Tokushima University / Educator and Researcher Directory --- Tamaki, Masanori

Personal Web Page

https://researchmap.jp/tamakimasanori (researchmap)

Field of Study

○	Life sciences [Nephrology]

Subject of Study

Book / Paper

Academic Paper (Judged Full Paper):

1.	Kazuhiro Hasegawa, Yusuke Sakamaki, Masanori Tamaki and Shu Wakino : PCK1 Protects against Mitoribosomal Defects in Diabetic Nephropathy in Mouse Models., Journal of the American Society of Nephrology, Vol.34, No.8, 1343-1365, 2023. (Summary) PCK1 preserves mitoribosomal function and may play a novel protective role in DN. (Keyword) Mice / Animals / Diabetic Nephropathies / Diabetes Mellitus, Experimental / Collagen Type IV / Albuminuria / Diabetes Mellitus, Type 2 / Phosphoenolpyruvate / Phosphoenolpyruvate Carboxykinase (GTP) / Sodium-Glucose Transporter 2 Inhibitors / Disease Models, Animal / Mice, Transgenic / Fibrosis / Mice, Knockout / Glucose (Link to Publication Site) ● Publication site (DOI): 10.1681/ASN.0000000000000156 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37199399 ● Search Scopus @ Elsevier (PMID): 37199399 ● Search Scopus @ Elsevier (DOI): 10.1681/ASN.0000000000000156 (DOI: 10.1681/ASN.0000000000000156, PubMed: 37199399)
2.	Masanori Minato, Taichi Murakami, Naoki Takahashi, Hiroyuki Ono, Kenji Nishimura, Masanori Tamaki, Kojiro Nagai, Hideharu Abe, Masayuki Iwano, Kensuke Joh and Toshio Doi : Glucocorticoid-dependent Tubulointerstitial Nephritis with IgM-positive Plasma Cells Presenting with Intracellular Crystalline Inclusions within the Rough Endoplasmic Reticulum., Internal Medicine, 2021. (Summary) Tubulointerstitial nephritis (TIN) with IgM-positive plasma cells (IgMPC-TIN) is an autoimmune kidney disease characterized by IgM/CD138-double-positive plasma cell infiltration in the tubulointerstitium. A 50-year-old man developed IgMPC-TIN and presented with crystalline inclusions in the rough endoplasmic reticulum. Intracellular crystal formation is a rare finding in paraprotein-related kidney diseases, but this case showed no pathogenic monoclonal immunoglobulin. Prednisolone (PSL, 30 mg) improved the TIN, but PSL tapering resulted in the recurrence of TIN. Combination therapy with 15 mg PSL and 150 mg mizoribine ultimately stabilized TIN. This case offers original evidence concerning the pathophysiology and treatment strategy of IgMPC-TIN. (Tokushima University Institutional Repository) ● Metadata: 118015 (Link to Publication Site) ● Publication site (DOI): 10.2169/internalmedicine.7118-21 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33840699 ● Search Scopus @ Elsevier (PMID): 33840699 ● Search Scopus @ Elsevier (DOI): 10.2169/internalmedicine.7118-21 (Tokushima University Institutional Repository: 118015, DOI: 10.2169/internalmedicine.7118-21, PubMed: 33840699)
3.	Kenji Nishimura, Kensei Taguchi, Seiji Kishi, R Craig Brooks, Arisa Ochi, Hiroyuki Kadoya, Yasumasa Ikeda, Masashi Miyoshi, Masanori Tamaki, Hideharu Abe, Ken-Ichi Aihara, Naoki Kashihara and Kojiro Nagai : Dual disruption of eNOS and ApoE gene accelerates kidney fibrosis and senescence after injury., Biochemical and Biophysical Research Communications, Vol.556, 142-148, 2021. (Summary) mice (DKO) were obtained by breeding. Unilateral ureteral obstruction (UUO) was performed on 8-10 week old male mice and the degree of renal tubular injury, fibrosis and kidney senescence were evaluated. DKO manifested elevated blood pressure, higher total cholesterol and lower HDL than WT. DKO showed sustained kidney injury molecule-1 protein expression. Kidney fibrosis was significantly higher in ApoEKO and DKO. mRNA expression of genes related to kidney fibrosis was the highest in DKO. The mRNA expression of Zinc-α2-Glycoprotein and heme oxygenase-1 were significantly decreased in DKO. Furthermore, mRNA expression of p53, p21 and p16 were increased both in ApoEKO and DKO, with DKO being the highest. Senescence associated β-gal positive tubule area was significantly increased in DKO. Increased DNA damage and target of rapamycin-autophagy spatial coupling compartments (TASCCs) formation was found in DKO. Mice with endothelial dysfunction and dyslipidemia developed kidney fibrosis and accelerated senescence even in young mice after injury. These data highlight the fact managing lifestyle-related diseases from a young age is important for CKD prevention. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbrc.2021.03.111 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33845306 ● Search Scopus @ Elsevier (PMID): 33845306 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbrc.2021.03.111 (DOI: 10.1016/j.bbrc.2021.03.111, PubMed: 33845306)
4.	Taichi Murakami, Kenji Nishimura, Hiroyuki Ono, Sayo Ueta, Eriko Shibata, Seiji Kishi, Masanori Tamaki, Keiko Miya, Hisato Shima, Manabu Tashiro, Tomoko Inoue, Kazuhiko Kawahara, Kojiro Nagai, Hideharu Abe, Jun Minakuchi and Toshio Doi : Clinical characteristics associated with 1-year tolvaptan efficacy in autosomal dominant polycystic kidney disease with a wide range of kidney functions., The Journal of Medical Investigation : JMI, Vol.67, No.3.4, 315-320, 2020. (Summary) Autosomal dominant polycystic kidney disease (ADPKD) develops into end-stage kidney disease by 65 years of age in an estimated 45%-70% of patients. Recent trials revealed that tolvaptan inhibits disease progression both in early-stage or late-stage ADPKD ; however, stratified analysis showed a difference of favorable factors correlated with tolvaptan efficacy between early-stage and late-stage ADPKD. Thus, we examined the efficacy of tolvaptan in ADPKD with a wide range of estimated glomerular filtration rates (eGFR). We enrolled 24 patients with eGFR 35.3 (28.0-65.5) ml / min / 1.73m2 and evaluated treatment effect as ΔΔeGFR (ml / min / 1.73m2 / year) or ΔΔtotal kidney volume (TKV) (% / year) that was calculated as post-treatment annual change - pre-treatment annual change. Pre ΔeGFR was significantly low in eGFR responders, defined as ΔΔeGFR > 0 ml / min / 1.73m2 / year. In eGFR responders, pre ΔeGFR, post ΔeGFR, eGFR, TKV, and proteinuria were significantly correlated with ΔΔeGFR. In TKV responders defined as ΔΔTKV > 5 % / year, we identified hypertension history, proteinuria, TKV, and post ΔTKV as significantly correlated factors with ΔΔTKV. In conclusion, pre ΔeGFR may be a predictive factor of therapeutic efficacy on kidney function. Tolvaptan may have greater efficacy in early-stage ADPKD with rapid GFR decline or with well-controlled blood pressure. J. Med. Invest. 67 : 315-320, August, 2020. (Tokushima University Institutional Repository) ● Metadata: 115436 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.67.315 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33148908 ● Summary page in Scopus @ Elsevier: 2-s2.0-85095569571 (Tokushima University Institutional Repository: 115436, DOI: 10.2152/jmi.67.315, PubMed: 33148908, Elsevier: Scopus)
5.	Kenji Nishimura, Taichi Murakami, Toshihiro Sakurai, Masashi Miyoshi, Kiyoe Kurahashi, Seiji Kishi, Masanori Tamaki, Tatsuya Tominaga, Sumiko Yoshida, Kojiro Nagai, Hideharu Abe, Shu-Ping Hui, Kazuhiko Kotani and Toshio Doi : Circulating Apolipoprotein L1 is associated with insulin resistance-induced abnormal lipid metabolism., Scientific Reports, Vol.9, No.1, 14869, 2019. (Summary) Circulating ApolipoproteinL1 (ApoL1) is a component of pre-β-high-density lipoprotein (HDL), however little is known about the relationship of ApoL1 with cardiometabolic factors. Considering previous studies reporting the correlation of ApoL1 to triglyceride, we have hypothesized that ApoL1 associates with insulin-related metabolism. The current study examined their associations in 126 non-diabetic subjects and 36 patients with type 2 diabetes (T2DM). Non-diabetic subjects demonstrated triglyceride (standardized coefficients [s.c.] = 0.204, p < 0.05), body mass index (s.c. =0.232, p < 0.05) and HDL cholesterol (s.c. = -0.203, p < 0.05) as independent determinant of ApoL1 levels, and the significant elevation of ApoL1 in metabolic syndrome. Lipoprotein fractionation analysis revealed the predominant distribution of ApoL1 in large HDL fraction, and the significant increase of ApoL1 in large LDL fraction in high ApoL1 samples with insulin resistance. In T2DM, ApoL1 was higher in T2DM with metabolic syndrome, however ApoL1 was lower with β cell dysfunction. Insulin significantly promotes ApoL1 synthesis and secretion in HepG2 cells. In conclusion, circulating ApoL1 may be associated with abnormal HDL metabolism in insulin resistant status. This may suggest a regulation of insulin signal on the ApoL1 level, leading to offer a novel insight to the ApoL1 biology. (Tokushima University Institutional Repository) ● Metadata: 114663 (Link to Publication Site) ● Publication site (DOI): 10.1038/s41598-019-51367-7 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31619724 ● Search Scopus @ Elsevier (PMID): 31619724 ● Search Scopus @ Elsevier (DOI): 10.1038/s41598-019-51367-7 (Tokushima University Institutional Repository: 114663, DOI: 10.1038/s41598-019-51367-7, PubMed: 31619724)
6.	Taichi Murakami, Masanori Tamaki, Seiji Kishi, Kojiro Nagai, Hideharu Abe, Yoshimi Bando, Yuko Toyoda, Hirokazu Ogino, Yasuhiko Nishioka, Sayo Ueda, Toshio Doi and Motokazu Matsuura : Systemic Sarcoidosis Presenting with Renal Involvement Caused by Various Sarcoidosis-associated Pathophysiological Conditions, Internal Medicine, Vol.58, No.5, 679-684, 2019. (Summary) A 61-year-old man was diagnosed with sarcoidosis involving the lungs, eyes, parotid gland and extrathoracic lymph nodes complicated by chronic kidney injury and hypercalcemia. Kidney biopsy showed non-specific interstitial nephritis and nephrosclerosis. However, immunohistochemical staining of cell surface markers revealed a multinucleated giant macrophage surrounded by T-cells, suggesting granulomatous interstitial nephritis. Corticosteroid improved the kidney function, and reduced the serum levels of calcium and angiotensin-converting enzyme. Sarcoid nephropathy may be caused by the combination of several sarcoidosis-associated pathophysiological conditions and a comprehensive kidney examination should be performed to assess the type of injury when determining a treatment strategy. (Keyword) Biomarkers / Biopsy / calcium / Glucocorticoids / Humans / Hypercalcemia / Kidney / male / Middle Aged / Nephritis, Interstitial / Nephrosclerosis / Peptidyl-Dipeptidase A / Radionuclide Imaging / Sarcoidosis (Tokushima University Institutional Repository) ● Metadata: 114405 (Link to Publication Site) ● Publication site (DOI): 10.2169/internalmedicine.1558-18 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30449791 ● Summary page in Scopus @ Elsevier: 2-s2.0-85062415769 (Tokushima University Institutional Repository: 114405, DOI: 10.2169/internalmedicine.1558-18, PubMed: 30449791, Elsevier: Scopus)
7.	Fumiaki Obata, Hideharu Abe, Taichi Murakami, Sayo Ueda, Taizo Inagaki, Masanori Minato, Hiroyuki Ono, Kenji Nishimura, Eriko Shibata, Masanori Tamaki, Fumi Kishi, Seiji Kishi, Kojiro Nagai and Toshio Doi : Direct oral anticoagulant successfully used to treat an adult nephrotic patient complicated with portal vein thrombosis., CEN Case Reports, Vol.8, No.2, 134-138, 2019. (Summary) Thromboembolism is a major complication of nephrotic syndrome, with the renal vein being the most frequent site. However, the incidence of portal vein thrombosis (PVT) in patients with nephrotic syndrome is rare. We report a case of a relapsed steroid-dependent minimal change disease with incidental PVT. A 38-year-old man presented with anasarca. Elevated liver enzymes were discovered during routine blood testing within days after commencing treatment. Although drug-induced liver injuries are frequently observed with mild aminotransferase abnormality during therapy with steroid or immune-suppressive agents, imaging revealed a massive thrombus of the portal vein, which was treated by anticoagulant therapy with edoxaban. Treatment with anticoagulant therapy could normalize liver function. Two months after the initiation of treatment with edoxaban, the follow-up CT scan and ultrasound showed the disappearance of PVT. Our case suggests that much attention should be paid to PVT as a cause of liver enzyme elevation when treating patients with nephrotic syndrome. (Link to Publication Site) ● Publication site (DOI): 10.1007/s13730-019-00381-9 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30721455 ● Search Scopus @ Elsevier (PMID): 30721455 ● Search Scopus @ Elsevier (DOI): 10.1007/s13730-019-00381-9 (DOI: 10.1007/s13730-019-00381-9, PubMed: 30721455)
8.	Masanori Tamaki, Tatsuya Tominaga, Yui Fujita, Yasuhiko Koezuka, Go Ichien, Taichi Murakami, Seiji Kishi, Keiichi Yamamoto, Hideharu Abe, Kojiro Nagai and Toshio Doi : All-trans retinoic acid suppresses bone morphogenetic protein 4 in mouse diabetic nephropathy through a unique retinoic acid response element., American Journal of Physiology, Endocrinology and Metabolism, Vol.316, No.3, E418-E431, 2019. (Summary) Diabetic nephropathy (DN) causes mesangial matrix expansion, which results in glomerulosclerosis and renal failure. Collagen IV (COL4) is a major component of the mesangial matrix that is positively regulated by bone morphogenetic protein 4 (BMP4)/suppressor of mothers against decapentaplegic (Smad1) signaling. Because previous studies showed that retinoids treatment had a beneficial effect on kidney disease, we investigated the therapeutic potential of retinoids in DN, focusing especially on the regulatory mechanism of BMP4. Diabetes was induced with streptozotocin in 12-wk-old male Crl:CD1(ICR) mice, and, 1 mo later, we initiated intraperitoneal injection of all-trans retinoic acid (ATRA) three times weekly. Glomerular matrix expansion, which was associated with increased BMP4, phosphorylated Smad1, and COL4 expression, worsened in diabetic mice at 24 wk of age. ATRA administration alleviated DN and downregulated BMP4, phosopho-Smad1, and COL4. In cultured mouse mesangial cells, treatment with ATRA or a retinoic acid receptor-α (RARα) agonist significantly decreased BMP4 and COL4 expression. Genomic analysis suggested two putative retinoic acid response elements (RAREs) for the mouse Bmp4 gene. Chromatin immunoprecipitation analysis and reporter assays indicated a putative RARE of the Bmp4 gene, located 11,488-11,501 bp upstream of exon 1A and bound to RARα and retinoid X receptor (RXR), which suppressed BMP4 expression after ATRA addition. ATRA suppressed BMP4 via binding of a RARα/RXR heterodimer to a unique RARE, alleviating glomerular matrix expansion in diabetic mice. These findings provide a novel regulatory mechanism for treatment of DN. (Link to Publication Site) ● Publication site (DOI): 10.1152/ajpendo.00218.2018 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30601699 ● Search Scopus @ Elsevier (PMID): 30601699 ● Search Scopus @ Elsevier (DOI): 10.1152/ajpendo.00218.2018 (DOI: 10.1152/ajpendo.00218.2018, PubMed: 30601699)
9.	Eriko Shibata, Kojiro Nagai, Sayo Ueda, Hiroyuki Ono, Kenji Nishimura, Taizo Inagaki, Masanori Minato, Fumi Kishi, Masanori Tamaki, Taichi Murakami, Seiji Kishi, Hideharu Abe, Narushi Yokota, Jun Minakuchi and Toshio Doi : The utility and limitation of inferior vena cava diameter as a dry weight marker., The Journal of Medical Investigation : JMI, Vol.66, No.1.2, 172-177, 2019. (Summary) IVCdexp was a rough marker to estimate volume status and only useful in suggesting apparent hypervolemia or hypovolemia. We should know that the IVCdexp value is affected by a lotof factors and not a definitive marker for estimating practical DW. J. Med. Invest. 66 : 172-177, February, 2019. (Tokushima University Institutional Repository) ● Metadata: 113414 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.66.172 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31064933 ● Search Scopus @ Elsevier (PMID): 31064933 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.66.172 (Tokushima University Institutional Repository: 113414, DOI: 10.2152/jmi.66.172, PubMed: 31064933)
10.	Hideharu Abe, Akiko Sakurai, Hiroyuki Ono, Sanae Hayashi, Sakiya Yoshimoto, Arisa Ochi, Sayo Ueda, Kenji Nishimura, Eriko Shibata, Masanori Tamaki, Fumi Kishi, Seiji Kishi, Taichi Murakami, Kojiro Nagai and Toshio Doi : Urinary Exosomal mRNA of WT1 as Diagnostic and Prognostic Biomarker for Diabetic Nephropathy, The Journal of Medical Investigation : JMI, Vol.65, No.3.4, 208-215, 2018. (Summary) Diabetic nephropathy (DN) is the major cause of end-stage renal failure and is associated with increased morbidity and mortality as compared to other causes of renal disease. Albuminuria is often the first clinical indicator of the presence of DN. However, albuminuria or proteinuria is a common symptom in patients with various renal disorders. Therefore, specific biomarkers for the diagnosis of DN are required. A primary hallmark of DN is the progressive damage and death of glomerular podocytes, resulting in the leaking of proteins into the urine. Urinary exosomes released by podocytes are microvesicles containing information of the originated cells. Podocyte-derived signal transduction factors (PDSTFs) are good candidates to assess podocyte injuries. The profile of PDSTFs in urinary exosomes from patients with DN is different from that from patients with minimal change nehrotic syndrome. In addition, PDSTFs molecules in exosomes were derived from primary murine podocytes under high glucose conditions. Among PDSTFs in urinary exosomes, Wilms tumor 1 (WT1) levels reflected damage of diabetic glomeruli in the patients. Urinary exosomal WT1 can predict the decline in eGFR for the following several years. In conclusion, urinary exosomal WT1 is a useful biomarker to improve risk stratification in patients with DN. J. Med. Invest. 65:208-215, August, 2018. (Keyword) Adolescent / Adult / Biomarkers / Case-Control Studies / Cells, Cultured / Diabetic Nephropathies / Exosomes / Genes, Wilms Tumor / Genetic Markers / Humans / Middle Aged / Nephrosis, Lipoid / Podocytes / Prognosis / RNA, Messenger / WT1 Proteins / Young Adult (Tokushima University Institutional Repository) ● Metadata: 112239 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.65.208 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30282862 ● Summary page in Scopus @ Elsevier: 2-s2.0-85054429444 (Tokushima University Institutional Repository: 112239, DOI: 10.2152/jmi.65.208, PubMed: 30282862, Elsevier: Scopus)
11.	Hiroyuki Ono, Hideharu Abe, Akiko Sakurai, Arisa Ochi, Tatsuya Tominaga, Masanori Tamaki, Seiji Kishi, Taichi Murakami, Kojiro Nagai, Masayuki Kohashi and Toshio Doi : Novel Interplay Between Smad1 and Smad3 Phosphorylation via AGE Regulates the Progression of Diabetic Nephropathy., Scientific Reports, Vol.8, No.1, 2018. (Summary) ; db/db mice and probucol-treated db/db mice, which was consistent with the attenuation of ECM overproduction. These results indicate that Smad3 expression and activation or probucol treatment alters Smad1 phosphorylation, thus suggesting new molecular mechanisms underlying DN development and progression. (Tokushima University Institutional Repository) ● Metadata: 112878 (Link to Publication Site) ● Publication site (DOI): 10.1038/s41598-018-28439-1 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30002389 ● Search Scopus @ Elsevier (PMID): 30002389 ● Search Scopus @ Elsevier (DOI): 10.1038/s41598-018-28439-1 (Tokushima University Institutional Repository: 112878, DOI: 10.1038/s41598-018-28439-1, PubMed: 30002389)
12.	Seiji Kishi, 小幡史明, Hirokazu Miki, Motokazu Matsuura, Masanori Tamaki, Fumi Kishi, 西村賢二, Taichi Murakami, Hideharu Abe, Kojiro Nagai, Masahiro Abe and Toshio Doi : A case of Lambda Light Chain Noncrystalline Proximal Tubulopathy with IgD lambda myeloma, Internal Medicine, 2018. (Tokushima University Institutional Repository) ● Metadata: 114401 (Link to Publication Site) ● Publication site (DOI): 10.2169/internalmedicine.1323-18 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30101939 ● Search Scopus @ Elsevier (PMID): 30101939 ● Search Scopus @ Elsevier (DOI): 10.2169/internalmedicine.1323-18 (Tokushima University Institutional Repository: 114401, DOI: 10.2169/internalmedicine.1323-18, PubMed: 30101939)
13.	Seiji Kishi, Masanori Minato, Atsuro Saijo, Naoka Murakami, Masanori Tamaki, Motokazu Matsuura, Taichi Murakami, Kojiro Nagai, Hideharu Abe, Yasuhiko Nishioka and Toshio Doi : IgA Nephropathy after Nivolumab Therapy for Postoperative Recurrence of Lung Squamous Cell Carcinoma., Internal Medicine, Vol.57, No.9, 1259-1263, 2018. (Summary) Immune checkpoint inhibitors (ICIs) are becoming a common and important cancer therapy. ICIs are associated with a unique category of side effects, termed immune-related adverse events (irAEs). We herein report the case of a 72-year-old man with postoperative recurrence of lung squamous cell carcinoma who was treated with nivolumab and who developed proteinuria and a worsening kidney function. A kidney biopsy revealed IgA nephropathy. After drug withdrawal, the proteinuria improved and the deterioration of the patient's renal function was halted. Although renal irAEs are considered to be rare and glomerulonephritis is not typical presentation, physicians need to pay more attention to renal irAEs and glomerular injury. (Keyword) Aged / Antibodies, Monoclonal / Antineoplastic Agents / Carcinoma, Squamous Cell / Glomerulonephritis, IGA / Humans / Lung Neoplasms / male / Neoplasm Recurrence, Local / Nivolumab / Proteinuria (Tokushima University Institutional Repository) ● Metadata: 114399 (Link to Publication Site) ● Publication site (DOI): 10.2169/internalmedicine.9814-17 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29279511 ● Summary page in Scopus @ Elsevier: 2-s2.0-85046287943 (Tokushima University Institutional Repository: 114399, DOI: 10.2169/internalmedicine.9814-17, PubMed: 29279511, Elsevier: Scopus)
14.	Kojiro Nagai, Hiroyuki Ono, Motokazu Matsuura, Michael Hann, Sayo Ueda, Sakiya Yoshimoto, Masanori Tamaki, Taichi Murakami, Hideharu Abe, Hisashi Ishikura and Toshio Doi : Progressive renal insufficiency related to ALK inhibitor, alectinib., Oxford Medical Case Reports, Vol.2018, No.4, 2018. (Summary) Alectinib is a second generation anaplastic lymphoma kinase (ALK) tyrosine kinase inhibitor and is generally effective and tolerated in patients who have demonstrated disease progression or adverse effects while on the first generation inhibitor, crizotinib. ALK inhibitors can cause a reversible chronic increase of serum creatinine concentration; however, they rarely induce progressive renal insufficiency. We herein report a case of a 68-year-old woman diagnosed with ALK-positive advanced non-small cell lung cancer and who received ALK inhibitors. Due to dysgeusia and transaminitis, her medication was switched from crizotinib to alectinib. Rapid progressive glomerulonephritis developed 1 year after the initiation of alectinib treatment. A renal biopsy revealed unique kidney lesions in both tubules and glomeruli. Glucocorticoid therapy partially reversed kidney impairment. However, re-administration of alectinib caused kidney dysfunction, which was improved by the cessation of alectinib. Our case suggests that much attention should be paid to kidney function when using ALK inhibitors. (Link to Publication Site) ● Publication site (DOI): 10.1093/omcr/omy009 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29713488 ● Search Scopus @ Elsevier (PMID): 29713488 ● Search Scopus @ Elsevier (DOI): 10.1093/omcr/omy009 (DOI: 10.1093/omcr/omy009, PubMed: 29713488)
15.	Fumi Kishi, Kojiro Nagai, Norimichi Takamatsu, Tatsuya Tominaga, Masanori Tamaki, E. Shibata, Taichi Murakami, Seiji Kishi, Hideharu Abe, Y Koezuka, N Minagawa, G Ichien and Toshio Doi : Urinary type IV collagen excretion is involved in the decline in estimated glomerular filtration rate in the Japanese general population without diabetes: A 5-year observational study., PLoS ONE, Vol.13, No.4, e0195523, 2018. (Summary) Urinary type IV collagen (U-Col4) and albumin excretion is evaluated to monitor the development of diabetic kidney disease. However, U-Col4 excretion in the general population without diabetes has not yet been fully elucidated. In this study, 1067 participants without diabetes and with urinary albumin-creatinine ratio <300 mg/gCr (normo- or microalbuminuria) who underwent an annual health examination in 2004 were enrolled and observed for 5 years. They were divided according to the amount of U-Col4 or urinary albumin excreted. The decline in estimated glomerular filtration rate (eGFR) was calculated. In participants with eGFR ≥80 mL/min, abnormal U-Col4 excretion was indicated as a significant independent risk factor for 10% eGFR change per year, which is one of the prognostic factors for the development of end-stage kidney disease. Moreover, in contrast to urinary albumin excretion, U-Col4 excretion was not related to age or kidney function, suggesting that some individuals with abnormal U-Col4 excretion can have an independent hidden risk for the development of kidney dysfunction. In conclusion, it is important to measure U-Col4 excretion in the general population without diabetes to determine changes in renal features in every individual and help detect future complications such as diabetic kidney disease. If U-Col4 excretion is abnormal, kidney manifestation should be carefully followed up, even if the kidney function and urinalysis findings are normal. (Keyword) Adult / Aged / Aged, 80 and over / Albuminuria / Asian Continental Ancestry Group / Collagen Type IV / Diabetic Nephropathies / Disease Progression / Female / Glomerular Filtration Rate / Humans / Japan / Kaplan-Meier Estimate / Male / Middle Aged / Prognosis / Renal Insufficiency / Risk Factors / Young Adult (Tokushima University Institutional Repository) ● Metadata: 112361 (Link to Publication Site) ● Publication site (DOI): 10.1371/journal.pone.0195523 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29624611 ● Search Scopus @ Elsevier (PMID): 29624611 ● Search Scopus @ Elsevier (DOI): 10.1371/journal.pone.0195523 (Tokushima University Institutional Repository: 112361, DOI: 10.1371/journal.pone.0195523, PubMed: 29624611)
16.	Hiroyuki Ono, Kojiro Nagai, Eriko Shibata, Motokazu Matsuura, Seiji Kishi, Taizo Inagaki, Masanori Minato, Sakiya Yoshimoto, Sayo Ueda, Fumiaki Obata, Kenji Nishimura, Masanori Tamaki, Fumi Kishi, Taichi Murakami, Hideharu Abe, Yukiko Kinoshita, Maki Urushihara, Shoji Kagami and Toshio Doi : Re-recognition of Age-dependent Reference Range for the Serum Creatinine Level in Teenagers - A Case of Slowly Progressive Tubulointerstitial Nephritis which Occurred in an Adolescent., Internal Medicine, Vol.56, No.16, 2187-2193, 2017. (Summary) For the first time, a 15-year-old boy was found to have a slight degree of proteinuria and microscopic hematuria during annual school urinalysis screening. His kidney function had already severely deteriorated. A kidney biopsy revealed tubulointerstitial nephritis (TIN) with diffuse inflammatory cell infiltration. His medical records showed his serum creatinine level to be 0.98 mg/dL two years ago, which was abnormally high considering his age. Although the etiology of slowly progressive TIN was unclear, glucocorticoid and immunosuppressant therapy improved his kidney function. This case report suggests that all doctors should recognize the reference range for the serum creatinine level in teenagers. (Tokushima University Institutional Repository) ● Metadata: 114406 (Link to Publication Site) ● Publication site (DOI): 10.2169/internalmedicine.8599-16 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28781321 ● Search Scopus @ Elsevier (PMID): 28781321 ● Search Scopus @ Elsevier (DOI): 10.2169/internalmedicine.8599-16 (Tokushima University Institutional Repository: 114406, DOI: 10.2169/internalmedicine.8599-16, PubMed: 28781321)
17.	Hiroyuki Ono, Taichi Murakami, Akira Mima, Eriko Shibata, Masanori Tamaki, Sakiya Yoshimoto, Sayo Ueda, Fumi Kishi, Seiji Kishi, Takashi Kawanaka, Motokazu Matsuura, Kojiro Nagai, Hideharu Abe, Masashi Harada and Toshio Doi : Successful treatment of highly advanced immunoglobulin G4-related kidney disease presenting renal mass-like regions with end-stage kidney failure: a case study., BMC Nephrology, Vol.18, No.1, 261, 2017. (Summary) In immunoglobulin G4-related kidney disease with severe kidney failure, radiological findings should be carefully examined. In addition, renal prognosis may be good despite highly advanced tubulointerstitial nephritis and fibrosis. (Tokushima University Institutional Repository) ● Metadata: 114372 (Link to Publication Site) ● Publication site (DOI): 10.1186/s12882-017-0676-5 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28774276 ● Search Scopus @ Elsevier (PMID): 28774276 ● Search Scopus @ Elsevier (DOI): 10.1186/s12882-017-0676-5 (Tokushima University Institutional Repository: 114372, DOI: 10.1186/s12882-017-0676-5, PubMed: 28774276)
18.	Fumiaki Obata, Taichi Murakami, Junko Miyagi, Sayo Ueda, Taizo Inagaki, Masanori Minato, Hiroyuki Ono, Kenji Nishimura, Eriko Shibata, Masanori Tamaki, Sakiya Yoshimoto, Fumi Kishi, Seiji Kishi, Motokazu Matsuura, Kojiro Nagai, Hideharu Abe and Toshio Doi : A case of rapid amelioration of hepatitis C virus-associated cryoglobulinemic membranoproliferative glomerulonephritis treated by interferon-free directly acting antivirals for HCV in the absence of immunosuppressant., CEN Case Reports, Vol.6, No.1, 55-60, 2016. (Summary) Mixed cryoglobulinemic syndrome, which is a systemic vasculitis characterized by the immune complex deposition in small- and medium-sized arteries and most often due to chronic hepatitis C virus (HCV) infection, sometimes clinically manifests as refractory glomerulonephritis or nephritic syndrome. Patients with mixed cryoglobulinemic nephropathy who have a rapidly progressive glomerulonephritis should receive immunosuppressive therapy. After disease stabilization, patients should receive concurrent therapy for the underlying HCV infection. The standard therapy of a chronic HCV infection is IFN monotherapy or IFN combined with ribavirin; however, after the introduction of direct-acting antivirals (DAAs), the standard therapy for patients with HCV genotype 1 has dramatically changed. We report a case of HCV-associated cryoglobulinemic membranoproliferative glomerulonephritis (MPGN) successfully treated by daclatasvir and asunaprevir, which are IFN-free DAAs for HCV, in combination with angiotensin II receptor blocker without immunosuppressive therapy. The patient developed severe nephrotic syndrome with progressive kidney dysfunction. Blood examination revealed a high copy number of HCV-RNA (6.4 log IU/mL, type 1), cryoglobulinemia, paraproteinemia of IgM-, and hypocomplementemia. Histological analysis showed MPGN type 1. These findings were compatible with those observed in HCV-associated cryoglobulinemic MPGN. This case offers original evidence for the application of newer generation of IFN-free DAAs in the treatment of HCV-associated cryoglobulinemic nephropathy. (Link to Publication Site) ● Publication site (DOI): 10.1007/s13730-016-0244-z (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28509128 ● Search Scopus @ Elsevier (PMID): 28509128 ● Search Scopus @ Elsevier (DOI): 10.1007/s13730-016-0244-z (DOI: 10.1007/s13730-016-0244-z, PubMed: 28509128)

Review, Commentary:

1.	Shu Wakino, Kazuhiro Hasegawa and Masanori Tamaki : 近位尿細管から見た糖尿病性腎臓病と肥満関連腎症, Cardioangiology, Vol.93, No.2, 182-189, Feb. 2023. (Keyword) proximal tabular cell / diabetic kidney disease / obesity / SGLT2 / Sirtuin (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1520013962704009344 (CiNii: 1520013962704009344)
2.	Masanori Tamaki, Kazuhiro Hasegawa and Shu Wakino : 【急性腎障害(AKI)】AKIの病態とその対応手術とAKI, Kidney and Dialysis, Vol.94, No.1, 83-86, Jan. 2023.
3.	Masanori Tamaki and Shu Wakino : 透析患者の血圧はどこまで下げるべきでしょうか?, Internal Medicine, Vol.130, No.3, 612-614, Sep. 2022.
4.	Kazuhiro Hasegawa, Masanori Tamaki, 坂巻裕介 and Shu Wakino : ミトコンドリアとSIRT1/NMNと腎臓病, Nephrology, Vol.15, No.5, 551-557, May 2022. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1520292395539278336 (CiNii: 1520292395539278336)

Proceeding of International Conference:

1.	Masanori Tamaki, Tatsuya Tominaga, Yui Fujita, Taichi Murakami, Seiji Kishi, Hideharu Abe, Kojiro Nagai and Toshio Doi : A Novel All-Trans Retinoic Acid Therapy Directly Suppresses Bone Morphogenetic Protein 4 in Mouse Diabetic Nephropathy, KIDNEY WEEK 2019 American Society of Nephrology, Nov. 2019.
2.	Kenji Nishimura, Seiji Kishi, Arisa Ochi, Hiroyuki Ono, Masanori Tamaki, Taichi Murakami, Hideharu Abe, Kenichi Aihara and Kojiro Nagai : Dual disruption of eNOS and ApoE gene accelerates kidney fibrosis and aging after injury, KIDNEY WEEK 2019 American Society of Nephrology, Nov. 2019.
3.	Masanori Tamaki, Taizo Inagaki, Masanori Minato, Fumi Kishi, Seiji Kishi, Taichi Murakami, Kojiro Nagai, Hideharu Abe and Toshio Doi : A case of Helicobacter cinaedi-induced PD-related peritonitis detected by blood culture, APCM-ISPD2019, Sep. 2019.
4.	Seiji Kishi, Kenji Nishimura, Hiroyuki Ono, Masanori Tamaki, Fumi Kishi, Taichi Murakami, Hideharu Abe and Kojiro Nagai : ENHANCED KIDNEY FIBROSIS AND AGING AFTER UUO IN ENOS/APOE DOUBLE KNOCKOUT MOUSE, 56th ERA-EDTA Congress, Jun. 2019.
5.	Maho Iwaki, Seiji Kishi, Masanori Minato, Masanori Tamaki, Fumi Kishi, Taichi Murakami, Hideharu Abe and Kojiro Nagai : Glomerular Injury Related to Immune Related Adverse Events: IgA Nephropathy After Nivolumab Therapy for Postoperative Recurrence of Lung Cancer, ASN Kidney week 2018, San Diego, Oct. 2018.
6.	Masanori Tamaki, Tatsuya Tominaga, Yui Fujita, Seiji Kishi, Taichi Murakami, Kojiro Nagai, Hideharu Abe and Toshio Doi : Mesangial Matrix Expansion Attenuated by All-Trans Retinoic Acid Through Direct Suppression of Bone Morphogenetic Protein 4 in Mouse Diabetic Nephropathy, KIDNEY WEEK 2018 American Society of Nephrology, Oct. 2018.
7.	Yui Fujita, Tatsuya Tominaga, Masanori Tamaki, Taichi Murakami, Seiji Kishi, Kojiro Nagai, Hideharu Abe and Toshio Doi : Palovarotene, Selective Retinoic Receptor- Agonist, Inhibited Both BMP4 and TGF- Signaling Pathways in Diabetic Nephropathy, KIDNEY WEEK 2017 American Society of Nephrology, Nov. 2017.
8.	Masanori Tamaki, Tatsuya Tominaga, Yui Fujita, Seiji Kishi, Taichi Murakami, Kojiro Nagai, Hideharu Abe and Toshio Doi : Glomerulosclerosis Attenuated by Retinoic Acid through Bone Morphogenetic Protein 4 Suppression in Mice with Streptozotocin-Induced Diabetes, KIDNEY WEEK 2017 American Society of Nephrology, Nov. 2017.

Proceeding of Domestic Conference:

1.	Shu Wakino, 柴田理恵子, Kazuhiro Hasegawa, Masanori Tamaki, Masanori Minato, Taizo Inagaki, 宮上慎司, 多田美穂 and Ichiro Hashimoto : 皮膚虚血・潰瘍病変患者における血中亜鉛濃度の意義, 第53回徳島透析療法研究会, Dec. 2023.
2.	Kazuhiro Hasegawa, Masanori Tamaki and Shu Wakino : 心血管内分泌の新知見尿細管糸球体連関とDKD, Folia endocrinologica Japonica, Vol.99, No.1, 171, May 2023.
3.	林成樹, Ryohei Sumitani, Masahiro Oura, Takeshi Harada, Shingen Nakamura, Ayaka Mori, Masanori Tamaki and Masahiro Abe : ITP，自己免疫性出血病F13に続発しTAFRO症候群を発症した1例, 第127回日本内科学会四国地方会, Dec. 2022.
4.	Yohjiroh Sunada, Sayo Ueda, Masanori Tamaki, Eriko Shibata and Shu Wakino : 胃癌による二次性血栓性微小血管症(TMA)の一例, Shikoku Acta Medica, Vol.78, No.5-6, 257-258, Dec. 2022.
5.	Kazuhiro Hasegawa, Masanori Tamaki and Shu Wakino : 時間空間的ネットワークで考えるDKDの基礎研究尿細管糸球体クロストークとDKD, Japanese Journal of Nephrology, Vol.64, No.6-W, 696, Oct. 2022.
6.	Masanori Tamaki, 宮上慎司, Ikuko Shimizu, 山口純代, Masanori Minato, Sayo Ueda, Eriko Shibata, Kazuhiro Hasegawa and Shu Wakino : ロキサデュスタット投与後に奇異性脳塞栓を発症した1例, Japanese Journal of Nephrology, Vol.64, No.6-W, 719, Oct. 2022.
7.	宮上慎司, Masanori Tamaki, Ikuko Shimizu, 山口純代, Masanori Minato, Sayo Ueda, Eriko Shibata, Kazuhiro Hasegawa and Shu Wakino : コロナウィルスワクチン後発症した悪性腎硬化症の一例, Japanese Journal of Nephrology, Vol.64, No.6-W, 719, Oct. 2022.
8.	Kazuhiro Hasegawa, Masanori Tamaki, 坂巻裕介 and Shu Wakino : 腎臓病治療に対する新たな切り口 DMミトコンドリア機能改善薬やNADがDKDのみならず腎臓病への切り口となる可能性, Japanese Journal of Nephrology, Vol.64, No.3, 189, May 2022.
9.	Kazuhiro Hasegawa, Masanori Tamaki, 坂巻裕介 and Shu Wakino : NMN消費酵素Nmnatのポドサイト発現調節はE-boxへのepigenetic制御が担う, Japanese Journal of Nephrology, Vol.64, No.3, 228, May 2022.
10.	Masanori Tamaki, 宮上慎司, Ikuko Shimizu, 山口純代, Masanori Minato, Sayo Ueda, Eriko Shibata, Motoyuki Tamaki, Motoyuki Tamaki, Kazuhiro Hasegawa, Kojiro Nagai and Shu Wakino : ESAからロキサデュスタットへ切り替えた保存期CKD症例の解析, Japanese Journal of Nephrology, Vol.64, No.3, 257, May 2022.
11.	Kazuhiro Hasegawa, Masanori Tamaki, 坂巻裕介 and Shu Wakino : FSGSへのNMN短期集中投与はNMN・NAD消費酵素の暴走連関を抑制し糸球体硬化を抑止する, Japanese Journal of Nephrology, Vol.64, No.3, 263, May 2022.
12.	Sayo Ueda, Eriko Shibata, Masanori Tamaki, Masanori Minato, 岩城真帆, Ikuko Shimizu, 山口純代, 宮上慎司, Kazuhiro Hasegawa and Shu Wakino : 急性間質性腎炎を認めた敗血症性AKIの症例, Journal of Japanese Society for Dialysis Therapy, Vol.55, No.Suppl.1, 507, May 2022.
13.	Masanori Tamaki, 宮上慎司, 岩城真帆, Ikuko Shimizu, 山口純代, Masanori Minato, Sayo Ueda, Eriko Shibata, Kojiro Nagai, Kazuhiro Hasegawa and Shu Wakino : 腹膜透析導入後に膵癌を発症した1例, Journal of Japanese Society for Dialysis Therapy, Vol.55, No.Suppl.1, 631, May 2022.
14.	Ikuko Shimizu, Masanori Tamaki, 宮上慎司, 山口純代, Masanori Minato, Sayo Ueda, Eriko Shibata, Kazuhiro Hasegawa and Shu Wakino : 慢性大動脈解離に伴う慢性DICのため腎代替療法導入に苦慮した1例, Journal of Japanese Society for Dialysis Therapy, Vol.55, No.Suppl.1, 663, May 2022.
15.	Masanori Tamaki, 宮上慎司, 岩城真帆, 清水郁子, 山口純代, 湊将典, Sayo Ueda, Eriko Shibata, Kazuhiro Hasegawa, Kojiro Nagai and Shu Wakino : 膵癌を合併した腹膜透析患者の1例, 第27回日本腹膜透析医学会学術集会・総会, Oct. 2021.
16.	宮上慎司, Masanori Tamaki, Kenji Nishimura, 岩城真帆, 清水郁子, 山口純代, Sayo Ueda, Eriko Shibata, Hideharu Abe, Kojiro Nagai and Shu Wakino : 繰り返す菌血症に対し予防的抗菌薬投与が奏功した1例, Journal of Japanese Society for Dialysis Therapy, Jun. 2021.
17.	Seiji Kishi, Kenji Nishimura, Masanori Tamaki, Fumi Kishi, Eriko Shibata, Taichi Murakami and Kojiro Nagai : 血液透析導入期の僧帽弁感染性心内膜炎による敗血症性肺塞栓 Embolism from left to right-sided heart, Journal of Japanese Society for Dialysis Therapy, Vol.53, No.Suppl.1, 481, Oct. 2020.
18.	Masanori Tamaki, 湊将典, Sayo Ueda, Eriko Shibata, Kenji Nishimura, Hiroyuki Ono, 小幡史明, 山本修三, 滝下佳寛, 田蒔正治, Hideharu Abe and Kojiro Nagai : 急性期と慢性期ともにトシリズマブが有効であったTAFRO症候群の1例, Journal of Japanese Society for Dialysis Therapy, Vol.53, No.Suppl.1, 391, Oct. 2020.
19.	Eriko Shibata, 三好雅士, Takayuki Nakao, Sayo Ueda, Kenji Nishimura, Hiroyuki Ono, Fumi Kishi, Masanori Tamaki, Taichi Murakami, Hideharu Abe, Seiji Kishi, Toshio Doi and Kojiro Nagai : プレセプシン濃度は検体処理や腎機能障害により影響をうける, 第63回日本腎臓学会学術総会, Aug. 2020.
20.	Masanori Tamaki, Hiroyuki Ono, Kenji Nishimura, Eriko Shibata, Sayo Ueda, 越智ありさ, Tatsuya Tominaga, Kojiro Nagai and Hideharu Abe : 骨形成因子4(BMP4)はメサンギウム細胞のミトコンドリア障害を惹起する, Japanese Journal of Nephrology, Vol.62, No.4, 282, Jul. 2020.
21.	山崎佳那子, Mio Yada, Yoshihiro Matsudate, Yoshiaki Kubo and Masanori Tamaki : Sore thumb症候群の1例, The Nishinihon Journal of Dermatology, Vol.82, No.2, 119, Apr. 2020.
22.	Masanori Tamaki : 慢性腎臓病と生活習慣, 腎疾患二次検診認定医取得講習会, Feb. 2020.
23.	山口純代, 岩城真帆, 清水郁子, 稲垣太造, 湊将典, Hiroyuki Ono, Sayo Ueda, Kenji Nishimura, Eriko Shibata, Masanori Tamaki, Kojiro Nagai and Hideharu Abe : 全身倦怠感，呼吸困難感を生じ，その後急性高Ca血症と判明した透析患者の一例, 第47回徳島透析療法研究会, Nov. 2019.
24.	Masanori Tamaki : 糖尿病性腎症重症化予防のためになすべきこと治療も含めて ―腎臓内科の立場から―, 徳島県糖尿病性腎症重症化予防対策フォーラム, Oct. 2019.
25.	湊将典, Taichi Murakami, Sayo Ueda, Hiroyuki Ono, Kenji Nishimura, Eriko Shibata, Masanori Tamaki, Kojiro Nagai and Hideharu Abe : Fanconi症候群を合併したTubulointerstitial nephritis with IgM-positive plasma cellsの一例, 第49回日本腎臓学会西部学術大会, Oct. 2019.
26.	清水郁子, Kojiro Nagai, 稲垣太造, 湊将典, 岩城真帆, 山口純代, Sayo Ueda, Kenji Nishimura, Hiroyuki Ono, Eriko Shibata, Masanori Tamaki, Fumi Kishi, Taichi Murakami, Seiji Kishi and Hideharu Abe : 慢性B型肝炎治療中に緩徐に進行する腎機能障害をみとめた一例, 第49回日本腎臓学会西部学術大会, Oct. 2019.
27.	近藤広宗, Masanori Tamaki, 湊将典, 稲垣太造, Eriko Shibata, Kenji Nishimura, Hiroyuki Ono, Taichi Murakami, Hideharu Abe and Kojiro Nagai : 早期診断に基づく分子標的薬治療で救命しえたTAFRO症候群の1例, 第49回日本腎臓学会西部学術大会, Oct. 2019.
28.	Seiji Kishi, Hiroyuki Ono, 稲垣太造, 湊将典, Kenji Nishimura, Fumi Kishi, Sayo Ueda, Eriko Shibata, Masanori Tamaki, Taichi Murakami, Hideharu Abe and Kojiro Nagai : PR-3 ANCA陽性化膿性脊椎炎合併シャント腎炎の1例, 第49回日本腎臓学会西部学術大会, Oct. 2019.
29.	山口純代, 岩城真帆, 清水郁子, 稲垣太造, 湊将典, Hiroyuki Ono, Sayo Ueda, Kenji Nishimura, Eriko Shibata, Masanori Tamaki, Kojiro Nagai, Masuda shiho, Itsuro Endo and Hideharu Abe : 透析導入期に急性高Ca血症を生じた一例, 第49回日本腎臓学会西部学術大会, Oct. 2019.
30.	田蒔正治, 山本修三, 滝下佳寛, Masanori Tamaki, 藤井泰宏, 安藤道夫 and 増田壽志 : 当院におけるエテルカルセチドの使用経験, 第53回四国透析療法研究会, Oct. 2019.
31.	Masanori Tamaki : 慢性腎臓病と生活習慣, 令和元年度健康を考える県民のつどい, Sep. 2019.
32.	Masanori Tamaki : 慢性腎臓病における高血圧管理の意義, 徳島透析療法研究会学術講演会, Aug. 2019.
33.	岸田盛吾, Masanori Tamaki, 稲垣太造, 湊将典, Fumi Kishi, Seiji Kishi, Taichi Murakami, Hideharu Abe and Kojiro Nagai : 血液培養でHelicobacter cinaediを同定した排液培養陰性腹膜透析関連腹膜炎の一例, 第259回徳島医学会学術集会, Aug. 2019.
34.	黒澤すみれ, 清水郁子, 稲垣太造, 湊将典, 岩城真帆, 山口純代, 上田紗代, Kenji Nishimura, Hiroyuki Ono, Eriko Shibata, Masanori Tamaki, Hideharu Abe, 早渕修 and Kojiro Nagai : B型肝炎治療薬によって緩徐に腎機能悪化をみとめた一例, 第259回徳島医学会学術集会, Aug. 2019.
35.	Masanori Tamaki : 慢性腎臓病と貧血とその他, 鳥居薬品株式会社社内勉強会, Jul. 2019.
36.	Masanori Tamaki : 慢性腎臓病と貧血管理, 名西郡・西医師会学術講演会, Jul. 2019.
37.	Masanori Tamaki : 慢性腎臓病と貧血と高齢化社会, 協和発酵キリン株式会社社内講演会, Jul. 2019.
38.	Kenji Nishimura, Seiji Kishi, Hiroyuki Ono, Fumi Kishi, Masanori Tamaki, Taichi Murakami, Hideharu Abe and Kojiro Nagai : 生活習慣病リスク増加は腎臓の線維化と老化を加速する, 第62回日本腎臓学会学術総会, Jun. 2019.
39.	Hiroyuki Ono, Hideharu Abe, Masanori Tamaki, Tatsuya Tominaga, Fumi Kishi, Seiji Kishi, Taichi Murakami, Kojiro Nagai and Toshio Doi : Smad1とSmad3の新規相互リン酸化制御機構による糖尿病性腎症の病態解析, 第62回日本腎臓学会学術総会, Jun. 2019.
40.	Kenji Nishimura, Taichi Murakami, Hiroyuki Ono, Sayo Ueda, Eriko Shibata, Masanori Tamaki, Seiji Kishi, Kojiro Nagai, Hideharu Abe and Toshio Doi : 血中HDLアポ蛋白ApoL1はインスリンシグナルに制御され2型糖尿病における糸球体濾過量と相関する, 第62回日本腎臓学会学術総会, Jun. 2019.
41.	Taichi Murakami, Hiroyuki Ono, 島久登, 田代学, 井上朋子, Masanori Tamaki, 川原和彦, Seiji Kishi, Kojiro Nagai, Hideharu Abe, 水口潤 and Toshio Doi : ADPKDにおけるトルバプタン治療反応性と臨床的特徴についての検討, 第62回日本腎臓学会学術総会, Jun. 2019.
42.	荒瀬美晴, Kojiro Nagai, 稲垣太造, Eriko Shibata, Fumi Kishi, Masanori Tamaki, Taichi Murakami, Seiji Kishi, Hideharu Abe and Motokazu Matsuura : 尿蛋白減少にシクロスポリンが有効であったアルポート症候群の1例, 日本内科学会第119回四国地方会, Dec. 2018.
43.	Taichi Murakami, Fumi Kishi, Masanori Tamaki, Kojiro Nagai, Hideharu Abe, Seiji Kishi, 湊将典 and Sayo Ueda : Fanconi症候群を合併したTubulointerstitial nephritis with IgM-positive plasma cellsの一例, 第119回四国地方会, Dec. 2018.
44.	Masanori Tamaki : よくわかるPD合併症の予防と対策, 第24回日本腹膜透析医学会学術集会・総会, Oct. 2018.
45.	岡田衣世, Masanori Tamaki, 稲垣太造, 湊将典, Fumi Kishi, Seiji Kishi, Taichi Murakami, Kojiro Nagai, Hideharu Abe and Toshio Doi : 血液培養でHelicobacter cinaediを同定した廃液培養陰性PD関連腹膜炎の一例, 第24回日本腹膜透析医学会学術集会・総会, Oct. 2018.
46.	Kenji Nishimura, Masanori Tamaki, Fumi Kishi, Taichi Murakami, Seiji Kishi, Kojiro Nagai, Hideharu Abe and Toshio Doi : 適切な腹膜透析廃液培養が早期診断・治療により有用であった真菌性腹膜炎の1例, 第24回日本腹膜透析医学会学術集会・総会, Oct. 2018.
47.	Masanori Tamaki, 湊将典, 稲垣太造, Taichi Murakami, Seiji Kishi, Kojiro Nagai, Hideharu Abe and Toshio Doi : 腎盂腎炎と鑑別困難であった化膿性脊椎炎に感染後腎炎の合併が疑われた1例, 第48回日本腎臓学会西部学術大会, Sep. 2018.
48.	Hiroyuki Ono, Kojiro Nagai, 松浦元一, 稲垣太造, 湊将典, Sayo Ueda, Kenji Nishimura, Eriko Shibata, Masanori Tamaki, 岸史, Taichi Murakami, Seiji Kishi, 水口潤, Hideharu Abe and Toshio Doi : ALK阻害薬関連の進行性腎障害を呈した1例, 第48回日本腎臓学会西部学術大会, Sep. 2018.
49.	Taichi Murakami, Fumi Kishi, Masanori Tamaki, Seiji Kishi, Kojiro Nagai and Hideharu Abe : 多彩な腎病変を合併し細胞表面マーカー染色により肉芽腫性間質性腎炎を診断しえた腎サルコイドーシスの一例, 第48回日本腎臓学会西部学術集会, Sep. 2018.
50.	Taichi Murakami, Fumi Kishi, Masanori Tamaki, Seiji Kishi, Kojiro Nagai and Hideharu Abe : 血栓性微小血管症による急性腎障害で末期腎不全に至ったクリオグロブリン血管炎の一例, 第48回日本腎臓学会西部学術集会, Sep. 2018.
51.	宮上慎司, Hiroyuki Ono, Seiji Kishi, Eiji Kondou, Nobuhito Naitoh, 稲垣太造, 湊将典, 上田紗代, Kenji Nishimura, Eriko Shibata, Masanori Tamaki, Fumi Kishi, Taichi Murakami, Hideharu Abe, Yasuhiko Nishioka and Kojiro Nagai : ANCA関連血管炎との鑑別を要したIgG4関連疾患の1例, 第257回徳島医学会学術集会, Aug. 2018.
52.	Fumi Kishi, Kojiro Nagai, Tatsuya Tominaga, Masanori Tamaki, 柴田恵理子, Taichi Murakami, Seiji Kishi, 肥塚靖彦, 皆川直人, 一圓剛, Norimichi Takamatsu and Toshio Doi : 尿中IV型コラーゲンは非糖尿病一般住民における糸球体濾過率低下に関与する, 第61回日本腎臓学会学術総会, Jun. 2018.
53.	Masanori Tamaki, Tatsuya Tominaga, 藤田結衣, Fumi Kishi, Seiji Kishi, Taichi Murakami, Kojiro Nagai, Hideharu Abe and Toshio Doi : レチノイン酸はBmp4遺伝子発現を直接制御して糖尿病マウスの糸球体硬化を改善する, 第61回日本腎臓学会学術総会, Jun. 2018.
54.	西村賢二, Seiji Kishi, Masanori Tamaki, Taichi Murakami, Kojiro Nagai, Hideharu Abe and Toshio Doi : 血液透析導入期に発症した左心系感染性心内膜炎の1例, 第48回徳島透析療法研究会, Nov. 2017.
55.	Hiroyuki Ono, Hideharu Abe, 上田紗代, Kenji Nishimura, Masanori Tamaki, Taichi Murakami, Seiji Kishi, Kojiro Nagai and Toshio Doi : 糖尿病性腎症の糸球体硬化抑制過程におけるSmad1の新規リン酸化部位の同定と解析, 第255回徳島医学会学術集会, Aug. 2017.
56.	Taichi Murakami, 稲垣太造, 湊将典, Eriko Shibata, Kenji Nishimura, Hiroyuki Ono, 上田紗代, Masanori Tamaki, 岸史, Seiji Kishi, Kojiro Nagai, Hideharu Abe and Toshio Doi : 過粘稠症候群に血漿交換が奏功した原発性マクログロブリン血症の一例, 第62回日本透析医学会学術集会, Jun. 2017.
57.	Hiroyuki Ono, Taichi Murakami, 稲垣太造, 上田紗代, Eriko Shibata, Masanori Tamaki, 岸史, Motokazu Matsuura, Seiji Kishi, Kojiro Nagai, Hideharu Abe and Toshio Doi : クリオグロブリン血栓性血管炎に続発した二次性血栓性微少血管症(TMA)に対して血漿交換，血液透析，ステロイド治療で救命しえた一例, 第62回日本透析医学会学術集会, Jun. 2017.
58.	Taichi Murakami, Toshio Doi, Hideharu Abe, Motokazu Matsuura, Kojiro Nagai, Sakiya Yoshimoto, Seiji Kishi, 上田紗代, 小野広幸 and Masanori Tamaki : 徳島大学腎臓内科における多発性嚢胞腎患者の診療現況, 第114回内科学会四国地方会, May 2016.
59.	Hiroyuki Ono, 平野隆弘, Akiko Sakurai, 新井美存, 上田紗代, Eriko Shibata, Sakiya Yoshimoto, Masanori Tamaki, Motokazu Matsuura, Taichi Murakami, Kojiro Nagai, Toshio Doi and Hideharu Abe : E2A新規結合分子FLASHによるTNFα-p21制御と細胞増殖・老化の調整による腎炎の修復機構, 第6回分子腎臓フォーラム, Sep. 2015.
60.	Taichi Murakami, Kojiro Nagai, Motokazu Matsuura, Masanori Tamaki, Eriko Shibata, Sakiya Yoshimoto, Hiroyuki Ono, 上田紗代, Hideharu Abe and Toshio Doi : Trophoblast glycoprotein:ポドサイト障害における発現・機能解析および尿中マーカーとしての検討, 第58回日本腎臓学会学術総会, Jun. 2015.
61.	Hiroyuki Ono, 平野隆弘, Akiko Sakurai, 新井美存, 上田紗代, Eriko Shibata, Sakiya Yoshimoto, Masanori Tamaki, Motokazu Matsuura, Taichi Murakami, Kojiro Nagai, Toshio Doi and Hideharu Abe : E2A新規結合因子FLASHによるTNFα-P21制御と細胞増殖・老化の調整による腎炎の修復機構, 第58回日本腎臓学会学術総会, Jun. 2015.
62.	Sakiya Yoshimoto, Kojiro Nagai, Hiroyuki Ono, Eriko Shibata, Sayo Ueda, Masanori Tamaki, Naoko Abe, Taichi Murakami, Akira Mima, Motokazu Matsuura, Hideharu Abe and Toshio Doi : サルコイドーシス，高カルシウム血症により間質障害を呈した一例, 第44回日本腎臓学会西部学術大会, Oct. 2014.
63.	Hiroyuki Ono, Taichi Murakami, Motokazu Matsuura, Akira Mima, Sakiya Yoshimoto, Sayo Ueda, Masanori Tamaki, Eriko Shibata, Kojiro Nagai, Hideharu Abe and Toshio Doi : ループス腎炎との鑑別を要したIgG4関連腎症の1例, 第44回日本腎臓学会西部学術大会, Oct. 2014.

Et cetera, Workshop:

1.	Masanori Tamaki, 湊将典, 宮上慎司, 岩城真帆, 清水郁子, 山口純代, Sayo Ueda, Eriko Shibata, Kazuhiro Hasegawa and Shu Wakino : ステントグラフト留置術がAVG頻回閉塞に有用であった一例, 第55回四国透析療法研究会, Oct. 2021.
2.	遠藤理子, 宮上慎司, 湊将典, Masanori Tamaki, 岩城真帆, 清水郁子, 山口純代, Sayo Ueda, Eriko Shibata, Kazuhiro Hasegawa and Shu Wakino : 膜性腎症に合併したIgG4関連腎臓病の一例, 第263回徳島医学会, Aug. 2021.

Grants-in-Aid for Scientific Research (KAKEN Grants Database @ NII.ac.jp)

多元的フェロトーシス治療に基づく慢性腎臓病治療戦略の開発 (Project/Area Number: 23K07674 )
ポドサイトの活性化シグナルの解析による各種腎障害の鑑別法の開発 (Project/Area Number: 21K07367 )
An investigation of novel therapeutic strategy for diabetic nephropathy based on control of mitochondrial turnover (Project/Area Number: 20K08609 )
Elucidation of the molecular mechanisms responsible for the recent increase in DKD (Project/Area Number: 20K08593 )
Nuclear receptor-targeted effective therapy for diabetic glomerulosclerosis through Chip-Seq analysis (Project/Area Number: 16K19490 )
Epigenetic analysis for reno-musclar correlation and optimal hormonal treatment for physical decline in patients with chronic kidney disease (Project/Area Number: 26860644 )
Elucidation of epigenetic alteration associated with aging in the muscle and the recovery by hormonal therapy targeting the mitochondria (Project/Area Number: 26460920 )
Search by Researcher Number (90528902)

Associate Professor : Tamaki, Masanori

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Grants-in-Aid for Scientific Research (KAKEN Grants Database @ NII.ac.jp)