Yujiro Kida

Publications (6)10.77 Total impact

• Article: A case report of thrombotic thrombocytopenic purpura and severe acute renal failure post non-myeloablative allogeneic peripheral blood stem cell transplantation treated with plasma exchange and hemodialysis.

  Yujiro Kida, Toshihide Ishii, Minoru Ando, Eiichiro Kanda, Hitoe Suzuki, Aiko Kida, Takuya Yamashita, Hisashi Sakamaki, Hiroshi Saito
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  ABSTRACT: A 59-year-old-woman received related non-myeloablative allogeneic peripheral blood stem cell transplantation (PBSCT) subsequent to autologous PBSCT in our hospital five years after she was diagnosed as oligo-secretory myeloma. She was admitted to our hospital because of vomiting and grayish diarrhea 4 months after non-myeloablative allogeneic PBSCT (mini-alloPBSCT). Although her initial symptoms improved after admission, she gradually showed thrombocytopenia, anemia, and oliguria during the 2 weeks after admission. Our diagnosis was thrombotic thrombocytopenic purpura (TTP) and acute renal failure (ARF) secondary to mini-alloPBSCT. After cessation of cyclosporine administration, we began to treat her with plasma exchange (PE) and hemodialysis. During the three and a half months after we started PE, the TTP gradually improved. Although PE had been reported to be ineffective for TTP post bone marrow transplantation, we could finally discontinue PE. In contrast, since her anuria continued, she was managed with hemodialysis. One month after PE was started, her activity of von Willebrand factor-cleaving protease was 41% (normal range, >50%) and the ultrasonographic investigation of both kidneys was normal. She could be discharged after four and a half months hospitalization and lived well as an outpatient for a further two months. She died shortly after readmission from multiple organ failure without the relapse of TTP. The patient's clinical course would suggest that TTP post mini-alloPBSCT could be treated with PE in some cases, despite the development of dialysis-requiring severe ARF being a poor prognostic factor.
  Therapeutic apheresis and dialysis: official peer-reviewed journal of the International Society for Apheresis, the Japanese Society for Apheresis, the Japanese Society for Dialysis Therapy 11/2007; 11(5):402-6. · 1.39 Impact Factor
• Article: Tuberous sclerosis, associated with renal cell carcinoma and angiomyolipoma, in a patient who developed endstage renal failure after nephrectomy.

  Yujiro Kida, Kenji Yamaguchi, Hitoe Suzuki, Eiichiro Kanda, Minoru Ando, Kenichi Ohashi, Nobuaki Funata, Hiroshi Saito
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  ABSTRACT: We report a case of tuberous sclerosis (TSC) associated with renal cell carcinoma and angiomyolipoma in a patient, who developed endstage renal failure that required hemodialysis after nephrectomy. A 37-year-old woman with TSC was admitted for further investigation of bilateral renal masses detected by computed tomography (CT). Angiography revealed a tumor stain (4 cm in diameter) in the medial portion of the right kidney. Because renal cell carcinoma (RCC) was strongly suspected, right nephrectomy was performed. Her serum creatinine level was already increased, moderately, at 2.4 mg/dl, before the right nephrectomy. Her renal function deteriorated quickly (in 1(1/2) years) after the right nephrectomy, and hemodialysis was introduced the next year. The histological findings of the resected right kidney revealed marked intimal thickening of the intralobular arteries. These findings suggested that the renal function loss was not only caused by the nephron mass reduction due to the nephrectomy but was also caused by nephrosclerosis. Though most patients with TSC die before developing endstage renal failure, this patient is currently receiving maintenance hemodialysis and has been followed for 3 years with no recurrence of RCC in the left kidney.
  Clinical and Experimental Nephrology 07/2005; 9(2):179-82. · 1.37 Impact Factor
• Article: Role of cytokines in anaphylactoid reaction with marked eosinophilia in a hemodialysis patient.

  Eiichiro Kanda, Yujiro Kida, Hitoe Suzuki, Minoru Ando, Hiroshi Nihei, Sei Sasaki, Hiroshi Saito
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  ABSTRACT: Hemodialysis is rarely terminated by events associated with anticoagulants. A 69-year-old woman on hemodialysis due to chronic renal failure (CRF) developed an anaphylactoid reaction with hypereosinophilia. On the basis of clinical and laboratory findings, we concluded that the causes of this anaphylactoid reaction were low-molecular-weight heparin and heparin. Our patient also showed high levels of soluble interleukin-2 receptor (sIL-2R) and eosinophil cationic protein (ECP), which decreased after the cessation of hemo-dialysis. To date, there has been no report of high levels of cytokines induced by hemodialysis-associated anaphylactoid reaction. In this report, we discuss the mechanism underlying drug-induced anaphylactoid reaction, particularly that involving eosinophilia and cytokines.
  Clinical and Experimental Nephrology 01/2005; 8(4):384-7. · 1.37 Impact Factor
• Article: A female patient with malarial nephropathy.

  Eiichiro Kanda, Yujiro Kida, Hitoe Suzuki, Minoru Ando, Masayoshi Negishi, Sei Sasaki, Hiroshi Saito
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  ABSTRACT: Malaria remains one of the world's major health problems, particularly in developing tropical countries. Imported malaria is reportedly increasing in Western countries. Acute renal failure (ARF) is the most common cause of death in severe malaria. We report the case of a 63-year-old female patient with a history of travel to a rural area in South Africa who was in coma and had a high fever on admission. Thirty percent of her erythrocytes were infected with Plasmodium falciparum. She had cerebral malaria, malarial nephropathy, anemia, hepatic dysfunction, and disseminated intravenous coagulation (DIC). Quinine and artesunate treatment decreased the number of parasites in the blood. To manage renal failure, hemodialysis was performed for 11 days. A relationship between ARF and hepatic dysfunction was suggested. This relationship is an indication of the clinical course of the disease. In this article, we discuss the mechanism underlying the development of malarial nephropathy and its management, particularly the usefulness of hemodialysis.
  Clinical and Experimental Nephrology 01/2005; 8(4):359-62. · 1.37 Impact Factor
• Article: CLC-3 deficiency leads to phenotypes similar to human neuronal ceroid lipofuscinosis.

  Momono Yoshikawa, Shinichi Uchida, Junji Ezaki, Tatemitsu Rai, Atsushi Hayama, Katsuki Kobayashi, Yujiro Kida, Masaki Noda, Masato Koike, Yasuo Uchiyama, Fumiaki Marumo, Eiki Kominami, Sei Sasaki
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  ABSTRACT: CLC-3 is a member of the CLC chloride channel family and is widely expressed in mammalian tissues. To determine the physiological role of CLC-3, we generated CLC-3-deficient mice (Clcn3-/- ) by targeted gene disruption. Together with developmental retardation and higher mortality, the Clcn3-/- mice showed neurological manifestations such as blindness, motor coordination deficit, and spontaneous hyperlocomotion. In histological analysis, the Clcn3-/- mice showed a pattern of progressive degeneration of the retina, hippocampus and ileal mucosa, which resembled the phenotype observed in cathepsin D knockout mice. The defect of cathepsin D results in a lysosomal accumulation of ceroid lipofuscin containing the mitochondrial F1F0 ATPase subunit c. In immunohistochemistry and Western blot analysis, we found that the subunit c was heavily accumulated in the lysosome of Clcn3-/- mice. Furthermore, we detected an elevation in the endosomal pH of the Clcn3-/- mice. These results indicated that the neurodegeneration observed in the Clcn3-/- mice was caused by an abnormality in the machinery which degrades the cellular protein and was associated with the phenotype of neuronal ceroid lipofuscinosis (NCL). The elevated endosomal pH could be an important factor in the pathogenesis of NCL.
  Genes to Cells 07/2002; 7(6):597-605. · 2.68 Impact Factor
• Article: Localization of mouse CLC-6 and CLC-7 mRNA and their functional complementation of yeast CLC gene mutant

  Yujiro Kida, Shinichi Uchida, Hiroaki Miyazaki, Sei Sasaki, Fumiaki Marumo
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  ABSTRACT: CLC-6 and CLC-7 belong to the family of voltage-dependent chloride channels. To learn more about the in vivo roles of CLC-6 and CLC-7, we performed in situ hybridization of these CLC channels in various mouse organs. Mouse CLC-6 (mCLC-6) was expressed in the peripheral region of seminiferous tubules in the testis, tracheal epithelium, epithelium of bronchioles, alveolar cells in the lung, acinar cells in the pancreas, and intestinal epithelium, but we could not detect signals from pancreatic islets. Mouse CLC-7 (mCLC-7) was expressed in neurons in the medulla oblongata, Purkinje cells in the cerebellum, proximal tubules in the kidney, and hepatocytes in the liver. The distribution of mCLC-6 and mCLC-7 were similar in the lung, pancreas, and testis. mCLC-6 functionally complemented the gef1 phenotype of a yeast strain in which a single CLC channel (GEF1) had been disrupted by homologous recombination. In contrast, mCLC-7 did not complement this gef1 phenotype. This study identified the cell types that express mCLC-6 and mCLC-7 in the mouse tissues, and the complementation assay suggested that mCLC-6 functions as an intracellular chloride channel.
  Histochemie 01/2001; 115(3):189-194. · 2.59 Impact Factor