Researchers Database

komada takanori

    DivisionofInflammationResearch Assistant Professor
Last Updated :2021/10/21

Researcher Information

J-Global ID

Published Papers

  • Homare Ito, Ai Sadatomo, Yoshiyuki Inoue, Naoya Yamada, Emi Aizawa, Erika Hishida, Ryo Kamata, Tadayoshi Karasawa, Hiroaki Kimura, Sachiko Watanabe, Takanori Komada, Hisanaga Horie, Joji Kitayama, Naohiro Sata, Masafumi Takahashi
    Biochemical and biophysical research communications 519 (1) 15 - 22 0006-291X 2019/10 [Refereed][Not invited]
    BACKGROUND: Intestinal ischemia/reperfusion (I/R) injury is a life-threatening complication that leads to inflammation and remote organ damage. However, the underlying mechanism is not yet fully understood. Toll-like receptor 5 (TLR5) is highly expressed in mucosa and recognizes flagellin, the main component of the bacterial flagella. Here, we investigated the role of TLR5 in inflammation and tissue damage after intestinal I/R injury using TLR5-deficient mice. METHODS AND RESULTS: Intestinal levels of TLR5 mRNA and flagellin protein were elevated in wild-type mice subjected to intestinal I/R. Although TLR5 deficiency had no effect on intestinal flagellin levels, it significantly attenuated intestinal injury and inflammatory responses after intestinal I/R. TLR5 deficiency also markedly improved survival in mice after intestinal I/R injury. In wild-type mice, intestinal I/R injury induced remote organ damage, particularly in the lung, which was attenuated by TLR5 deficiency. Furthermore, TLR5 deficiency prevented lung inflammatory responses and vascular permeability after intestinal I/R injury. CONCLUSION: These findings demonstrate a novel role of TLR5 and provide new insights into the mechanism underlying inflammation and tissue damage after intestinal I/R injury.
  • Komada T, Muruve DA
    Nature reviews. Nephrology 15 (8) 501 - 520 1759-5061 2019/08 [Refereed][Not invited]
  • Hishida E, Ito H, Komada T, Karasawa T, Kimura H, Watanabe S, Kamata R, Aizawa E, Kasahara T, Morishita Y, Akimoto T, Nagata D, Takahashi M
    Scientific reports 9 (1) 10363 - 10363 2019/07 [Refereed][Not invited]
    Long-term peritoneal dialysis (PD) therapy leads to peritoneal inflammation and fibrosis. However, the mechanism underlying PD-related peritoneal inflammation and fibrosis remains unclear. NLRP3 inflammasome regulates the caspase-1-dependent release of interleukin-1β and mediates inflammation in various diseases. Here, we investigated the role of NLRP3 inflammasome in a murine model of PD-related peritoneal fibrosis induced by methylglyoxal (MGO). Inflammasome-related proteins were upregulated in the peritoneum of MGO-treated mice. MGO induced parietal and visceral peritoneal fibrosis in wild-type mice, which was significantly reduced in mice deficient in NLRP3, ASC, and interleukin-1β (IL-1β). ASC deficiency reduced the expression of inflammatory cytokines and fibrotic factors, and the infiltration of macrophages. However, myeloid cell-specific ASC deficiency failed to inhibit MGO-induced peritoneal fibrosis. MGO caused hemorrhagic ascites, fibrin deposition, and plasminogen activator inhibitor-1 upregulation, but all of these manifestations were inhibited by ASC deficiency. Furthermore, in vitro experiments showed that MGO induced cell death via the generation of reactive oxygen species in vascular endothelial cells, which was inhibited by ASC deficiency. Our results showed that endothelial NLRP3 inflammasome contributes to PD-related peritoneal inflammation and fibrosis, and provide new insights into the mechanisms underlying the pathogenesis of this disorder.
  • Mizushina Y, Karasawa T, Aizawa K, Kimura H, Watanabe S, Kamata R, Komada T, Mato N, Kasahara T, Koyama S, Bando M, Hagiwara K, Takahashi M
    Journal of immunology (Baltimore, Md. : 1950) 0022-1767 2019/05 [Refereed][Not invited]
  • Platnich JM, Chung H, Lau A, Sandall CF, Bondzi-Simpson A, Chen HM, Komada T, Trotman-Grant AC, Brandelli JR, Chun J, Beck PL, Philpott DJ, Girardin SE, Ho M, Johnson RP, MacDonald JA, Armstrong GD, Muruve DA
    Cell reports 25 (6) 1525 - 1536.e7 2018/11 [Refereed][Not invited]
  • Lau A, Chung H, Komada T, Platnich JM, Sandall CF, Choudhury SR, Chun J, Naumenko V, Surewaard BG, Nelson MC, Ulke-Lemée A, Beck PL, Benediktsson H, Jevnikar AM, Snelgrove SL, Hickey MJ, Senger DL, James MT, Macdonald JA, Kubes P, Jenne CN, Muruve DA
    The Journal of clinical investigation 128 (7) 2894 - 2913 0021-9738 2018/07 [Refereed][Not invited]
  • Komada T, Chung H, Lau A, Platnich JM, Beck PL, Benediktsson H, Duff HJ, Jenne CN, Muruve DA
    Journal of the American Society of Nephrology : JASN 29 (4) 1165 - 1181 1046-6673 2018/04 [Refereed][Not invited]
  • Hiroaki Kimura, Fumitake Usui, Tadayoshi Karasawa, Akira Kawashima, Koumei Shirasuna, Yoshiyuki Inoue, Takanori Komada, Motoi Kobayashi, Yoshiko Mizushina, Tadashi Kasahara, Koichi Suzuki, Yusaku Iwasaki, Toshihiko Yada, Patrizio Caturegli, Masafumi Takahashi
    SCIENTIFIC REPORTS 5 15883  2045-2322 2015/10 [Refereed][Not invited]
    Inflammation plays an important role in the development of obesity and metabolic disorders; however, it has not been fully understood how inflammation occurs and is regulated in their pathogenesis. Low-molecular mass protein-7 (LMP7) is a proteolytic subunit of the immunoproteasome that shapes the repertoire of antigenic peptides on major histocompatibility complex class I molecule. In this study, we investigated the role of LMP7 in the development of obesity and metabolic disorders using LMP7-deficient mice. LMP7 deficiency conveyed resistant to obesity, and improved glucose intolerance and insulin sensitivity in mice fed with high-fat diet (HFD). LMP7 deficiency decreased pancreatic lipase expression, increased fecal lipid contents, and inhibited the increase of plasma triglyceride levels upon oral oil administration or HFD feeding. Using bone marrow-transferred chimeric mice, we found that LMP7 in both bone marrow-and non-bone marrow-derived cells contributes to the development of HFD-induced obesity. LMP7 deficiency decreased inflammatory responses such as macrophage infiltration and chemokine expression while it increased serum adiponection levels. These findings demonstrate a novel role for LMP7 and provide new insights into the mechanisms underlying inflammation in the pathophysiology of obesity and metabolic disorders.
  • Takanori Komada, Fumitake Usui, Akira Kawashima, Hiroaki Kimura, Tadayoshi Karasawa, Yoshiyuki Inoue, Motoi Kobayashi, Yoshiko Mizushina, Tadashi Kasahara, Shun'ichiro Taniguchi, Shigeaki Muto, Daisuke Nagata, Masafumi Takahashi
    SCIENTIFIC REPORTS 5 10901  2045-2322 2015/06 [Refereed][Not invited]
    Rhabdomyolysis is one of the main causes of community-acquired acute kidney injury (AKI). Although inflammation is involved in the pathogenesis of rhabdomyolysis-induced AKI (RIAKI), little is known about the mechanism that triggers inflammation during RIAKI. Recent evidence has indicated that sterile inflammation triggered by tissue injury can be mediated through multiprotein complexes called the inflammasomes. Therefore, we investigated the role of NLRP3 inflammasomes in the pathogenesis of RIAKI using a glycerol-induced murine rhabdomyolysis model. Inflammasomerelated molecules were upregulated in the kidney of RIAKI. Renal tubular injury and dysfunction preceded leukocyte infiltration into the kidney during the early phase of RIAKI, and they were markedly attenuated in mice deficient in NLRP3, ASC, caspase-1, and interleukin (IL)-1 beta compared with those in wild-type mice. No difference in leukocyte infiltration was observed between wild-type and NLRP3-deficient mice. Furthermore, NLRP3 deficiency strikingly suppressed the expression of renal injury markers and inflammatory cytokines and apoptosis of renal tubular cells. These results demonstrated that NLRP3 inflammasomes contribute to inflammation, apoptosis, and tissue injury during the early phase of RIAKI and provide new insights into the mechanism underlying the pathogenesis of RIAKI.
  • Yamazaki T, Akimoto T, Iwazu Y, Sugase T, Takeshima E, Numata A, Komada T, Yoshizawa H, Otani N, Morishita Y, Saito O, Takemoto F, Muto S, Kusano E, Nagata D
    CEN case reports 4 (1) 106 - 111 2015/05 [Refereed][Not invited]
  • Yoshiko Mizushina, Koumei Shirasuna, Fumitake Usui, Tadayoshi Karasawa, Akira Kawashima, Hiroaki Kimura, Motoi Kobayashi, Takanori Komada, Yoshiyuki Inoue, Naoko Mato, Hideaki Yamasawa, Eicke Latz, Yoichiro Iwakura, Tadashi Kasahara, Masashi Bando, Yukihiko Sugiyama, Masafumi Takahashi
    JOURNAL OF BIOLOGICAL CHEMISTRY 290 (8) 5065 - 5077 0021-9258 2015/02 [Refereed][Not invited]
    Supplemental oxygen inhalation is frequently used to treat severe respiratory failure; however, prolonged exposure to hyperoxia causes hyperoxic acute lung injury (HALI), which induces acute respiratory distress syndrome and leads to high mortality rates. Recent investigations suggest the possible role of NLRP3 inflammasomes, which regulate IL-1 beta production and lead to inflammatory responses, in the pathophysiology of HALI; however, their role is not fully understood. In this study, we investigated the role of NLRP3 inflammasomes in mice with HALI. Under hyperoxic conditions, NLRP3(-/-) mice died at a higher rate compared with wild-type and IL-1 beta(-/-) mice, and there was no difference in IL-1 beta production in their lungs. Under hyperoxic conditions, the lungs of NLRP3(-/-) mice exhibited reduced inflammatory responses, such as inflammatory cell infiltration and cytokine expression, as well as increased and decreased expression of MMP-9 and Bcl-2, respectively. NLRP3(-/-) mice exhibited diminished expression and activation of Stat3, which regulatesMMP-9 and Bcl-2, in addition to increased numbers of apoptotic alveolar epithelial cells. In vitro experiments revealed that alveolar macrophages and neutrophils promoted Stat3 activation in alveolar epithelial cells. Furthermore, NLRP3 deficiency impaired the migration of neutrophils and chemokine expression by macrophages. These findings demonstrate that NLRP3 regulates Stat3 signaling in alveolar epithelial cells by affecting macrophage and neutrophil function independent of IL-1 beta production and contributes to the pathophysiology of HALI.
  • Tadayoshi Karasawa, Akira Kawashima, Fumitake Usui, Hiroaki Kimura, Koumei Shirasuna, Yoshiyuki Inoue, Takanori Komada, Motoi Kobayashi, Yoshiko Mizushina, Junji Sagara, Masafumi Takahashi
    FEBS OPEN BIO 5 348 - 356 2211-5463 2015 [Refereed][Not invited]
    Increasing evidence indicates that caspase recruitment domain (CARD)-mediated caspase-1 (CASP1) assembly is an essential process for its activation and subsequent interleukin (IL)-1 beta release, leading to the initiation of inflammation. Both CARD16 and CARD17 were previously reported as inhibitory homologs of CASP1; however, their molecular function remains unclear. Here, we identified that oligomerization activity allows CARD16 to function as a CASP1 activator. We investigated the molecular characteristics of CARD16 and CARD17 in transiently transfected HeLa cells. Although both CARD16 and CARD17 interacted with CASP1CARD, only CARD16 formed a homo-oligomer. Oligomerized CARD16 formed a filament-like structure with CASP1CARD and a speck with apoptosis-associated speck-like protein containing a CARD. A filament-like structure formed by CARD16 promoted CASP1 filament assembly and IL-1 beta release. In contrast, CARD17 did not form a homo-oligomer or filaments and inhibited CASP1-dependent IL-1 beta release. Mutated CARD16(D27G), mimicking the CARD17 amino acid sequence, formed a homo-oligomer but failed to form a filament-like structure. Consequently, CARD16D27G weakly promoted CASP1 filament assembly and subsequent IL-1 beta release. These results suggest that oligomerized CARD16 promotes CARD-mediated molecular assembly and CASP1 activation. (C) 2015 The Authors. Published by Elsevier B.V. on behalf of the Federation of European Biochemical Societies. This is an open access article under the CC BY-NC-ND license.
  • Takanori Komada, Fumitake Usui, Koumei Shirasuna, Akira Kawashima, Hiroaki Kimura, Tadayoshi Karasawa, Satoshi Nishimura, Junji Sagara, Tetsuo Noda, Shun'ichiro Taniguchi, Shigeaki Muto, Daisuke Nagata, Eiji Kusano, Masafumi Takahashi
    AMERICAN JOURNAL OF PATHOLOGY 184 (5) 1287 - 1298 0002-9440 2014/05 [Refereed][Not invited]
    Inflammation plays a crucial role in the pathophysiologicat characteristics of chronic kidney disease; however, the inflammatory mechanisms underlying the chronic kidney disease process remain unclear. Recent evidence indicates that sterile inflammation triggered by tissue injury is mediated through a muttiprotein complex called the inflammasome. Therefore, we investigated the role of the inflammasome in the development of chronic kidney disease using a murine unilateral ureteral obstruction (UUO) model. Inflammasome-related molecules were up-regulated in the kidney after UUO. Apoptosis-associated speck-like protein containing a caspase recruitment domain deficiency significantly reduced inflammatory responses, such as inflammatory cell infiltration and cytokine expression, and improved subsequent renal injury and fibrosis. Furthermore, apoptosis-associated speck-like protein containing a caspase recruitment domain was specifically up-regulated in collecting duct (CD) epithelial cells of the UUO-treated kidney. In vitro experiments showed that extracellular adenosine triphosphate (ATP) induced inflammasome activation in CD epithelial cells through P2X(7)-potassium efflux and reactive oxygen species dependent pathways. These results demonstrate the molecular basis for the inflammatory response in the process of chronic kidney disease and suggest the CD inflammasome as a potential therapeutic target for preventing chronic kidney disease progression.
  • Tomoyuki Yamazaki, Tetsu Akimoto, Kousuke Okuda, Taro Sugase, Eri Takeshima, Akihiko Numata, Yoshiyuki Morishita, Yoshitaka Iwazu, Hiromichi Yoshizawa, Takanori Komada, Kana Iwazu, Osamu Saito, Fumi Takemoto, Shigeaki Muto, Eiji Kusano
    INTERNAL MEDICINE 53 (2) 115 - 119 0918-2918 2014 [Refereed][Not invited]
    Mixed cryoglobulinemia is occasionally seen in patients with hepatitis B virus (HBV) infection. This report presents the case of a quiescent HBV carrier who had type II mixed cryoglobulinemia, protracted purpura, ulcerative skin lesions and advanced chronic kidney disease. The cutaneous manifestations of the patient improved along with a decrease in the serum cryoglobulin and HBV-deoxyribonucleic acid levels following the initiation of oral entecavir in combination with plasmapheresis. However, the patient ultimately required prednisolone due to the limited benefits of these treatments. We also discuss various concerns regarding steroid treatment in patients with mixed cryoglobulinemia complicated by HBV infection.
  • Takanori Komada, Yoshiyuki Morishita, Masafumi Kitamura, Kana Iwazu, Akihiko Numata, Takahisa Kobayashi, Hisashi Yamamoto, Tetsu Akimoto, Osamu Saito, Yasuhiro Ando, Fumi Takemoto, Shigeaki Muto, Wako Yumura, Eiji Kusano
    INTERNAL MEDICINE 52 (12) 1383 - 1387 0918-2918 2013 [Refereed][Not invited]
    We herein report the case of a 75-year-old man who developed an increased serum creatinine level (4.93 mg/dL) and oliguria with massive proteinuria (7.14 g/day) on the second day after a single oral administration of high-dose (56 mg) minodronate. The histology of a renal biopsy showed one area of glomerular sclerosis among 20 glomeruli with global foot process effacement of podocytes and mild infiltration of lymphocytes and eosinophils into the interstitial space. Acute kidney injury in nephrotic syndrome due to focal segmental glomerular sclerosis induced by minodronate was diagnosed. Following cessation of minodronate without the administration of immunosuppressive agents, the patient's renal function and proteinuria markedly improved.
  • Ayako Kokuzawa, Yoshiyuki Morishita, Hiromichi Yoshizawa, Kana Iwazu, Takanori Komada, Tetsu Akimoto, Osamu Saito, Takashi Oda, Fumi Takemoto, Yasuhiro Ando, Shigeaki Muto, Wako Yumura, Eiji Kusano
    Internal Medicine 52 (18) 2087 - 2091 0918-2918 2013 [Refereed][Not invited]
    We herein report the case of a 17-year-old man who developed an increased plasma creatinine level (11.1 mg/dL) and oliguria with massive proteinuria (27.3 g/day) four weeks after an abraded wound to his right knee. The histology of the renal biopsy specimens showed diffuse endocapillary proliferative glomerulonephritis with the deposition of nephritis-associated plasmin receptor in the glomerulus. A case of acute kidney injury due to nephrotic syndrome caused by acute post-streptococcal glomerulonephritis was diagnosed. His renal function and proteinuria were improved with supportive care, including hemodialysis, without the administration of immunosuppressive agents. © 2013 The Japanese Society of Internal Medicine.
  • Tetsu Akimoto, Hiromichi Yoshizawa, Yuko Watanabe, Akihiko Numata, Tomoyuki Yamazaki, Eri Takeshima, Kana Iwazu, Takanori Komada, Naoko Otani, Yoshiyuki Morishita, Chiharu Ito, Kazuhiro Shiizaki, Yasuhiro Ando, Shigeaki Muto, Makoto Kuro-o, Eiji Kusano
    BMC nephrology 13 155 - 155 2012/11 [Refereed][Not invited]
    BACKGROUND: Klotho is a single-pass transmembrane protein, which appears to be implicated in aging. The purpose of the present study was to characterize the relationship between the soluble Klotho level and renal function in patients with various degrees of chronic kidney disease (CKD). METHODS: The levels of soluble Klotho in the serum and urine obtained from one hundred thirty-one CKD patients were determined by a sandwich enzyme-linked immunosorbent assay system. RESULTS: The amount of urinary excreted Klotho during the 24 hr period ranged from 1.6 to 5178 ng/day (median 427 ng/day; interquartile range [IR] 56.8-1293.1), and the serum Klotho concentration ranged from 163.9 to 2123.7 pg/ml (median 759.7 pg/ml; IR 579.5-1069.1). The estimated glomerular filtration rate (eGFR) was significantly correlated with the log-transformed values of the amount of 24 hr urinary excreted Klotho (r = 0.407, p < 0.01) and the serum Klotho levels (r = 0.232, p < 0.01). However, a stepwise multiple regression analysis identified eGFR to be a variable independently associated only with the log-transformed value of the amount of 24-hr urinary excreted Klotho but not with the log-transformed serum Klotho concentration. Despite the strong correlation between random urine protein-to-creatinine ratio and the 24 hr urinary protein excretion (r = 0.834, p < 0.01), a moderate linear association was observed between the log-transformed value of the amount of 24 hr urinary excreted Klotho and that of the urinary Klotho-to-creatinine ratio (Klotho/Cr) in random urine specimens (r = 0.726, p < 0.01). CONCLUSIONS: The amount of urinary Klotho, rather than the serum Klotho levels, should be linked to the magnitude of the functioning nephrons in CKD patients. The use of random urine Klotho/Cr as a surrogate for the amount of 24-hr urinary excreted Klotho needs to be evaluated more carefully.
  • Jun Suzuki, Takanori Komada, Keiji Hirai, Hirohisa Tsuruoka, Honami Mori, Izumi Yoshida, Kaoru Tabei
    INTERNAL MEDICINE 51 (6) 629 - 634 0918-2918 2012 [Refereed][Not invited]
    Epstein-Barr virus (EBV) infection is common in adolescence, but fulminant infection is very rare. A 40-year-old man presented with high fever and sore throat. Symptoms, including cervical lymphadenopathy, jaundice, atypical lymphocytosis, respiratory distress and oliguria, suggested infectious mononucleosis with multiple organ failure that required mechanical ventilation and renal replacement therapy. Virus markers were consistent with primary EBV infection. Renal function was gradually improved by corticosteroid therapy. Renal biopsy revealed acute tubulointerstitial nephritis. In situ hybridizaion EBV-encoded RNA 1 did not show the presence of virus in the kidney, but acute kidney injury may be explained by cytotoxic/suppressor T lymphocyte infiltration,
  • Izumi Yoshida, Susumu Ookawara, Katsunobu Ando, Takayuki Uchida, Atsushi Horiguchi, Itsuro Nakajima, Takanori Komada, Honami Mori, Kaoru Tabei
    THERAPEUTIC APHERESIS AND DIALYSIS 15 (3) 319 - 326 1744-9979 2011/06 [Refereed][Not invited]
    Together with Nikkiso in Shizuoka, Japan, we developed a new method for measuring the rate of vascular access recirculation by the blood volume monitor. This measurement is performed via a method of dilution that employs a marker produced by rapid ultrafiltration using a dialysis machine. In this paper, we evaluate the reliability and safety of this machine, in vitro and in vivo. The safety of this method was evaluated by investigating hemolysis after rapid ultrafiltration. The measurement of free hemoglobin, potassium and haptoglobin in the circulating blood were performed before and after rapid ultrafiltration. No data was found to indicate hemolysis in vivo, detected by an increase in potassium or a decrease in haptoglobin. Evaluation of reliability in an experimental system was also performed on an in vitro recirculation system at a rate of 0, 10, 25, 50, and 70%. Almost all of the measured rates were within +/- 10% of the theoretical rate. We performed 20 hemodialysis experiments with vascular access recirculation applying this monitor and simultaneous urea and creatinine dilution methods, which were the recommended standard measurements for vascular recirculation. In 53 measurements of standard vascular shunts with no postural change, differences of the results between the monitor and both dilution methods were only 4.0% and 3.2%, respectively. Regression analysis showed a significant and positive correlation between them (P < 0.0001). We conclude that this new method for measuring vascular access recirculation is applicable in terms of both accuracy and ease of operation.
  • Izumi Yoshida, Katsunobu Ando, Yasuhiro Ando, Susumu Ookawara, Masayuki Suzuki, Hiroaki Furuya, Osamu Iimura, Daisuke Takada, Masaharu Kajiya, Takanori Komada, Honami Mori, Kaoru Tabei
    THERAPEUTIC APHERESIS AND DIALYSIS 14 (6) 560 - 565 1744-9979 2010/12 [Refereed][Not invited]
    We developed a new optical device (Nikkiso) to assess changes through blood volume monitoring (BVM) during hemodialysis and were able to determine the ideal levels in which changes in blood volume percentage (BV%) occur among hemodialysis patients in one hemodialysis center. We evaluated both the reliability of BVM and these ideal levels in a multicenter group. The purpose of this manuscript is to develop a navigating system to set dry weight in a variety of situations as the final goal. First, based on the obtained BVM (BV%(BVM)) measurements, the relationships between BV% and hematocrit (BV%(HT)) and between BV% and CRIT-LINE (BV%(CLM); Hema Metrics, Kaysville, UT, USA) were then evaluated. In 30 hemodialysis patients, there was a close correlation between both BV%(BVM) vs. BV%(HT) and BV%(BVM) vs. BV%(CLM) (n = 30, r = 0.967, P < 0.001, and n = 36, r = 0.7867, P < 0.001, respectively). Second, BV% data were obtained from 464 treatment cases performed on 26 subjects in one satellite hemodialysis center on patients whose body weight was deemed clinically suitable. The formulas for the levels of BV% (standardized by the percent change in body weight at the end of hemodialysis treatment: BW%end) were determined. Finally, we revalidated the reliability of the above levels. A total of 1126 measurements were performed on 201 patients whose body weights were deemed suitable in seven hemodialysis centers. New ideal levels were then recalculated. We therefore conclude that BVM is a sufficiently accurate method of monitoring BV% in hemodialysis treatment. Most well-controlled hemodialysis patients display the same pattern of BV%/BW%end. Monitoring BV% during hemodialysis is beneficial for determining dry weight (DW).
  • Izumi Yoshida, Takanori Komada, Yuki Sakuma, Honami Mori, Izumi Funayama, Kaoru Tabei
    Japanese Journal of Nephrology 51 (2) 121 - 129 0385-2385 2009 [Refereed][Not invited]
    Background : Oral adsorbent AST-120 reduces uremic toxins, such as indoxyl sulfate, and retards the progression of chronic kidney disease (CKD). The present study was conducted to elucidate the association between the progression of CKD and the combined effect of AST-120 and standard care based on diet therapy and medications such as ACE inhibitor and ARB Method : Retrospective analysis was performed using forty-four CKD patients (chronic glomerular nephritis 16, diabetic nephropathy 9, nephrosclerosis 13, and others 6) who were treated by AST-120 during the period from October, 2001 through December, 2004 and followed up for more than 6 months. The selection criteria were an estimated creatinine clearance (eCCr) of 30 mL/min or under at the initiation of treatment and a negative change in eCCr over time (ΔeCCr (mL/min/year)) before AST-120 treatment. The eCCr was calculated using the Cockcroft-Gault equation and the ΔeCCr was evaluated as a marker for the progression of chronic renal failure. Result : Overall ΔeCCr before and after AST-120 treatment significantly improved from -7.28 ± 6.33 to - 4.29±5.09(paired Wilcoxon test, p< 0.05). AST-120 led to greater +improvement of ΔeCCr in patients with an AeCCr of less than - 10 mL/min/year before AST-120 treatment and who had higher blood uric acid, urinary protein, and urinary specific gravity valves. Conclusion : This finding suggests that AST-120 treatment is effective in slowing the progression of chronic kidney disease, especially, in patients who exhibit a poor response to standard care.

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