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8. 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

9. Primary and secondary glomerulonephritis II

Author

Valdivia Vega, R. P., primary, Perez Carlos, J., additional, LI, X., additional, Xu, X., additional, Zhang, W., additional, Ren, H., additional, Chen, N., additional, Yorioka, N., additional, Doi, T., additional, Hirashio, S., additional, Arita, M., additional, Hirabayashi, A., additional, Tilkiyan, E., additional, Chonova, E., additional, Ronchev, Y., additional, Kumchev, E., additional, Giamalis, P., additional, Spartalis, M., additional, Stangou, M., additional, Tsouchnikas, I., additional, Moysiades, D., additional, Dimopoulou, D., additional, Garyfalos, A., additional, Efstratiadis, G., additional, Memmos, D., additional, Schonermarck, U., additional, Eichhorn, P., additional, Sitter, T., additional, Wendler, T., additional, Vielhauer, V., additional, Lederer, S., additional, Fechner, K., additional, Fischereder, M., additional, Bantis, C., additional, Heering, P., additional, Kouri, N.-M., additional, Schwandt, C., additional, Kuhr, N., additional, Ivens, K., additional, Rump, L.-C., additional, Matta, V., additional, Melis, P., additional, Conti, M., additional, Cao, R., additional, Binda, V., additional, Altieri, P., additional, Asunis, A. M., additional, Catani, W., additional, Floris, M., additional, Angioi, A., additional, Congia, M., additional, Cucca, F., additional, Minerba, L., additional, Peri, M., additional, Pani, A., additional, Beck, L. H., additional, Fervenza, F. C., additional, Bomback, A. S., additional, Ayalon, R., additional, Irazabal, M. V., additional, Eirin, A., additional, Cattran, D. C., additional, Appel, G. B., additional, Salant, D. J., additional, Santoro, D., additional, Postorino, A., additional, Costantino, G., additional, Bellinghieri, G., additional, Savica, V., additional, Weiner, M., additional, Goh, S. M., additional, Mohammad, A., additional, Eriksson, P., additional, Westman, K., additional, Selga, D., additional, Salama, A., additional, Segelmark, M., additional, Chocova, Z., additional, Hruskova, Z., additional, Mareckova, H., additional, Svobodova, B., additional, Jancova, E., additional, Bednarova, V., additional, Rysava, R., additional, Tesar, V., additional, Hanzal, V., additional, Zamboch, K., additional, Grussmannova, M., additional, Svojanovsky, J., additional, Klaboch, J., additional, Kubisova, M., additional, Sevcik, J., additional, Olsanska, R., additional, Sobotkova, M., additional, Becvar, R., additional, Nemec, P., additional, Kodeda, M., additional, Jilek, D., additional, Hussain, M., additional, Dhaygude, A., additional, Cartery, C., additional, Huart, A., additional, Plaisier, E., additional, Bongard, V., additional, Montastruc, F., additional, Ronco, P., additional, Pourrat, J., additional, Chauveau, D., additional, Prasad, N., additional, Gurjar, D., additional, Bhadauria, D., additional, Sharma, R. K., additional, Gupta, A., additional, Kaul, A., additional, Jain, M., additional, Venning, M., additional, Brown, N., additional, Bruce, I., additional, Noor, S., additional, Bekker, P., additional, Potarca, A., additional, Dairaghi, D., additional, Miao, S., additional, Powers, J. P., additional, Jaen, J. C., additional, Schall, T. J., additional, Kalavrizioti, D., additional, Gerolymos, M., additional, Komninakis, D., additional, Rodi, M., additional, Mouzaki, A., additional, Kalliakmani, P., additional, Goumenos, D., additional, Choi, B. S., additional, Park, C. W., additional, Kim, Y.-S., additional, Yang, C. W., additional, Sun, I. O., additional, Qin, W., additional, Xie, L., additional, Tan, C., additional, Mian, W., additional, Fu, P., additional, Kaminskyy, V., additional, Hao, X., additional, Wang, W., additional, Cengiz, C., additional, Nur, C., additional, Nurdan, Y., additional, Selman, G., additional, Pinar, T., additional, Mehmet, T., additional, Lale, S., additional, Caliskan, S., additional, Shinzawa, M., additional, Yamamoto, R., additional, Nagasawa, Y., additional, Oseto, S., additional, Mori, D., additional, Niihata, K., additional, Fukunaga, M., additional, Yamauchi, A., additional, Tsubakihara, Y., additional, Rakugi, H., additional, Isaka, Y., additional, Chen, J.-S., additional, Lin, Y.-F., additional, Lin, W.-Y., additional, Shu, K.-H., additional, Chen, H.-H., additional, Wu, C.-J., additional, Yang, C.-S., additional, Tseng, T.-L., additional, Zaza, G., additional, Bernich, P., additional, Lupo, A., additional, Panizo, N., additional, Rivera, F., additional, Lopez Gomez, J. M., additional, Regn, S. R. o. G., additional, Ceresini, G., additional, Vaglio, A., additional, Urban, M. L., additional, Corradi, D., additional, Usberti, E., additional, Palmisano, A., additional, Buzio, C., additional, Zineb, H., additional, Ramdani, B., additional, Marques, L. P. J., additional, Rioja, L. D. S., additional, Rocco, R., additional, Nery, A. C. F., additional, Novaes, B. C., additional, Bridoux, F., additional, Sicard, A., additional, Labatut, D., additional, Touchard, G., additional, Sarkozy, C., additional, Vanhille, P., additional, Callard, P., additional, Essig, M., additional, Provot, F., additional, Nony, A., additional, Karras, A., additional, Agustin, C. P., additional, M Belen, H. R., additional, Carmen, C. P., additional, Eliana, O., additional, Elisa, P., additional, Luis, P., additional, Alberto, M.-C., additional, Javier, N., additional, Isabel, F., additional, Atzeni, A., additional, Fois, A., additional, Piras, D., additional, Maxia, S., additional, Sau, G., additional, Pili, G., additional, Porcu, M., additional, Derudas, D., additional, Angelucci, E., additional, Ledda, A., additional, La Nasa, G., additional, Ossareh, S., additional, Asgari, M., additional, Savaj, S., additional, Ataipour, Y., additional, Abdi, E., additional, Malakoutian, T., additional, Rajaa, R., additional, Berkchi, F. Z., additional, Haffane, L., additional, Squalli, Z., additional, Rouass, L., additional, Al Hamany, Z., additional, Ezzaitouni, F., additional, Benamar, L., additional, Bayahya, R., additional, Ouzeddoun, N., additional, Gao-Yuan, H., additional, Yao, X., additional, Xin, C., additional, Zhen, C., additional, Yong-Chun, G., additional, Qing-Wen, W., additional, Hui-Ping, C., additional, Da-XI, J., additional, De-Hua, G., additional, Wei-Xin, H., additional, Zhi-Hong, L., additional, Fatima Zahra, B., additional, Laila, H., additional, Zoubair, S., additional, Naima, O., additional, Smykal-Jankowiak, K., additional, Niemir, Z., additional, Polcyn-Adamczak, M., additional, Szramka-Pawlak, B., additional, Zaba, R., additional, Zhang, C., additional, MA, Y., additional, Shen, P., additional, Ouyang, Y., additional, Pan, X., additional, Wang, Z., additional, Feng, X., additional, and Ni, L., additional

Published
2012
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10. Angiotensin II induces thrombospondin-1 production in human mesangial cells via p38 MAPK and JNK: A mechanism for activation of latent TGF-beta 1.

Author

Yorioka N., Kohno N., Naito T., Masaki T., Nikolic-Paterson D.J., Tanji C., Yorioka N., Kohno N., Naito T., Masaki T., Nikolic-Paterson D.J., and Tanji C.

Abstract

ANG II induces secretion and activation of transforming growth factor-beta (TGF-beta) by glomerular mesangial cells. However, the mechanisms that operate this are unclear. Thrombospondin-1 (TSP-1), which is produced by mesangial cells in damaged glomeruli, is one of several molecules known to activate the latent TGF-beta1 complex. Therefore, we examined whether the ANG II-induced activation of latent TGF-beta1 in human mesangial cells (HMC) operates via TSP-1. The addition of ANG II (1-100 nM) to HMC significantly increased TSP-1 mRNA within 6 h, followed by an increase in TSP-1 protein production as shown by Western blot analysis of cells and immunoassay of the culture supernatant. Production of ANG II-induced TSP-1 mRNA and protein was completely inhibited by an ANG II type 1 (AT 1)-receptor antagonist but was unaffected by an AT 2-receptor antagonist. Use of a TSP-1-specific blocking peptide demonstrated that the ANG II-induced activation of latent TGF-beta 1 operates via TSP-1. Next, we investigated the role of ERK1/2, p38 MAPK, and JNK in ANG II-induced TSP-1 production in HMC. The addition of the upstream ERK1/2 inhibitor PD-98059 did not affect ANG II-induced TSP-1 production, whereas addition of either the p38 MAPK inhibitor SB-203580 or the JNK inhibitor SP-600125 significantly reduced TSP-1 production. In conclusion, this study has demonstrated that ANG II-induced activation of latent TGF-beta1 in HMC operates via TSP-1. Furthermore, ANG II-induced TSP-1 production is dependent on p38 MAPK and JNK signaling.

Published
2004

40. Effect of a carbonaceous oral adsorbent on the progression of CKD: a multicenter, randomized, controlled trial.

Author

Akizawa T, Asano Y, Morita S, Wakita T, Onishi Y, Fukuhara S, Gejyo F, Matsuo S, Yorioka N, Kurokawa K, and CAP-KD Study Group

Abstract

BACKGROUND: The carbonaceous oral adsorbent AST-120 slows the deterioration of kidney function in patients with advanced chronic kidney disease (CKD). However, information about AST-120 in patients with less severe stages of CKD is lacking. STUDY DESIGN: Randomized controlled trial. SETTING & PARTICIPANTS: 75 medical facilities, 460 patients with CKD with serum creatinine (sCr) concentrations less than 5.0 mg/dL (not undergoing dialysis). INTERVENTION: Random assignment to either a low-protein diet and antihypertensive medication in the control group or that treatment combined with AST-120 (6 g/d). OUTCOMES & MEASUREMENTS: Composite primary end point: doubling of sCr level, increase in sCr level to 6.0 mg/dL or more, need for dialysis or transplantation, or death. Secondary outcomes: adverse events and changes in estimated creatinine clearance (CCr) rate, proteinuria (protein in milligrams per day), and quality of life. RESULTS: Mean sCr level was 2.66 mg/dL and estimated CCr was 22.4 mL/min in both groups. During 56 weeks, numbers of primary end-point events (43 for control versus 42 for AST-120) and event-free survival (P = 0.9) did not differ between groups. Gastrointestinal adverse events were less common in the control group than the AST-120 group (2 versus 32 events). Estimated CCr decreased more in the control group than in the AST-120 group (-0.15 versus -0.12 mL/min/y; P = 0.001). Median proteinuria changed from protein of 1,162 to 1,167 mg/d in the control group versus 1,102 to 906 mg/d in the AST-120 group (P = 0.2). LIMITATION: Infrequent primary end-point events. CONCLUSION: AST-120 did not substantially slow the progression of kidney disease in patients with moderate to severe CKD during 1 year. Copyright © 2009 National Kidney Foundation, Inc. [ABSTRACT FROM AUTHOR]

Published
2009
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42. Screening for gastroenterological malignancies in new and maintenance dialysis patients.

Author

Ito, Takafumi, Tanaka, Issei, Kadoya, Takayuki, Kimura, Mari, Ooshiro, Takafumi, Ooishi, Kouichi, Tanaka, Junko, Yorioka, Noriaki, Ito, T, Tanaka, I, Kadoya, T, Kimura, M, Ooshiro, T, Ooishi, K, Tanaka, J, and Yorioka, N

Subjects
CHRONIC kidney failure, HEMODIALYSIS patients, GASTROENTEROLOGY, MEDICAL screening
Abstract

To screen for gastroenterological malignancies in dialysis patients, we used the fecal occult blood test, examined the upper and lower gastrointestinal tract, and used abdominal ultrasonography in 178 patients starting dialysis (171 on hemodialysis and 7 on continuous ambulatory peritoneal dialysis (CAPD)) and 34 patients on maintenance dialysis (27 on hemodialysis and 7 on CAPD). Screening disclosed ten cancers (one esophageal cancer, three gastric cancers, four colorectal cancers, and two hepatocellular carcinomas) in 9 of the patients starting dialysis. Six cancers (one esophageal, three gastric, one colorectal, and one renal) were detected in 5 of the patients on maintenance dialysis. Since an increased incidence of malignancy has been reported in dialysis patients, gastroenterological screening appears to be worthwhile. [ABSTRACT FROM AUTHOR]

Published
1999
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46. Serum Cross-Linked N-Terminal Telopeptide of Type I Collagen for Evaluation of Renal Osteodystrophy in Hemodialysis Patients

Author

Nakashima, A., Yorioka, N., Mizutani, T., Yamagata, Z., Ueno, T., and Takasugi, N.

Abstract

AbstractBackground: Useful markers of bone resorption are needed for hemodialysis patients with renal osteodystrophy. This study investigated the use of a new immunoassay for cross-linked N-terminal telopeptide of type 1 collagen to assess bone changes in hemodialysis patients. Methods: Radial bone mineral density was examined in 178 hemodialysis patients at baseline and after 12 months. Serum levels of N-terminal telopeptide and other markers were measured. Results: The annual percent change of radial bone mineral density was negatively correlated with the levels of N-terminal telopeptide, intact osteocalcin, tartrate-resistant acid phosphatase, bone-specific alkaline phosphatase, and intact parathyroid hormone. The annual percent change of radial bone mineral density showed a stronger correlation with N-terminal telopeptide levels than with the other markers, except for intact parathyroid hormone. Also, intact parathyroid hormone and N-terminal telopeptide levels showed a stronger correlation than that of either tartrate-resistant acid phosphatase or cross-linked carboxyterminal telopeptide of type 1 collagen with intact parathyroid hormone. Conclusion: Serum N-terminal telopeptide may be the most useful bone resorption marker in renal osteodystrophy and its use combined with bone formation markers may improve the management of this condition.Copyright © 2005 S. Karger AG, Basel

Published
2005

47. Effect of Glucose Polymer on the Intercellular Junctions of Cultured Human Peritoneal Mesothelial Cells

Author

Ito, T., Yorioka, N., Kyuden, Y., Asakimori, Y., Kiribayashi, K., Ogawa, T., and Kohno, N.

Abstract

AbstractBackground: Glucose polymer is an active osmotic agent that is increasingly used as an alternative to glucose in peritoneal dialysis fluids. It was recently reported that the duration of peritoneal dialysis can be extended by using glucose polymer in patients with poor ultrafiltration. We previously demonstrated that high glucose levels damage the intercellular junctions of cultured human peritoneal mesothelial cells (HPMC), but little is known about the influence of glucose polymer. Therefore, we investigated the effects of glucose polymer on the intercellular junctions of HPMC. Methods: HPMC were isolated, cultured, and identified according to the modified method of Stylianou. M199 medium was supplemented with peritoneal dialysis solutions containing 7.5% glucose polymer or 1.5, 2.5, and 4.25% glucose. After 6 h, cell viability was assessed, intercellular junction proteins were examined by immunofluorescence techniques, and the concentration of transforming growth factor-β1 in the culture supernatant was determined. Results: Glucose significantly suppressed cell viability and significantly increased transforming growth factor-β1 production when compared with control or glucose polymer cultures. Peritoneal dialysis solutions containing 4.25% glucose caused the detachment of HPMC. Immunofluorescence of intercellular junction proteins (tight junctions: ZO-1, occludin, and claudin-1; adherens junctions: β-catenin) became weak and uneven after culture with glucose. On the other hand, glucose polymer caused little change in the immunofluorescence of these proteins when compared with control cultures. Conclusions: Glucose polymer seems to be less toxic to HPMC than glucose itself, suggesting that the glucose polymer may be better for peritoneal dialysis.Copyright © 2003 S. Karger AG, Basel

Published
2003

48. Role of Transforming Growth Factor-β1in Glomerulonephritis

Author

Taniguchi, Y, Yorioka, N, Masaki, T, Yamashita, K, Ito, T, Ueda, H, and Yamakido, M

Abstract

The role of transforming growth factor-β1(TGF-β1) in human glomerulonephritis is still poorly understood. The relationship between expression of TGF-β1protein or TGF-β1mRNA and tissue damage was investigated using the enzyme–antibody and in situhybridization method in frozen slices of renal tissue from 30 patients: 25 with glomerulonephritis (18 with immunoglobulin A nephropathy; two with focal glomerulosclerosis, one with membranous nephropathy, one with crescentic glomerulonephritis and three with lupus nephritis) and five control patients with minimal change disease. The expression of TGF-β1mRNA was high in sclerotic and proliferative glomeruli, as well as in the tubular epithelial cells within tubulointerstitial lesions. There was significant correlation between the severity of tissue damage in immunoglobulin A nephropathy and the presence of TGF-β1protein and TGF-β1mRNA. These findings suggest that TGF-β1is involved in glomerulosclerosis and the development of tubulointerstitial lesions, indicating its potential importance in the progression and aggravation of immunoglobulin A nephropathy.

Published
1997
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50. Fatal hepatic failure caused by miliary tuberculosis in a hemodialysis patient: Case report

Author

Kushihata, S., Yorioka, N., Nishida, Y, Amimoto, D., Takasugi, T., Taniyama, K., and Yamakido, M.

Abstract

A 57 year-old male dialysis patient died soon after the onset of high fever, hypoglycemia, and disturbance of consciousness. Autopsy revealed granulomatous lesions associated with caseous necrosis mainly found in the liver, despite the absence of pulmonary changes on chest radiographs performed during the patients illness. It appears that tubercle bacilli were hematogenously disseminated mainly to the liver causing miliary tuberculosis without producing typical diffuse lesions in the lungs. Since tuberculosis is a common complication in hemodialysis patients, the potential development of atypical miliary tuberculosis should always be borne in mind. (Int J Artif Organs 1998; 21:23–5)

Published
1998
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