Search

Your search keyword '"Magistroni R"' showing total 9 results
Start Over Author "Magistroni R" Topic adult
9 results on '"Magistroni R"'

1. Is there long-term value of pathology scoring in immunoglobulin A nephropathy? A validation study of the Oxford Classification for IgA Nephropathy (VALIGA) update

Author

Coppo, R., D'Arrigo, G., Tripepi, G., Russo, M. L., Roberts, I. S. D., Bellur, S., Cattran, D., Cook, T. H., Feehally, J., Tesar, V., Maixnerova, D., Peruzzi, L., Amore, A., Lundberg, S., Di Palma, A. M., Gesualdo, L., Emma, F., Rollino, C., Praga, M., Biancone, L., Pani, A., Feriozzi, S., Polci, R., Barratt, J., Del Vecchio, L., Locatelli, F., Pierucci, A., Caliskan, Y., Perkowska-Ptasinska, A., Durlik, M., Moggia, E., Ballarin, J. C., Wetzels, J. F. M., Goumenos, D., Papasotiriou, M., Galesic, K., Toric, L., Papagianni, A., Stangou, M., Benozzi, L., Cusinato, S., Berg, U., Topaloglu, R., Maggio, M., Ots-Rosenberg, M., D'Amico, M., Geddes, C., Balafa, O., Quaglia, M., Cravero, R., Cirami, C. L., Fellstrom, B., Floege, J., Egido, J., Mallamaci, F., Zoccali, C., Fuiano, L., Beltrame, G., Camilla, R., Segoloni, G., Colla, L., Angioi, A., Piras, L., Cancarini, G., Ravera, S., Ballarin, J., Di Giulio, S., Pugliese, F., Serriello, I., Sever, M., Kilicaslan, I., Peters, H., Carvalho, F., Da Costa Ferreira, A. C., Wiecek, A., Magistroni, R., Bilginer, Y., Giacchino, F., Papastirou, M., Siamopoulos, K., Galliani, M., Stratta, P., Bergia, R., Salvadori, M., Cirami, L., Kloster Smerud, H., Ferrario, F., Stellato, T., Martin, C., Eitner, F., Rauen, T., Lupo, A., Bernich, P., Mene, P., Morosetti, M., Van Kooten, C., Rabelink, T., Reinders, M. E. J., Boria Grinyo, J. M., Savoldi, S., Licata, C., Mizerska-Wasiak, M., Roszkowska-Blaim, M., Martina, G., Messuerotti, A., Dal Canton, A., Esposito, C., Migotto, C., Triolo, G., Mariano, F., Pozzi, C., Boero, R., Mazzucco, G., Giannakakis, C., Honsova, E., Sundelin, B., Gutierrez, E., Asunis, A. M., Tardanico, R., Arce Terroba, J., Fortunato, M., Pantzaki, A., Ozluk, Y., Steenbergen, E., Soderberg, M., Riispere, Z., Furci, L., Orhan, D., Kipgen, D., Casartelli, D., Galesic Ljubanovic, D., Akiopoulou, H., Bertoni, E., Cannata Ortiz, P., Karkoszka, H., Groene, H. J., Stoppacciaro, A., Bajema, I., Bruijn, J., Fulladosa Oliveras, X., Maldyk, J., Ioachim, E., and Internal Medicine

Subjects
Adult, Male, Pathology, medicine.medical_specialty, Adolescent, 030232 urology & nephrology, Renal function, 030204 cardiovascular system & hematology, Kidney, Nephropathy, Cohort Studies, 03 medical and health sciences, Glomerulonephritis, 0302 clinical medicine, renal biopsy, Interquartile range, IgA nephropathy, progression, risk factors, Child, Disease Progression, Female, Follow-Up Studies, Glomerular Filtration Rate, Glomerulonephritis, IGA, Humans, Prognosis, Medicine, Endocapillary hypercellularity, IGA, Transplantation, medicine.diagnostic_test, business.industry, medicine.disease, medicine.anatomical_structure, Renal pathology, Nephrology, Cohort, Renal biopsy, Renal disorders Radboud Institute for Health Sciences [Radboudumc 11], business
Abstract

Background It is unknown whether renal pathology lesions in immunoglobulin A nephropathy (IgAN) correlate with renal outcomes over decades of follow-up. Methods In 1130 patients of the original Validation Study of the Oxford Classification for IgA Nephropathy (VALIGA) cohort, we studied the relationship between the MEST score (mesangial hypercellularity, M; endocapillary hypercellularity, E; segmental glomerulosclerosis, S; tubular atrophy/interstitial fibrosis, T), crescents (C) and other histological lesions with both a combined renal endpoint [50% estimated glomerular filtration rate (eGFR) loss or kidney failure] and the rate of eGFR decline over a follow-up period extending to 35 years [median 7 years (interquartile range 4.1–10.8)]. Results In this extended analysis, M1, S1 and T1–T2 lesions as well as the whole MEST score were independently related with the combined endpoint (P Conclusion Long-term follow-up analyses of the VALIGA cohort showed that the independent relationship between kidney biopsy findings and the risk of progression towards kidney failure in IgAN remains unchanged across all age groups and decades after the renal biopsy.

Published
2020
Full Text
View/download PDF

2. Quantifying duration of proteinuria remission and association with clinical outcome in IgA nephropathy

Author

Canney, M., Barbour, S. J., Zheng, Y., Coppo, R., Zhang, H., Liu, Z. -H., Matsuzaki, K., Suzuki, Y., Katafuchi, R., Reich, H. N., Cattran, D., Russo, M. L., Troyanov, S., Cook, H. T., Roberts, I., Tesar, V., Maixnerova, D., Lundberg, S., Gesualdo, L., Emma, F., Fuiano, L., Beltrame, G., Rollino, C., Amore, A., Camilla, R., Peruzzi, L., Praga, M., Feriozzi, S., Polci, R., Segoloni, G., Colla, L., Pani, A., Piras, D., Angioi, A., Cancarini, G., Ravera, S., Durlik, M., Moggia, E., Ballarin, J., Di Giulio, S., Pugliese, F., Serriello, I., Caliskan, Y., Sever, M., Kilicaslan, I., Locatelli, F., Del Vecchio, L., Wetzels, J. F. M., Peters, H., Berg, U., Carvalho, F., da Costa Ferreira, A. C., Maggio, M., Wiecek, A., Ots-Rosenberg, M., Magistroni, R., Topaloglu, R., Bilginer, Y., D'Amico, M., Stangou, M., Giacchino, F., Goumenos, D., Kalliakmani, P., Gerolymos, M., Galesic, K., Geddes, C., Siamopoulos, K., Balafa, O., Galliani, M., Stratta, P., Quaglia, M., Bergia, R., Cravero, R., Salvadori, M., Cirami, L., Fellstrom, B., Kloster Smerud, H., Ferrario, F., Stellato, T., Egido, J., Martin, C., Floege, J., Eitner, F., Lupo, A., Bernich, P., Mene, P., Morosetti, M., van Kooten, C., Rabelink, T., Reinders, M. E. J., Boria Grinyo, J. M., Cusinato, S., Benozzi, L., Savoldi, S., Licata, C., Mizerska-Wasiak, M., Martina, G., Messuerotti, A., Dal Canton, A., Esposito, C., Migotto, C., Triolo, G., Mariano, F., Pozzi, C., Boero, R., Bellur, S., Mazzucco, G., Giannakakis, C., Honsova, E., Sundelin, B., Di Palma, A. M., Gutierrez, E., Asunis, A. M., Barratt, J., Tardanico, R., Perkowska-Ptasinska, A., Arce Terroba, J., Fortunato, M., Pantzaki, A., Ozluk, Y., Steenbergen, E., Soderberg, M., Riispere, Z., Furci, L., Orhan, D., Kipgen, D., Casartelli, D., Galesic Ljubanovic, D., Gakiopoulou, H., Bertoni, E., Cannata Ortiz, P., Karkoszka, H., Groene, H. J., Stoppacciaro, A., Bajema, I., Bruijn, J., Fulladosa Oliveras, X., Maldyk, J., Ioachim, E., Bavbek, N., Cook, T., Alpers, C., Feehally, J., Berthoux, F., Bonsib, S., D'Agati, V., D'Amico, G., Emancipator, S., Emmal, F., Fervenza, F., Florquin, S., Fogo, A., Groene, H., Haas, M., Hill, P., Hogg, R., Hsu, S., Hunley, T., Hladunewich, Jennette, C., Joh, K., Julian, B., Kawamura, T., Lai, F., Leung, C., Li, L., Li, P., Liu, Z., Massat, A., Mackinnon, B., Mezzano, S., Schena, F., Tomino, Y., Walker, P., Wang, H., Weening, J., Yoshikawa, N., Zeng, C. -H., Shi, S., Nogi, C., Suzuki, H., Koike, K., Hirano, K., Yokoo, T., Hanai, M., Fukami, K., Takahashi, K., Yuzawa, Y., Niwa, M., Yasuda, Y., Maruyama, S., Ichikawa, D., Suzuki, T., Shirai, S., Fukuda, A., Fujimoto, S., Trimarchi, H., Anesthesiology, Pathology, Graduate School, ACS - Heart failure & arrhythmias, and ACS - Atherosclerosis & ischemic syndromes

Subjects
Male, Time Factors, glomerular disease, 030232 urology & nephrology, 030204 cardiovascular system & hematology, Gastroenterology, 0302 clinical medicine, Outcome Assessment, Health Care, Clinical endpoint, Medicine, Clinical Epidemiology, Proteinuria, medicine.diagnostic_test, Remission Induction, Hazard ratio, IgA nephropathy, General Medicine, Middle Aged, end stage kidney disease, epidemiology and outcomes, proteinuria, renal function decline, renal pathology, 3. Good health, Renal pathology, Nephrology, Disease Progression, Female, medicine.symptom, Glomerular Filtration Rate, Adult, medicine.medical_specialty, Nephropathy, 03 medical and health sciences, Internal medicine, Biopsy, Humans, Proportional Hazards Models, Retrospective Studies, business.industry, Surrogate endpoint, Glomerulonephritis, IGA, medicine.disease, Confidence interval, Renal disorders Radboud Institute for Molecular Life Sciences [Radboudumc 11], Kidney Failure, Chronic, Renal disorders Radboud Institute for Health Sciences [Radboudumc 11], business
Abstract

Contains fulltext : 232930.pdf (Publisher’s version ) (Closed access) BACKGROUND: On the basis of findings of observational studies and a meta-analysis, proteinuria reduction has been proposed as a surrogate outcome in IgA nephropathy. How long a reduction in proteinuria needs to be maintained to mitigate the long-term risk of disease progression is unknown. METHODS: In this retrospective multiethnic cohort of adult patients with IgA nephropathy, we defined proteinuria remission as a ≥25% reduction in proteinuria from the peak value after biopsy, and an absolute reduction in proteinuria to

Published
2021

3. Evaluating a New International Risk-Prediction Tool in IgA Nephropathy

Author

Barbour, S.J., Coppo, R., Zhang, H., Liu, Z.H., Suzuki, Y., Matsuzaki, K., Katafuchi, R., Er, L., Espino-Hernandez, G., Kim, S.J., Reich, H.N., Feehally, J., Cattran, D.C., Russo, M.L., Troyanov, S., Cook, H.T., Roberts, I., Tesar, V., Maixnerova, D., Lundberg, S., Gesualdo, L., Emma, F., Fuiano, L., Beltrame, G., Rollino, C., Amore, A., Camilla, R., Peruzzi, L., Praga, M., Feriozzi, S., Polci, R., Segoloni, G., Colla, L., Pani, A., Piras, D., Angioi, A., Cancarini, G., Ravera, S., Durlik, M., Moggia, E., Ballarin, J., Giulio, S. di, Pugliese, F., Serriello, I., Caliskan, Y., Sever, M., Kilicaslan, I., Locatelli, F., Vecchio, L. del, Wetzels, J.F.M., Peters, H., Berg, U., Carvalho, F., Ferreira, A.C.D., Maggio, M., Wiecek, A., Ots-Rosenberg, M., Magistroni, R., Topaloglu, R., Bilginer, Y., D'Amico, M., Stangou, M., Giacchino, F., Goumenos, D., Kalliakmani, P., Gerolymos, M., Galesic, K., Geddes, C., Siamopoulos, K., Balafa, O., Galliani, M., Stratta, P., Quaglia, M., Bergia, R., Cravero, R., Salvadori, M., Cirami, L., Fellstrorn, B., Smerud, H.K., Ferrario, F., Stellato, T., Egido, J., Martin, C., Floege, J., Eitner, F., Lupo, A., Bernich, P., Mene, R., Morosetti, M., Kooten, C. van, Rabelink, T., Reinders, M.E.J., Grinyo, J.M.B., Cusinato, S., Benozzi, L., Savoldi, S., Licata, C., Mizerska-Wasiak, M., Martina, G., Messuerotti, A., Canton, A. dal, Esposito, C., Migotto, C., Triolo, G., Mariano, F., Pozzi, C., Boero, R., Bellur, S., Mazzucco, G., Giannakakis, C., Honsova, E., Sundelin, B., Palma, A.M. di, Gutierrez, E., Asunis, A.M., Barratt, J., Tardanico, R., Perkowska-Ptasinska, A., Terroba, J.A., Fortunato, M., Pantzaki, A., Ozluk, Y., Steenbergen, E., Soderberg, M., Riispere, Z., Furci, L., Orhan, D., Kipgen, D., Casartelli, D., Ljubanovic, D.G., Gakiopoulou, H., Bertoni, E., Ortiz, P.C., Karkoszka, H., Groene, H.J., Stoppacciaro, A., Bajema, I., Bruijn, J., Oliveras, X.F., Maldyk, J., Loachim, E., Bavbek, N., Cook, T., Alpers, C., Berthoux, F., Bonsib, S., D'Agati, V., D'Amico, G., Emancipator, S., Emmal, F., Fervenza, F., Florquin, S., Fogo, A., Groene, H., Haas, M., Hill, P., Hogg, R., Hsu, S., Hunley, T., Hladunewich, Jennette, C., Joh, K., Julian, B., Kawamura, T., Lai, F., Leung, C., Li, L., Li, P., Liu, Z., Massat, A., Mackinnon, B., Mezzano, S., Schena, F., Tomino, Y., Walker, P., Wang, H., Weening, J., Yoshikawa, N., Zeng, C.H., Shi, S.F., Nogi, C., Suzuki, H., Koike, K., Hirano, K., Yokoo, T., Hanai, M., Fukami, K., Takahashi, K., Yuzawa, Y., Niwa, M., Yasuda, Y., Maruyama, S., Ichikawa, D., Suzuki, T., Shirai, S., Fukuda, A., Fujimoto, S., Trimarchi, H., Int IgA Nephropathy Network, and Pathology

Subjects
Adult, Male, medicine.medical_specialty, Risk Assessment, 01 natural sciences, Nephropathy, 03 medical and health sciences, 0302 clinical medicine, Interquartile range, Internal medicine, Internal Medicine, Humans, Medicine, 030212 general & internal medicine, 0101 mathematics, business.industry, Proportional hazards model, Clinical study design, 010102 general mathematics, Glomerulonephritis, IGA, Middle Aged, Models, Theoretical, medicine.disease, Clinical trial, Cohort, Female, business, Risk assessment, Kidney disease
Abstract

ImportanceAlthough IgA nephropathy (IgAN) is the most common glomerulonephritis in the world, there is no validated tool to predict disease progression. This limits patient-specific risk stratification and treatment decisions, clinical trial recruitment, and biomarker validation. ObjectiveTo derive and externally validate a prediction model for disease progression in IgAN that can be applied at the time of kidney biopsy in multiple ethnic groups worldwide. Design, Setting, and ParticipantsWe derived and externally validated a prediction model using clinical and histologic risk factors that are readily available in clinical practice. Large, multi-ethnic cohorts of adults with biopsy-proven IgAN were included from Europe, North America, China, and Japan. Main Outcomes and MeasuresCox proportional hazards models were used to analyze the risk of a 50% decline in estimated glomerular filtration rate (eGFR) or end-stage kidney disease, and were evaluated using the R-D(2) measure, Akaike information criterion (AIC), C statistic, continuous net reclassification improvement (NRI), integrated discrimination improvement (IDI), and calibration plots. ResultsThe study included 3927 patients; mean age, 35.4 (interquartile range, 28.0-45.4) years; and 2173 (55.3%) were men. The following prediction models were created in a derivation cohort of 2781 patients: a clinical model that included eGFR, blood pressure, and proteinuria at biopsy; and 2 full models that also contained the MEST histologic score, age, medication use, and either racial/ethnic characteristics (white, Japanese, or Chinese) or no racial/ethnic characteristics, to allow application in other ethnic groups. Compared with the clinical model, the full models with and without race/ethnicity had better R-D(2) (26.3% and 25.3%, respectively, vs 20.3%) and AIC (6338 and 6379, respectively, vs 6485), significant increases in C statistic from 0.78 to 0.82 and 0.81, respectively (Delta C, 0.04; 95% CI, 0.03-0.04 and Delta C, 0.03; 95% CI, 0.02-0.03, respectively), and significant improvement in reclassification as assessed by the NRI (0.18; 95% CI, 0.07-0.29 and 0.51; 95% CI, 0.39-0.62, respectively) and IDI (0.07; 95% CI, 0.06-0.08 and 0.06; 95% CI, 0.05-0.06, respectively). External validation was performed in a cohort of 1146 patients. For both full models, the C statistics (0.82; 95% CI, 0.81-0.83 with race/ethnicity; 0.81; 95% CI, 0.80-0.82 without race/ethnicity) and R-D(2) (both 35.3%) were similar or better than in the validation cohort, with excellent calibration. Conclusions and RelevanceIn this study, the 2 full prediction models were shown to be accurate and validated methods for predicting disease progression and patient risk stratification in IgAN in multi-ethnic cohorts, with additional applications to clinical trial design and biomarker research.

Published
2019

4. Tolvaptan in Patients with Autosomal Dominant Polycystic Kidney Disease

Author

Torres VE, Chapman AB, Devuyst O, Gansevoort RT, Grantham JJ, Higashihara E, Perrone RD, Krasa HB, Ouyang J, Czerwiec FS, Tempo team, Gross P, Schulze B, Bichet D, Chauveau D, Peeters P, Voiculescu M, Manunta P, Tuazon J, Watnick T, Goral S, Horie S, Nutahara K, Torres V, Chapman A, Gansevoort R, Perrone R, Czerwiec F, Goldstein S, Cowley B, Fukagawa M, Torra R, Wei LJ, Cook T, Toto R, Agarwal R, August P, Bakris G, Beddhu S, Corwin H, Ruilope L, Rosa-Diez G, De La Fuente J, Martin R, Massari P, Novoa P, Rial M, Wasserman A, Faull R, Fraser I, Johnson D, Pedagagos E, Lian M, Pollock C, Cooper B, Rangan G, Russ G, McDonald S, Thomas M, Khoo D, Walker R, Pirson Y, Laecke V, Van der Niepen P, Sennesael J, Barre P, Alam A, Soroka S, Dieperink H, Strandgaard S, Petersen L, Berthoux F, Canaud B, Gontiers-Picard A, Huart A, Combe C, Delmas Y, Dussol B, Laville M, Guebre-Egziabher F, Mignon F, Michel C, Rieu P, Noel N, Ryckelynck J, Lobbedez T, Dellanna F, Kleophas W, Feldkamp T, Witzke O, Nurnberger J, Zeltner R, Walz G, Zeier M, Sommerer C, Bianchi S, Capasso G, Miranda N, Magistroni R, Bracale M, Remuzzi G, Rota S, Villa G, Tilocca P, Asahi K, Kato T, Endo M, Umezono T, Fujigaki Y, Kato A, Fukatsu A, Hasegawa H, Tayama Y, Hasegawa M, Hosoya T, Hanaoka K, Iehara N, Iino Y, Tsuruoka S, Imai E, Isaka Y, Ishimura E, Ito S, Sato H, Kamata K, Sakamoto H, Kamura K, Kusano E, Muto S, Kuwahara M, Matsubara A, Yorioka N, Mochizuki T, Narita I, Naya Y, Nihei N, Yukio N, Nishio S, Nitta K, Tsuchiya K, Okamura M, Sasaki S, Rai T, Seta K, Sugawara A, Shibazaki S, Sugiyama S, Tabei K, Takaichi K, Tomita K, Kitamura K, Tsukamoto Y, Tsuruya K, Nakano T, Ubara Y, Watanabe T, Yamamoto T, Yoshida K, Ishii D, Yuzawa Y, Meijer E, Vervloet M, Ciechanowski K, Wisniewska M, Gutowska-Jablonska M, Marcinkowska-Królewicz M, Klatko W, Wiśniewski T, Klinger M, Krajewska M, Ksiazek A, Orłowska G, Malecki R, Gontarek-Kacprzak J, Nowicki M, Makówka A, Rutkowski B, Wołyniec W, Rydzewski A, Sulowicz W, Jasik P, Covic A, Volovat C, Mircescu G, Petrescu L, Bobeica R, Barbarash O, Chesnokova L, Borovoy S, Demina L, Shostka G, Idovu M, Tkalich L, Geynits O, Tomilina N, Foggensteiner L, Holt S, Kingswood J, Lambie S, Peel R, MacDougall I, Tucker B, MacPhee I, Maxwell A, Brown H, Mikhail A, Bastin L, Turner N, Neary J, Wheeler D, Maxwell P, Wilkie M, Ong A, Zehnder D, Aldridge N, Adler S, Klein M, Battle D, Bennett W, Berger B, Dell K, Blumenfeld J, Donahue S, Bolin P, Browder R, Perry A, Oskoui F, Culpepper M, Dahl N, Edelstein C, Clegg L, Fischer D, Kaplan M, Kaveh K, Pankhaniya R, Koren M, Mansur K, Lafayette R, Lamar W, Lee J, Mahnensmith R, Nachman P, Mottl A, Miskulin D, Petersen J, Radhakrishnan J, Roppolo M, Basireddy M, Rosner M, Bolton W, Schulman G, Steed L, Steinman T, Hogan M, Venuto R, Turban S, Winklhofer F., Cardiovascular Centre (CVC), Groningen Kidney Center (GKC), Torres, Ve, Chapman, Ab, Devuyst, O, Gansevoort, Rt, Grantham, Jj, Higashihara, E, Perrone, Rd, Krasa, Hb, Ouyang, J, Czerwiec, F, Tempo, Team, Gross, P, Schulze, B, Bichet, D, Chauveau, D, Peeters, P, Voiculescu, M, Manunta, P, Tuazon, J, Watnick, T, Goral, S, Horie, S, Nutahara, K, Torres, V, Chapman, A, Gansevoort, R, Perrone, R, Goldstein, S, Cowley, B, Fukagawa, M, Torra, R, Wei, Lj, Cook, T, Toto, R, Agarwal, R, August, P, Bakris, G, Beddhu, S, Corwin, H, Ruilope, L, Rosa-Diez, G, De La Fuente, J, Martin, R, Massari, P, Novoa, P, Rial, M, Wasserman, A, Faull, R, Fraser, I, Johnson, D, Pedagagos, E, Lian, M, Pollock, C, Cooper, B, Rangan, G, Russ, G, Mcdonald, S, Thomas, M, Khoo, D, Walker, R, Pirson, Y, Laecke, V, Van der Niepen, P, Sennesael, J, Barre, P, Alam, A, Soroka, S, Dieperink, H, Strandgaard, S, Petersen, L, Berthoux, F, Canaud, B, Gontiers-Picard, A, Huart, A, Combe, C, Delmas, Y, Dussol, B, Laville, M, Guebre-Egziabher, F, Mignon, F, Michel, C, Rieu, P, Noel, N, Ryckelynck, J, Lobbedez, T, Dellanna, F, Kleophas, W, Feldkamp, T, Witzke, O, Nurnberger, J, Zeltner, R, Walz, G, Zeier, M, Sommerer, C, Bianchi, S, Capasso, G, Miranda, N, Magistroni, R, Bracale, M, Remuzzi, G, Rota, S, Villa, G, Tilocca, P, Asahi, K, Kato, T, Endo, M, Umezono, T, Fujigaki, Y, Kato, A, Fukatsu, A, Hasegawa, H, Tayama, Y, Hasegawa, M, Hosoya, T, Hanaoka, K, Iehara, N, Iino, Y, Tsuruoka, S, Imai, E, Isaka, Y, Ishimura, E, Ito, S, Sato, H, Kamata, K, Sakamoto, H, Kamura, K, Kusano, E, Muto, S, Kuwahara, M, Matsubara, A, Yorioka, N, Mochizuki, T, Narita, I, Naya, Y, Nihei, N, Yukio, N, Nishio, S, Nitta, K, Tsuchiya, K, Okamura, M, Sasaki, S, Rai, T, Seta, K, Sugawara, A, Shibazaki, S, Sugiyama, S, Tabei, K, Takaichi, K, Tomita, K, Kitamura, K, Tsukamoto, Y, Tsuruya, K, Nakano, T, Ubara, Y, Watanabe, T, Yamamoto, T, Yoshida, K, Ishii, D, Yuzawa, Y, Meijer, E, Vervloet, M, Ciechanowski, K, Wisniewska, M, Gutowska-Jablonska, M, Marcinkowska-Królewicz, M, Klatko, W, Wiśniewski, T, Klinger, M, Krajewska, M, Ksiazek, A, Orłowska, G, Malecki, R, Gontarek-Kacprzak, J, Nowicki, M, Makówka, A, Rutkowski, B, Wołyniec, W, Rydzewski, A, Sulowicz, W, Jasik, P, Covic, A, Volovat, C, Mircescu, G, Petrescu, L, Bobeica, R, Barbarash, O, Chesnokova, L, Borovoy, S, Demina, L, Shostka, G, Idovu, M, Tkalich, L, Geynits, O, Tomilina, N, Foggensteiner, L, Holt, S, Kingswood, J, Lambie, S, Peel, R, Macdougall, I, Tucker, B, Macphee, I, Maxwell, A, Brown, H, Mikhail, A, Bastin, L, Turner, N, Neary, J, Wheeler, D, Maxwell, P, Wilkie, M, Ong, A, Zehnder, D, Aldridge, N, Adler, S, Klein, M, Battle, D, Bennett, W, Berger, B, Dell, K, Blumenfeld, J, Donahue, S, Bolin, P, Browder, R, Perry, A, Oskoui, F, Culpepper, M, Dahl, N, Edelstein, C, Clegg, L, Fischer, D, Kaplan, M, Kaveh, K, Pankhaniya, R, Koren, M, Mansur, K, Lafayette, R, Lamar, W, Lee, J, Mahnensmith, R, Nachman, P, Mottl, A, Miskulin, D, Petersen, J, Radhakrishnan, J, Roppolo, M, Basireddy, M, Rosner, M, Bolton, W, Schulman, G, Steed, L, Steinman, T, Hogan, M, Venuto, R, Turban, S, Winklhofer, F., University of Zurich, Torres, Vicente E, Feldkamp, Thorsten (Beitragende*r), and Witzke, Oliver (Beitragende*r)

Subjects
Male, Tolvaptan, Medizin, 2700 General Medicine, SIROLIMUS, Kidney, V2 RECEPTOR ANTAGONIST, 10052 Institute of Physiology, Aquaretic, VASOPRESSIN V-2-RECEPTOR ANTAGONIST, Polycystic Kidney, 10035 Clinic for Nephrology, Medicine (all), General Medicine, Organ Size, Middle Aged, Adolescent, Adult, Benzazepines, Double-Blind Method, Female, Glomerular Filtration Rate, Humans, Polycystic Kidney, Autosomal Dominant, Sodium, Young Adult, Antidiuretic Hormone Receptor Antagonists, LONG-ACTING SOMATOSTATIN, Autosomal Dominant, 10076 Center for Integrative Human Physiology, OPC-41061, medicine.symptom, medicine.drug, medicine.medical_specialty, RENAL-FUNCTION, CYST GROWTH, Autosomal dominant polycystic kidney disease, Urology, Renal function, Kidney Volume, 610 Medicine & health, Placebo, Article, VOLUME PROGRESSION, Cystic kidney disease, Internal medicine, medicine, HYPONATREMIA, business.industry, urogenital system, ORAL TOLVAPTAN, medicine.disease, Endocrinology, Albuminuria, 570 Life sciences, biology, business
Abstract

BACKGROUND: The course of autosomal dominant polycystic kidney disease (ADPKD) is often associated with pain, hypertension, and kidney failure. Preclinical studies indicated that vasopressin V 2 -receptor antagonists inhibit cyst growth and slow the decline of kidney function. METHODS: In this phase 3, multicenter, double-blind, placebo-controlled, 3-year trial, we randomly assigned 1445 patients, 18 to 50 years of age, who had ADPKD with a total kidney volume of 750 ml or more and an estimated creatinine clearance of 60 ml per minute or more, in a 2:1 ratio to receive tolvaptan, a V 2 -receptor antagonist, at the highest of three twice-daily dose regimens that the patient found tolerable, or placebo. The primary outcome was the annual rate of change in the total kidney volume. Sequential secondary end points included a composite of time to clinical progression (defined as worsening kidney function, kidney pain, hypertension, and albuminuria) and rate of kidney-function decline. RESULTS: Over a 3-year period, the increase in total kidney volume in the tolvaptan group was 2.8% per year (95% confidence interval [CI], 2.5 to 3.1), versus 5.5% per year in the placebo group (95% CI, 5.1 to 6.0; P

Published
2012

5. Genetic variation of DKK3 may modify renal disease severity in ADPKD

Author

Liu, M., Shi, S., Senthilnathan, S., Yu, J., Wu, E., Bergmann, C., Zerres, K., Bogdanova, N., Coto, E., Constantinou-Deltas, Constantinos D., Pierides, Alkis M., Demetriou, Kyproula, Devuyst, O., Gitomer, B., Laakso, M., Lumiaho, A., Lamnissou, Klea, Magistroni, R., Parfrey, P., Breuning, M., Peters, D. J. M., Torra, R., Winearls, C. G., Torres, V. E., Harris, Peter C., Paterson, A. D., Pei, Y., Constantinou-Deltas, Constantinos D. [0000-0001-5549-9169], UCL - SSS/IREC/NEFR - Pôle de Néphrologie, and UCL - (SLuc) Service de néphrologie

Subjects
Oncology, Nephrology, Candidate gene, glomerulus filtration rate, genotype, kidney disease, urologic and male genital diseases, Cohort Studies, single nucleotide polymorphism, middle aged, genetic variability, kidney cyst, genetics, gene mutation, Genetics, adult, article, General Medicine, Middle Aged, cohort analysis, Polycystic Kidney, Autosomal Dominant, female genital diseases and pregnancy complications, Phenotype, priority journal, beta catenin, polycystin, Intercellular Signaling Peptides and Proteins, Chemokines, Adult, medicine.medical_specialty, TRPP Cation Channels, gene locus, Genotype, phenotype, Autosomal dominant polycystic kidney disease, Single-nucleotide polymorphism, Biology, DKK3 protein, human, Polymorphism, Single Nucleotide, Internal medicine, Genetic variation, medicine, Humans, signal peptide, Genetic variability, human, DKK3 gene, gene, Adaptor Proteins, Signal Transducing, ADPKD, PKD1, medicine.disease, major clinical study, Wnt protein, kidney failure, kidney polycystic disease, polycystic kidney disease 1 protein, Basic Research, adolescent, Mutation, mutation, Kidney disease
Abstract

Significant variation in the course of autosomal dominant polycystic kidney disease (ADPKD) within families suggests the presence of effect modifiers. Recent studies of the variation within families harboring PKD1 mutations indicate that genetic background may account for 32 to 42% of the variance in estimated GFR (eGFR) before ESRD and 43 to 78% of the variance in age at ESRD onset, but the genetic modifiers are unknown. Here, we conducted a high-throughput single-nucleotide polymorphism (SNP) genotyping association study of 173 biological candidate genes in 794 white patients from 227 families with PKD1. We analyzed two primary outcomes: (1) eGFR and (2) time to ESRD (renal survival). For both outcomes, we used multidimensional scaling to correct for population structure and generalized estimating equations to account for the relatedness among individuals within the same family. We found suggestive associations between each of 12 SNPs and at least one of the renal outcomes. We genotyped these SNPs in a second set of 472 white patients from 229 families with PKD1 and performed a joint analysis on both cohorts. Three SNPs continued to show suggestive/significant association with eGFR at the Dickkopf 3 (DKK3) gene locus no SNPs significantly associated with renal survival. DKK3 antagonizes Wnt/β-catenin signaling, which may modulate renal cyst growth. Pending replication, our study suggests that genetic variation of DKK3 may modify severity of ADPKD resulting from PKD1 mutations. Copyright © 2010 by the American Society of Nephrology. 21 1510 1520 Cited By :31

Published
2010

6. Genotype-renal function correlation in type 2 autosomal dominant polycystic kidney disease

Author

Magistroni, R., He, N., Wang, K., Andrew, R., Johnson, A., Gabow, P., Dicks, E., Parfrey, P., Torra, R., San-Millan, J. L., Coto, E., Van Dijk, M., Breuning, M., Peters, D., Bogdanova, N., Ligabue, G., Albertazzi, A., Hateboer, N., Demetriou, Kyproula, Pierides, Alkis M., Constantinou-Deltas, Constantinos D., St. George-Hyslop, P., Ravine, D., Pei, Y., and Constantinou-Deltas, Constantinos D. [0000-0001-5549-9169]

Subjects
Male, genotype, correlation analysis, pkd1 gene, DNA Mutational Analysis, urologic and male genital diseases, Kidney, Gastroenterology, Severity of Illness Index, genetic heterogeneity, Cohort Studies, Locus heterogeneity, pkd2 gene, gene mutation, Age of Onset, kidney function, Frameshift Mutation, Aged, 80 and over, adult, article, General Medicine, chronic kidney failure, Middle Aged, Polycystic Kidney, Autosomal Dominant, female genital diseases and pregnancy complications, aged, female, priority journal, Nephrology, Codon, Nonsense, disease severity, Allelic heterogeneity, Female, survival rate, onset age, Adult, medicine.medical_specialty, TRPP Cation Channels, Genotype, sex difference, Autosomal dominant polycystic kidney disease, Mutation, Missense, Renal function, Biology, Open Reading Frames, male, Internal medicine, Severity of illness, medicine, ADPKD, mutation, renal function, Humans, Family, human, Sex Distribution, gene, Aged, PKD1, Membrane Proteins, Proteins, medicine.disease, major clinical study, kidney failure, kidney polycystic disease, Endocrinology, RNA Splice Sites, Age of onset, Gene Deletion, Kidney disease
Abstract

Autosomal dominant polycystic kidney disease (ADPKD) is a common Mendelian disorder that affects approximately 1 in 1000 live births. Mutations of two genes, PKD1 and PKD2, account for the disease in approximately 80 to 85% and 10 to 15% of the cases, respectively. Significant interfamilial and intrafamilial renal disease variability in ADPKD has been well documented. Locus heterogeneity is a major determinant for interfamilial disease variability (i.e., patients from PKD1-linked families have a significantly earlier onset of ESRD compared with patients from PKD2-linked families). More recently, two studies have suggested that allelic heterogeneity might influence renal disease severity. The current study examined the genotype-renal function correlation in 461 affected individuals from 71 ADPKD families with known PKD2 mutations. Fifty different mutations were identified in these families, spanning between exon 1 and 14 of PKD2. Most (94%) of these mutations were predicted to be inactivating. The renal outcomes of these patients, including the age of onset of end-stage renal disease (ESRD) and chronic renal failure (CRF defined as creatinine clearance ≤ 50 ml/min, calculated using the Cockroft and Gault formula), were analyzed. Of all the affected individuals clinically assessed, 117 (25.4%) had ESRD, 47 (10.2%) died without ESRD, 65 (14.0%) had CRF, and 232 (50.3%) had neither CRF nor ESRD at the last follow-up. Female patients, compared with male patients, had a later mean age of onset of ESRD (76.0 [95% CI, 73.8 to 78.1] versus 68.1 [95% CI, 66.0 to 70.2] yr) and CRF (72.5 [95% CI, 70.1 to 74.9] versus 63.7 [95% CI, 61.4 to 66.0] yr). Linear regression and renal survival analyses revealed that the location of PKD2 mutations did not influence the age of onset of ESRD. However, patients with splice site mutations appeared to have milder renal disease compared with patients with other mutation types (P < 0.04 by log rank test adjusted for the gender effect). Considerable renal disease variability was also found among affected individuals with the same PKD2 mutations. This variability can confound the determination of allelic effects and supports the notion that additional genetic and/or environmental factors may modulate the renal disease severity in ADPKD. 14 1164 1174 Cited By :80

7. Application of the International IgA Nephropathy Prediction Tool one or two years post-biopsy

Author

Sean J. Barbour, Rosanna Coppo, Hong Zhang, Zhi-Hong Liu, Yusuke Suzuki, Keiichi Matsuzaki, Lee Er, Heather N. Reich, Jonathan Barratt, Daniel C. Cattran, M.L. Russo, S. Troyanov, H.T. Cook, I. Roberts, V. Tesar, D. Maixnerova, S. Lundberg, L. Gesualdo, F. Emma, L. Fuiano, G. Beltrame, C. Rollino, A. Amore, R. Camilla, L. Peruzzi, M. Praga, S. Feriozzi, R. Polci, G. Segoloni, L. Colla, A. Pani, D. Piras, A. Angioi, G. Cancarini, S. Ravera, M. Durlik, E. Moggia, J. Ballarin, S. Di Giulio, F. Pugliese, I. Serriello, Y. Caliskan, M. Sever, I. Kilicaslan, F. Locatelli, L. Del Vecchio, J.F.M. Wetzels, H. Peters, U. Berg, F. Carvalho, A.C. da Costa Ferreira, M. Maggio, A. Wiecek, M. Ots-Rosenberg, R. Magistroni, R. Topaloglu, Y. Bilginer, M. D’Amico, M. Stangou, F. Giacchino, D. Goumenos, E. Papachristou, K. Galesic, C. Geddes, K. Siamopoulos, O. Balafa, M. Galliani, P. Stratta, M. Quaglia, R. Bergia, R. Cravero, M. Salvadori, L. Cirami, B. Fellstrom, H. Kloster Smerud, F. Ferrario, T. Stellato, J. Egido, C. Martin, J. Floege, F. Eitner, A. Lupo, P. Bernich, P. Menè, M. Morosetti, C. van Kooten, T. Rabelink, M.E.J. Reinders, J.M. Boria Grinyo, S. Cusinato, L. Benozzi, S. Savoldi, C. Licata, M. Mizerska-Wasiak, G. Martina, A. Messuerotti, A. Dal Canton, C. Esposito, C. Migotto, G. Triolo, F. Mariano, C. Pozzi, R. Boero, S. Bellur, G. Mazzucco, C. Giannakakis, E. Honsova, B. Sundelin, A.M. Di Palma, E. Gutiérrez, A.M. Asunis, J. Barratt, R. Tardanico, A. Perkowska-Ptasinska, J. Arce Terroba, M. Fortunato, A. Pantzaki, Y. Ozluk, E. Steenbergen, M. Soderberg, Z. Riispere, L. Furci, D. Orhan, D. Kipgen, D. Casartelli, D. Galesic Ljubanovic, H. Gakiopoulou, E. Bertoni, P. Cannata Ortiz, H. Karkoszka, H.J. Groene, A. Stoppacciaro, I. Bajema, J. Bruijn, X. Fulladosa Oliveras, J. Maldyk, E. Ioachim, N. Bavbek, T. Cook, C. Alpers, F. Berthoux, S. Bonsib, V. D’Agati, G. D’Amico, S. Emancipator, F. Emmal, F. Fervenza, S. Florquin, A. Fogo, H. Groene, M. Haas, P. Hill, R. Hogg, S. Hsu, T. Hunley, M. Hladunewich, C. Jennette, K. Joh, B. Julian, T. Kawamura, F. Lai, C. Leung, L. Li, P. Li, Z. Liu, A. Massat, B. Mackinnon, S. Mezzano, F. Schena, Y. Tomino, P. Walker, H. Wang, J. Weening, N. Yoshikawa, C.-H. Zeng, S. Shi, C. Nogi, H. Suzuki, K. Koike, K. Hirano, T. Yokoo, M. Hanai, K. Fukami, K. Takahashi, Y. Yuzawa, M. Niwa, Y. Yasuda, S. Maruyama, D. Ichikawa, T. Suzuki, S. Shirai, A. Fukuda, S. Fujimoto, H. Trimarchi, Triolo, G., Mariano, F., Pozzi, C., Boero, R., Bellur, S., Mazzucco, G., Giannakakis, C., Honsova, E., Sundelin, B., Di Palma, A. M., Russo, M. L., Ferrario, F., Gutiérrez, E., Asunis, A. M., Barratt, J., Tardanico, R., Perkowska-Ptasinska, A., Terroba, J. Arce, Fortunato, M., Pantzaki, A., Ozluk, Y., Troyanov, S., Steenbergen, E., Soderberg, M., Riispere, Z., Furci, L., Orhan, D., Kipgen, D., Casartelli, D., Ljubanovic, D. Galesic, Gakiopoulou, H., Bertoni, E., Cook, H. T., Cannata Ortiz, P., Karkoszka, H., Groene, H. J., Stoppacciaro, A., Bajema, I., Bruijn, J., Fulladosa Oliveras, X., Maldyk, J., Ioachim, E., Bavbek, N., Roberts, I., Cook, T., Alpers, C., Amore, A., Berthoux, F., Bonsib, S., D'Agati, V., D'Amico, G., Tesar, V., Emancipator, S., Emmal, F., Fervenza, F., Florquin, S., Fogo, A., Geddes, C., Groene, H., Haas, M., Hill, P., Maixnerova, D., Hogg, R., Hsu, S., Hunley, T., Hladunewich, M., Jennette, C., Joh, K., Julian, B., Kawamura, T., Lai, F., Leung, C., Lundberg, S., Li, L., Li, P., Liu, Z., Massat, A., Mackinnon, B., Mezzano, S., Schena, F., Tomino, Y., Walker, P., Wang, H., Gesualdo, L., Weening, J., Yoshikawa, N., Zeng, C.-H., Shi, S., Nogi, C., Suzuki, H., Koike, K., Hirano, K., Yokoo, T., Emma, F., Hanai, M., Fukami, K., Takahashi, K., Yuzawa, Y., Niwa, M., Yasuda, Y., Maruyama, S., Ichikawa, D., Suzuki, T., Shirai, S., Fuiano, L., Fukuda, A., Fujimoto, S., Trimarchi, H., Beltrame, G., Rollino, C., Camilla, R., Peruzzi, L., Praga, M., Feriozzi, S., Polci, R., Segoloni, G., Colla, L., Pani, A., Piras, D., Angioi, A., Cancarini, G., Ravera, S., Durlik, M., Moggia, E., Ballarin, J., Di Giulio, S., Pugliese, F., Serriello, I., Caliskan, Y., Sever, M., Kilicaslan, I., Locatelli, F., Del Vecchio, L., Wetzels, J. F. M., Peters, H., Berg, U., Carvalho, F., da Costa Ferreira, A. C., Maggio, M., Wiecek, A., Ots-Rosenberg, M., Magistroni, R., Topaloglu, R., Bilginer, Y., D'Amico, M., Stangou, M., Giacchino, F., Goumenos, D., Papachristou, E., Galesic, K., Siamopoulos, K., Balafa, O., Galliani, M., Stratta, P., Quaglia, M., Bergia, R., Cravero, R., Salvadori, M., Cirami, L., Fellstrom, B., Smerud, H. Kloster, Stellato, T., Egido, J., Martin, C., Flöge, Jürgen, Eitner, F., Lupo, A., Bernich, P., Menè, P., Morosetti, M., van Kooten, C., Rabelink, T., Reinders, M. E. J., Boria Grinyo, J. M., Cusinato, S., Benozzi, L., Savoldi, S., Licata, C., Mizerska-Wasiak, M., Martina, G., Messuerotti, A., Dal Canton, A., Esposito, C., Migotto, C., Pathology, Center of Experimental and Molecular Medicine, Graduate School, and ACS - Heart failure & arrhythmias

Subjects
Adult, disease progression, end-stage kidney disease, IgA nephropathy, prediction tool, risk prediction, Biopsy, Glomerulonephritis, IGA, Prognosis, Cohort Studies, Renal disorders Radboud Institute for Molecular Life Sciences [Radboudumc 11], Nephrology, Humans, Renal Insufficiency, Renal disorders Radboud Institute for Health Sciences [Radboudumc 11], Glomerular Filtration Rate
Abstract

Kidney international 102(1), 160-172 (2022). doi:10.1016/j.kint.2022.02.042, Published by Elsevier, New York, NY

Published
2022
Full Text
View/download PDF

8. Reliability of Total Renal Volume Computation in Polycystic Kidney Disease From Magnetic Resonance Imaging

Author

Cristiana Corsi, Renzo Mignani, Stefano Severi, Dario Turco, Riccardo Magistroni, Valeria Aiello, Turco, D., Severi, S., Mignani, R., Aiello, V., Magistroni, R., and Corsi, C.

Subjects
Adult, Male, medicine.medical_specialty, Autosomal dominant polycystic kidney disease, kidney segmentation, Image processing, Kidney, End stage renal disease, Magnetic resonance imaging, Nuclear Medicine and Imaging, Linear regression, medicine, Polycystic kidney disease, Image Processing, Computer-Assisted, Humans, Radiology, Nuclear Medicine and imaging, Prospective Studies, Reliability (statistics), Aged, Observer Variation, Reproducibility, autosomal dominant polycystic kidney disease, medicine.diagnostic_test, business.industry, Reproducibility of Results, Organ Size, renal volume, Middle Aged, medicine.disease, Polycystic Kidney, Autosomal Dominant, Magnetic Resonance Imaging, Kidney segmentation, Renal volume, Radiology, Nuclear Medicine and Imaging, Disease Progression, Regression Analysis, Female, Radiology, business
Abstract

Rationale and Objectives Total renal volume (TRV) is an important quantitative indicator of the progression of autosomal dominant polycystic kidney disease (ADPKD). The Consortium for Radiologic Imaging Studies of Polycystic Kidney Disease proposes a method for TRV computation based on manual tracing and geometric modeling. Alternative approaches for TRV computation are represented by the application of advanced image processing techniques. In this study, we aimed to compare TRV estimates derived from these two different approaches. Materials and Methods The nearly automated technique for the analysis of magnetic resonance (MR) images was tested on 30 ADPKD patients. TRV was computed from both axial (KV ax ) and coronal (KV cor ) acquisitions and compared to measurements based on geometric modeling (KV ap ) by linear regression and Bland–Altman analysis. In addition, to assess reproducibility, intraobserver and interobserver variabilities were computed. Results Linear regression analysis between KV ax and KV cor resulted in an excellent correlation (KV ax = 1KV cor − 0.78; r 2 = 0.997). Bland–Altman analysis showed a negligible bias and narrow limits of agreement (bias: −11.7 mL; SD: 54.3 mL). Similar results were obtained by comparison of volumes obtained applying the nearly automated method and the one based on geometric modeling ( y = 0.98 x + 75.9; r 2 = 0.99; bias: −53.7 mL; SD: 108.1 mL). Importantly, geometric modeling does not provide reliable TRV estimates in huge kidney affected by regional deformation. Intraobserver and interobserver variability resulted in very small percentage error Conclusions The results of this study provide the feasibility of using a nearly automated approach for accurate and fast evaluation of TRV also in markedly enlarged ADPKD kidneys including exophytic cysts.

Published
2014

9. Coexistence of different circulating anti-podocyte antibodies in membranous nephropathy

Author

Corrado Murtas, Pietro Ravani, Francesca Bruno, Maurizio Bruschi, Piergiorgio Messa, Riccardo Magistroni, Francesco Scolari, Giovanni Candiano, Landino Allegri, Andrea Magnano, Fernando C. Fervenza, Maria Luisa Carnevali, Gian Marco Ghiggeri, Lucia Argentiero, L. Furci, Renato Alberto Sinico, Antonella Radice, Gabriella Moroni, Loreto Gesualdo, Murtas, C, Bruschi, M, Candiano, G, Moroni, G, Magistroni, R, Magnano, A, Bruno, F, Radice, A, Furci, L, Argentiero, L, Carnevali, M, Messa, P, Scolari, F, Sinico, R, Gesualdo, L, Fervenza, F, Allegri, L, Ravani, P, and Ghiggeri, G

Subjects
Male, Registrie, nefrologia, Time Factors, Epidemiology, glomerulonefrite membranosa, Critical Care and Intensive Care Medicine, Glomerulonephritis, Membranous, Immunoglobulin G, Retrospective Studie, Medicine, Registries, antigene, Proteinuria, biology, Podocytes, Glomerulosclerosis, Focal Segmental, Middle Aged, Glomerulonephritis, Membranou, Isotype, Autoantibodie, sindrome nefrosica, Italy, Nephrology, Linear Model, Female, Neprilysin, medicine.symptom, Human, Adult, Adolescent, Logistic Model, Time Factor, Podocyte, Nephropathy, Young Adult, Antigen, Membranous nephropathy, Aldehyde Reductase, Humans, Autoantibodies, Retrospective Studies, Aged, Transplantation, business.industry, Superoxide Dismutase, Receptors, Phospholipase A2, Autoantibody, Glomerulonephritis, IGA, Original Articles, medicine.disease, Logistic Models, Phosphopyruvate Hydratase, Immunology, Linear Models, biology.protein, business
Abstract

Summary Background and objectives The discovery of different podocyte autoantibodies in membranous nephropathy (MN) raises questions about their pathogenetic and clinical meaning. This study sought to define antibody isotypes and correlations; to compare levels in MN, other glomerulonephritides, and controls; and to determine their association with clinical outcomes. Design, setting, participants, & measurements Serum IgG1 ,I gG3 ,a nd IgG4 against aldose reductase (AR), SOD2, and a-enolase (aENO) were measured at diagnosis in 186 consecutive MN patients, in 96 proteinuric controls (36 with FSGS, and 60 with IgA nephropathy), and in 92 healthy people recruited in four Italian nephrology units. Anti-phospholipase A2 receptor (PLA2r) and anti-neutral endopeptidase (NEP) IgG4 were titrated in the same specimens. Association with 1-year follow-up clinical parameters was studied in 120 patients. Results IgG4 was the most common isotype for all antibodies; IgG1 and IgG3 were nearly negligible. IgG4 levels werepositiveinasignificantproportionofMNpatients(AR,34%;SOD2,28%;aENO,43%).Antibodytiterswere higher in MN than in healthy and pathologic controls (P,0.005). Anti-NEP IgG4 did not differ from normal controls (P=0.12). Anti-PLA2r IgG4 was detected in 60% of patients and correlated with anti-AR, anti-SOD2, and anti-aENO IgG4 (P,0.001). In MN patients negative for the whole antibody panel (20%), 1-year proteinuria was lower compared with patients with at least one antibody positivity (P,0.05). Conclusions Our data suggest that IgG4 is the prevalent isotype for antibodies against cytoplasmic antigens of podocytes (AR, SOD2, aENO). Their levels were higher than in other proteinuric glomerulonephritides and in normal controls and were correlated with anti-PLA2r. Only baseline negativity for all known antibodies predicted lower 1-year proteinuria. Clin J Am Soc Nephrol 7: ccc–ccc, 2012. doi: 10.2215/CJN.02170312

Published
2012

Catalog

Books, media, physical & digital resources
See catalog results