Researchers Database

kobayashi takahisa

    Regional Clinical Education Center, Associate Professor
Last Updated :2021/10/19

Researcher Information

J-Global ID

Published Papers

  • Warangkana Pichaiwong, Kelly L. Hudkins, Tomasz Wietecha, Tri Q. Nguyen, Chiraporn Tachaudomdach, Wei Li, Bardia Askari, Takahisa Kobayashi, Kevin D. O'Brien, Jeffrey W. Pippin, Stuart J. Shankland, Charles E. Alpers
    JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY 24 (7) 1088 - 1102 1046-6673 2013/07 [Refereed][Not invited]
    The reversibility of diabetic nephropathy remains controversial. Here, we tested whether replacing leptin could reverse the advanced diabetic nephropathy modeled by the leptin-deficient BTBR ob/ob mouse. Leptin replacement, but not inhibition of the renin-angiotensin-aldosterone system (RAAS), resulted in near-complete reversal of both structural (mesangial matrix expansion, mesangiolysis, basement membrane thickening, podocyte loss) and functional (proteinuria, accumulation of reactive oxygen species) measures of advanced diabetic nephropathy. Immunohistochemical labeling with the podocyte markers Wilms tumor 1 and p57 identified parietal epithelial cells as a possible source of regenerating podocytes. Thus, the leptin-deficient BTBR ob/ob mouse provides a model of advanced but reversible diabetic nephropathy for further study. These results also suggest that restoration of lost podocytes is possible but is not induced by RAAS inhibition, possibly explaining the limited efficacy of RAAS inhibitors in promoting repair of diabetic nephropathy.
  • T Kobayashi, Y Ando, T Umino, Y Miyata, S Muto, M Hironaka, Y Asano, E Kusano
    CLINICAL NEPHROLOGY 65 (6) 423 - 426 0301-0430 2006/06 [Refereed][Not invited]
    We report a case of a 17-year-old male with relapse of minimal-change nephrotic syndrome (MCNS), in whom apheresis monotherapy without steroids or immunosuppressants resulted in complete remission. The patient initially developed nephrotic syndrome in February 1998. The first renal biopsy confirmed the diagnosis of MCNS. The patient was also found to be a carrier of hepatitis B virus. Steroid therapy was started with oral prednisolone 60 mg/day. Complete remission was achieved in 3 months, and the steroid treatment was tapered off in May 2001. During the steroid tapering, temporal exacerbation of liver function was noted. In July 2002, the patient was admitted to our hospital again due to relapse of nephrotic syndrome. Second biopsy reconfirmed the diagnosis of MCNS. Since the serum titer of HBV was elevated, apheresis monotherapy was selected to avoid the risk of steroid-induced fulminant hepatitis. Four sessions of low-density lipoprotein apheresis (LDL-A) and 5 sessions of double-filtration plasmapheresis (DFPP) reduced the proteinuria from 9.2 g/day to 0.2 g/day over 38 days without any additional medication. Proteinuria remained suppressed below 0.2 g/day for more than 12 months and no exacerbation of liver function was observed up to the final follow-up in September 2003. The present case suggested the potential of apheresis monotherapy to induce and maintain complete remission of MCNS and an important role of circulating factors in the pathogenesis of MCNS.
  • T Kobayashi, S Muto, J Nemoto, Y Miyata, S Ishiharajima, M Hironaka, Y Asano, E Kusano
    CLINICAL NEPHROLOGY 6 65 (6) 427 - 432 0301-0430 2006/06 [Refereed][Not invited]
    Tubulointerstitial nephritis is a well-recognized complication in primary Sjogrens syndrome. Fanconi's syndrome is a far less frequent complication compared with distal tubular dysfunction. We here describe a 49-year-old woman with primary Sjogren's syndrome. In 1997, she was diagnosed with primary Sjogren's syndrome with tubulointerstitial nephritis, and was then treated with oral prednisolone for the tubulointerstitial nephritis. In 2002, she was referred to our hospital because of progressive fatigue. At that time, biclonal spike on serum protein (IgG-kappa and IgA-kappa) and Bence-Jones protein in urine were found. Bone marrow aspiration showed 1.0% plasma cell infiltration. Thus, a diagnosis of monoclonal gammopathy of undetermined significance (MGUS) was made. In 2004, she was again admitted to our hospital because of mild renal dysfunction and hypokalemia. Laboratory evaluation showed inappropriate, alkaline urine in hyperchloremic metabolic acidosis and a positive urine anion gap, indicating the presence of distal (Type 1) renal tubular acidosis (RTA). The urine concentration defect was also found. Further studies revealed proximal tubular dysfunction, including renal glycosuria, generalized aminoaciduria, phosphaturia, uricosuria and proximal RTA. The kidney biopsy represented diffuse and severe tubulointerstitial nephritis with dense infiltrates of lymphocytes and IgA and kappa light chain-positive plasma cells. No findings of multiple myeloma or malignant lymphoma were observed. In conclusion, our patient had Sjogren's syndrome with MGUS and exhibited dysfunction of both proximal tubule (Fanconi's syndrome) and distal tubule, which may be attributed to diffuse tubulointerstitial nephritis.

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