after 5 years and 2.3-fold higher than that observed in CKD at 10 years. R2 analysis in unmatched patients showed that the proportion of the outcome variance explained by traditional ESKD determinants was smaller in KTR versus native CKD (31% versus 70%). After PS matching, the risk of ESKD [hazard ratio (HR), 95% confidence interval (95% CI)] was significantly associated with systolic blood pressure (1.02, 1.01-1.02), phosphorus (1.31, 1.05-1.64), 24-h proteinuria (1.11, 1.05-1.17) and haemoglobin (0.85, 0.78-0.93) irrespective of KTR status. Similar data were obtained after matching also for modifiable risk factors., Conclusions: In KTR, when compared with matched native CKD patients, the risk of ESKD is lower in the first 5 years and higher later on. Traditional determinants of ESKD account for one-third of the variability of time-to-graft failure., (© The Author(s) 2022. Published by Oxford University Press on behalf of the ERA.)
Published: 2023
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24. Eradication of HCV by direct antiviral agents restores mitochondrial function and energy homeostasis in peripheral blood mononuclear cells.

Author: Villani R, Sangineto M, Pontrelli P, Bellanti F, Bukke VN, Moola A, Gesualdo L, Vendemiale G, Grandaliano G, Stallone G, and Serviddio G
Subjects: Humans, Antiviral Agents pharmacology, Antiviral Agents therapeutic use, Leukocytes, Mononuclear, Homeostasis, Mitochondria, Hepacivirus, Hepatitis C drug therapy
Abstract: Hepatitis C virus (HCV) adopts several immune evasion mechanisms such as interfering with innate immunity or promoting T-cell exhaustion. However, the recent direct-antiviral agents (DAAs) rapidly eliminate the virus, and the repercussions in terms of immune system balance are unknown. Here we compared the PBMCs transcriptomic profile of patients with HCV chronic infection at baseline (T0) and 12 weeks after the end of the therapy (SVR12) with DAAs. 3862 genes were differently modulated, identifying oxidative phosphorylation as the top canonical pathway differentially activated. Therefore, we dissected PBMCs bioenergetic profile by analyzing mitochondrial respiration and glycolysis at 4 timepoints: T0, 4 weeks of therapy, end of therapy (EoT), and SVR12. Maximal and reserve respiratory capacity considerably increased at EoT, persisting until SVR12. Notably, over time a significant increase was observed in respiratory chain (RC) complexes protein levels and the enzymatic activity of complexes I, II, and IV. Mitochondrial-DNA integrity improved over time, and the expression of mitochondrial biogenesis key regulators such as TFAM, Nrf-1, and PPARGC1A significantly increased at SVR12; hence, RC complexes synthesis and mitochondrial respiration were supported after treatment. HCV clearance with DAAS profoundly changed PBMCs bioenergetic profile, suggesting the immunometabolism study as a new approach to the understanding of viral immune evasion mechanisms and host adaptations during infections and therapies., (© 2022 Federation of American Societies for Experimental Biology.)
Published: 2022
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25. Increased Complement Gene Expression in Circulating B Cells From Kidney Transplant Recipients With Chronic Antibody-Mediated Rejection.

Author: Cravedi P, Bruschi M, Pontrelli P, Grandaliano G, Zaza G, and Fribourg M
Published: 2022
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26. Extracellular vesicles derived from patients with antibody-mediated rejection induce tubular senescence and endothelial to mesenchymal transition in renal cells.

Author: Franzin R, Stasi A, Sallustio F, Bruno S, Merlotti G, Quaglia M, Grandaliano G, Pontrelli P, Thurman JM, Camussi G, Stallone G, Cantaluppi V, Gesualdo L, and Castellano G
Subjects: Endothelial Cells metabolism, Epithelial Cells metabolism, Humans, RNA, Messenger metabolism, Extracellular Vesicles metabolism, MicroRNAs genetics
Abstract: Extracellular vesicles (EV) are emerging mediators in several diseases. However, their role in the pathophysiology of antibody-mediated allograft rejection (AMR) has been poorly investigated. Here, we investigated the role of EV isolated from AMR patients in inducing tubular senescence and endothelial to mesenchymal transition (EndMT) and analyzed their miRNA expression profile. By multiplex bead flow cytometry, we characterized the immunophenotype of plasma AMR-derived EV and found a prevalent platelet and endothelial cell origin. In vitro, AMR-derived EV induced tubular senescence by upregulating SA-β Gal and CDKN1A mRNA. Furthermore, AMR-derived EV induced EndMT. The occurrence of tubular senescence and EndMT was confirmed by analysis of renal biopsies from the same AMR patients. Moreover, AMR-derived EV induced C3 gene upregulation and CFH downregulation in tubular epithelial cells, with C4d deposition on endothelial cells. Interestingly, RNase-mediated digestion of EV cargo completely abrogated tubular senescence and EndMT. By microarray analysis, miR-604, miR-515-3p, miR-let-7d-5p, and miR-590-3p were significantly upregulated in EV from AMR group compared with transplant controls, whereas miR-24-3p and miR-29a-3p were downregulated. Therefore, EV-associated miRNA could act as active player in AMR pathogenesis, unraveling potential mechanisms of accelerated graft senescence, complement activation and early fibrosis that might lead to new therapeutic intervention., (© 2022 The Authors. American Journal of Transplantation published by Wiley Periodicals LLC on behalf of The American Society of Transplantation and the American Society of Transplant Surgeons.)
Published: 2022
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27. Can SGLT2 inhibitors answer unmet therapeutic needs in chronic kidney disease?

Author: De Nicola L, Cozzolino M, Genovesi S, Gesualdo L, Grandaliano G, and Pontremoli R
Subjects: Albuminuria, Humans, Kidney, Diabetes Mellitus, Type 2 drug therapy, Renal Insufficiency, Chronic complications, Renal Insufficiency, Chronic drug therapy, Sodium-Glucose Transporter 2 Inhibitors pharmacology, Sodium-Glucose Transporter 2 Inhibitors therapeutic use
Abstract: Chronic kidney disease (CKD) is a global health problem, affecting more than 850 million people worldwide. The number of patients receiving renal replacement therapy (dialysis or renal transplantation) has increased over the years, and it has been estimated that the number of people receiving renal replacement therapy will more than double from 2.618 million in 2010 to 5.439 million in 2030, with wide differences among countries. The main focus of CKD treatment has now become preserving renal function rather than replacing it. This is possible, at least to some extent, through the optimal use of multifactorial therapy aimed at preventing end-stage kidney disease and cardiovascular events. Sodium/glucose cotransporter 2 inhibitors (SGLT2i) reduce glomerular hypertension and albuminuria with beneficial effects on progression of renal damage in both diabetic and non-diabetic CKD. SGLT2 inhibitors also show great benefits in cardiovascular protection, irrespective of diabetes. Therefore, the use of these drugs will likely be extended to the whole CKD population as a new standard of care., (© 2022. The Author(s).)
Published: 2022
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28. Crystal-induced colitis.

Author: Spasiano A, Castri F, Giustiniani MC, Riccioni ME, Naticchia A, Grandaliano G, and Panocchia N
Subjects: Humans, Colitis chemically induced
Published: 2022
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29. Pre-Transplant Expression of CCR-2 in Kidney Transplant Recipients Is Associated With the Development of Delayed Graft Function.

Author: Pontrelli P, Simone S, Rascio F, Pesce F, Conserva F, Infante B, Castellano G, Sallustio F, Fiorentino M, Zaza G, Gallone A, Battaglia M, Ditonno P, Stallone G, Gesualdo L, and Grandaliano G
Subjects: Epidermal Growth Factor, Humans, Receptors, Chemokine, Risk Factors, Delayed Graft Function, Kidney Transplantation adverse effects, Kidney Transplantation methods
Abstract: Background: Delayed graft function (DGF) leads to a reduced graft survival. Donors' features have been always considered as key pathogenic factors in this setting. The aim of our study was to evaluate the recipients' characteristics in the development of DGF., Methods: We enrolled 932 kidney graft recipients from 466 donors; 226 recipients experienced DGF. In 290 donors, both recipients presented with early graft function (EGF, group A), in 50 both recipients experienced DGF (group B), and in 126 one recipient presented with DGF and the other with EGF (group C). In group C, we selected 7 couples of DGF/EGF recipients and we evaluated the transcriptomic profile by microarray on circulating mononuclear cells harvested before transplantation. Results were validated by qPCR in an independent group of 25 EGF/DGF couples., Findings: In the whole study group, DGF was associated with clinical characteristics related to both donors and recipient. In group C, DGF was significantly associated with body mass index, hemodialysis, and number of mismatches. In the same group, we identified 411 genes differently expressed before transplantation between recipients discordant for the transplant outcome. Those genes were involved in immune dysfunction and inflammation. In particular, we observed a significant increase in DGF patients in the expression of C-C chemokine receptor type 2 (CCR2), the monocyte chemoattractant protein-1 (MCP-1) receptor. CCR-2 upregulation was confirmed in an independent cohort of patients., Conclusions: Our results suggest that recipients' clinical/immunological features, potentially modulated by dialysis, are associated with the development of DGF independently of donors' features., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Pontrelli, Simone, Rascio, Pesce, Conserva, Infante, Castellano, Sallustio, Fiorentino, Zaza, Gallone, Battaglia, Ditonno, Stallone, Gesualdo and Grandaliano.)
Published: 2022
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30. On-line hemodiafiltration modulates atherosclerosis signaling in peripheral lymphomonocytes of hemodialysis patients.

Author: Simone S, Chieti A, Pontrelli P, Rascio F, Castellano G, Stallone G, Infante B, Gesualdo L, Grandaliano G, and Pertosa G
Subjects: Cross-Sectional Studies, Humans, Leukocytes, Mononuclear, Renal Dialysis, Vascular Endothelial Growth Factor C, Atherosclerosis diagnosis, Atherosclerosis genetics, Hemodiafiltration
Abstract: Background: Hemodialysis patients present a dramatic increase in cardiovascular morbidity/mortality. Circulating immune cells, activated by both uremic milieu and dialysis, play a key role in the pathogenesis of dialysis-related vascular disease. The aim of our study was to identify, through a high-throughput approach, differences in gene expression profiles in the peripheral blood mononuclear cells (PBMCs) of patients treated with on-line hemodiafiltration and bicarbonate hemodialysis., Methods: The transcriptomic profile was investigated in PBMCs isolated from eight patients on on-line hemodiafiltration and eight patients on bicarbonate hemodialysis by microarray analysis. The results were evaluated by statistical and functional pathway analysis and validated by real time PCR (qPCR) in an independent cohort of patients (on-line hemodiafiltration N = 20, bicarbonate hemodialysis n = 20)., Results: Eight hundred and forty-seven genes were differentially expressed in patients treated with on-line hemodiafiltration and bicarbonate hemodialysis. Thirty-seven functional gene networks were identified and atherosclerosis signaling was the top canonical pathway regulated by on-line hemodiafiltration. Among the genes of this pathway, on-line hemodiafiltration was associated with a reduced expression of Platelet-derived growth factor A chain (PDGF A), Clusterin, Monoamine Oxidase A, Interleukin-6 (IL-6) and Vascular Endothelial Growth Factor C (VEGF-)C and with an increase of Apolipoprotein E. qPCR confirmed the microarray results. Platelet derived growth factor AA (PDGF-AA), IL-6 and VEGF-C serum levels were significantly lower in the on-line hemodiafiltration group. Finally, 10 patients previously on bicarbonate hemodialysis were switched to on-line hemodiafiltration and PBMCs were harvested after 6 months. The qPCR results from this perspective group confirmed the modulation of atherosclerotic genes observed in the cross-sectional analysis., Conclusions: Our data suggest that type of dialysis (on-line hemodiafiltration versus bicarbonate hemodialysis) may modulate the expression of several genes involved in the pathogenesis of atherosclerotic disease., (© 2021. The Author(s).)
Published: 2021
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31. Emerging biomarkers of delayed graft function in kidney transplantation.

Author: Mezzolla V, Pontrelli P, Fiorentino M, Stasi A, Pesce F, Franzin R, Rascio F, Grandaliano G, Stallone G, Infante B, Gesualdo L, and Castellano G
Subjects: Biomarkers, Delayed Graft Function epidemiology, Delayed Graft Function etiology, Graft Rejection epidemiology, Graft Rejection etiology, Graft Survival, Humans, Kidney, Risk Factors, Tissue Donors, Kidney Transplantation adverse effects
Abstract: Delayed Graft Function (DGF) is one of the most common early complications in kidney transplantation, associated with poor graft outcomes, prolonged post-operative hospitalization and higher rejection rates. Given the severe shortage of high-quality organs for transplantation, DGF incidence is expected to raise in the next years because of the use of nonstandard kidneys from Extended Criteria Donors (ECD) and from Donors after Circulatory Death (DCD). Alongside conventional methods for the evaluation of renal allograft [e.g. serum creatinine Glomerular Filtration Rate (GFR), needle biopsy], recent advancements in omics technologies, including proteomics, metabolomics and transcriptomics, may allow to discover novel biomarkers associated with DGF occurrence, in order to identify early preclinical signs of renal dysfunction and to improve the quality of graft management. Here, we gather contributions from basic scientists and clinical researchers to describe new omics studies in renal transplantation, reporting the emerging biomarkers of DGF that may implement and improve conventional approaches., (Copyright © 2021. Published by Elsevier Inc.)
Published: 2021
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31 results on '"Grandaliano G"'

1. Clinical and Economic Impact of Early Diagnosis of Chronic Kidney Disease in General Practice: The Endorse Study

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

4. Risk of end-stage kidney disease in kidney transplant recipients versus patients with native chronic kidney disease: multicentre unmatched and propensity-score matched analyses

5. Eradication of HCV by direct antiviral agents restores mitochondrial function and energy homeostasis in peripheral blood mononuclear cells

6. Increased Complement Gene Expression in Circulating B Cells From Kidney Transplant Recipients With Chronic Antibody-Mediated Rejection

7. New-onset anemia and associated risk of ESKD and death in non-dialysis CKD patients: A multicohort observational study

8. Can SGLT2 inhibitors answer unmet therapeutic needs in chronic kidney disease?

9. Crystal-induced colitis

10. Can SGLT2 inhibitors answer unmet therapeutic needs in chronic kidney disease?

11. Epitope Spreading in Immune-Mediated Glomerulonephritis: The Expanding Target.

12. Potential Add-On Benefits of Dietary Intervention in the Treatment of Autosomal Dominant Polycystic Kidney Disease.

13. Updates on C3 Glomerulopathy in Kidney Transplantation: Pathogenesis and Treatment Options.

14. A novel scenario in the therapeutic management of anemia of chronic kidney disease: placement and use of roxadustat.

15. Fragility Fractures in End-Stage Chronic Kidney Disease (CKD) Population: Patient-Related and CKD-Related Factor Analysis-A Single-Center Experience.

16. Consensus commentary and position of the Italian Society of Nephrology on KDIGO controversies conference on novel anemia therapies in chronic kidney disease.

17. Assessment and management of heart failure in patients with chronic kidney disease.

18. Effects of low-sodium bread on dietary compliance and fecal cultivable bacteria in a randomized controlled pilot trial in hypertensive subjects.

19. Immunosuppressive therapy and oral anticoagulation in kidney transplant recipients: Direct oral anticoagulants versus vitamin-k antagonists.

20. COVID-19: The Dysregulated Response to Infection - Why Consider Polymethylmethacrylate Membrane in Hemodialysis Patients?

21. Underlying Genetics of aHUS: Which Connection with Outcome and Treatment Discontinuation?

22. Prevalence, incidence, and treatment of anaemia in patients with non-dialysis-dependent chronic kidney disease: findings from a retrospective real-world study in Italy.

23. Risk of end-stage kidney disease in kidney transplant recipients versus patients with native chronic kidney disease: multicentre unmatched and propensity-score matched analyses.

24. Eradication of HCV by direct antiviral agents restores mitochondrial function and energy homeostasis in peripheral blood mononuclear cells.

25. Increased Complement Gene Expression in Circulating B Cells From Kidney Transplant Recipients With Chronic Antibody-Mediated Rejection.

26. Extracellular vesicles derived from patients with antibody-mediated rejection induce tubular senescence and endothelial to mesenchymal transition in renal cells.

27. Can SGLT2 inhibitors answer unmet therapeutic needs in chronic kidney disease?

28. Crystal-induced colitis.

29. Pre-Transplant Expression of CCR-2 in Kidney Transplant Recipients Is Associated With the Development of Delayed Graft Function.

30. On-line hemodiafiltration modulates atherosclerosis signaling in peripheral lymphomonocytes of hemodialysis patients.

31. Emerging biomarkers of delayed graft function in kidney transplantation.

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31 results on '"Grandaliano G"'

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