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Masashi Nishida

Publications and source records attributed to Masashi Nishida.

15 recordsLinked to original sources
PubMed2006

MMP-2 inhibition reduces renal macrophage infiltration with increased fibrosis in UUO.

We examined the role of matrix metalloproteinase-2 (MMP-2) in renal fibrosis and its effect on interstitial macrophage infiltration in a mouse model of unilateral ureteral obstruction (UUO). TISAM, a selective inhibitor of MMP-2, was administered during early stage (day -2 to 4; protocol A) and late stage (day 7 to 13; protocol B) after UUO. Treatment with TISAM accelerated fibrosis both at day 5 (A) and at day 14 (B). The degree of macrophage infiltration was decreased by the treatment with TISAM at day 14, but not at day 5. In vitro macrophage migration assay showed a greater migration to renal tissue of control UUO kidney (day 14) than to TISAM-treated kidney, which was suppressed by preincubating macrophages with RGDS, a fibronectin degradation peptide. These results suggest that MMP-2 acts to accelerate macrophage infiltration in the late stage of UUO, possibly by degrading extracellular matrix components.

Animals↗
PubMed2006

How does G-CSF act on the kidney during acute tubular injury?

Recent findings in stem cell research have demonstrated multi-lineage plasticity of bone marrow cells, and also the contribution of hematopoietic bone marrow stem cells to the regeneration of injured organs including the kidney. These findings suggested the possibility of the use of granulocyte colony-stimulating factor (G-CSF) as a therapeutic option to regenerate injured organs. Recently, several studies regarding the effect of G-CSF on renal function have been reported in mouse models of acute renal failure. This series of experiments provided potentially important information regarding the treatment of patients with renal injury. This review summarizes the possible actions of G-CSF on the kidney, especially during acute tubular injury caused by toxic or ischemic insults.

Acute Kidney Injury↗
PubMed2006

Renal function and cardiac angiography.

OBJECTIVE: To study the effect of non-ionic contrast medium on renal function in children with cardiovascular disease. METHODS: Analysis of renal function in 98 children with cardiovascular disease before and after the use of Iopamidol, Iohexol, and Ioversol was done for angiography. Serum creatinine (s-Cre), urinary N-acetyl-beta-D-glucosaminase (u-NAG), urinary beta 2-microglobulin (u-BMG), and urinary alpha 1-microglobulin (u-AMG) levels were evaluated. RESULTS: Although s-Cre levels remained unchanged, u-NAG/Cre, u-AMG/Cre and u-BMG/Cre significantly increased 12 hours after angiography. Levels of u-NAG/Cre, u-BMG/Cre, and u-AMG/Cre after angiography were significantly higher in neonates and infants (age< 12-months, n=32) than in children (age>1-year, n=61), in patients with more than 5 ml/kg of contrast medium (n=25) than in those with less than 5 ml/kg (n=70) and in cyanotic patients (n=13) than in non-cyanotic (n=80) patients. CONCLUSION: Transient renal tubular dysfunction occurred in all of these three non-ionic contrast mediums. Although renal tubular function was intact on a long-term basis, one should be careful of contrast medium-induced nephropathy, especially in neonates and infants, in patients receiving more than 5 ml/kg of contrast mediums in total, and in patients with cyanotic heart disease in using non-ionic contrast mediums.

Adolescent↗
PubMed2006

Complex formation of p-nitrocalix[6]arene with rare earth metal ions.

p-Nitrocalix[6]arene (CALX-N6, L) formed a 1:1 metal complex, ML, with light rare earth metal ions (M3+), such as La3+, Pr3+ and Nd3+ except Ce3+, but formed a 1:2 (M(3+):L) complex, ML2 (the charge of the complex is omitted) with heavy rare earth metal ions, such as Sm(3+)-Lu3+ including Y3+. The conditional stability constants of these 1:1 and 1:2 complexes, KML and KML2, were measured by a ligand displacement method using absorption spectrophotometry in 4% (v/v) acetone aqueous solution at pH 9.65 +/- 0.15 and 25 degrees C.

Journal Article↗
PubMed2005

C1q nephropathy with asymptomatic urine abnormalities.

We found four cases of C1q nephropathy (C1qN) among a total of 193 pediatric series of first renal biopsies. Among them, 94 biopsies were performed because of asymptomatic urine abnormalities detected by school urinary screening program in Japan; three cases out of these 94 biopsies (3.2%) met the criteria of C1qN. One case out of the remaining 99 biopsies with symptomatic renal diseases (1%) also met the criteria of C1qN. Three cases with asymptomatic onset presenting with mild proteinuria with or without hematuria equally showed histologic features of membranoproliferative glomerulonephritis and showed improvements in urinalysis without corticosteroid treatment. Our data suggest that membranoproliferative glomerulonephritis may be a common histological feature of asymptomatic pediatric C1qN in Japan and that this type of glomerulopathy may follow a relatively good clinical course without steroid therapy.

Adolescent↗
PubMed2005

Adoptive transfer of macrophages ameliorates renal fibrosis in mice.

We performed adoptive transfer of bone marrow-derived (BM) macrophages following pharmacological depletion of leukocytes in a mouse model of unilateral ureteral obstruction (UUO). Treatment with cyclophosphamide (CPM) caused marked decrease in the numbers of F4/80-positive interstitial macrophages as well as in peripheral blood leukocyte counts, and adoptive transfer of BM macrophages to CPM-treated mice resulted in significant increase in the numbers of interstitial macrophages both at day 5 and at day 14 after UUO. At day 5 after UUO, no significant change was observed in the degree of renal interstitial fibrosis either by treatment with CPM or with CPM+macrophage. However, at day 14 after UUO, treatment with CPM caused significant increase in the degree of interstitial fibrosis, and adoptive macrophage transfer to these mice attenuated this enhancement in renal fibrosis. Our result suggests the role of infiltrating macrophages on facilitating tissue repair at late stage of UUO.

Adoptive Transfer↗
PubMed2005

Rapidly progressive IgA nephropathy.

A 14-year-old boy presented with macroscopic hematuria and a rapid deterioration in renal function. Percutaneous renal biopsy demonstrated severe crescentic IgA nephropathy (IgAN) with extensive (88%) glomerular crescent formation. After started intravenous administration of high-dose pulse methylprednisolone, severe nausea and general malaise accompanied by a rapid increase in Blood Urea Nitrogen (BUN) and serum creatinine levels appeared, however, the renal function ameliorated rapidly and fully recovered by following oral administration of corticosteroid. The clinical presentation of our case seems to be very remarkable compared to previously reported cases of rapidly progressive IgAN.

Adolescent↗
PubMed2004

Effect of hematopoietic cytokines on renal function in cisplatin-induced ARF in mice.

In this study, the effect of hematopoietic cytokines, i.e., granulocyte-colony stimulating factor (G-CSF), stem cell factor (SCF), and granulocyte-macrophage-colony stimulating factor (GM-CSF), on renal function was studied in cisplatin-induced acute renal failure in mice. Treatment with G-CSF significantly ameliorated both BUN and serum creatinine increase induced by cisplatin administration with concomitant alleviation in the degree of necrotic change, enhancement in DNA synthesis, and decrease in apoptosis of renal tubular cells. There was no significant change observed among these parameters following treatment with SCF or with GM-CSF. Serum hepatocyte growth factor level was significantly lower in mice treated with cisplatin and G-CSF compared with that in those treated with cisplatin only. In conclusion, G-CSF, but not SCF or GM-CSF, acts to accelerate regeneration and prevent apoptosis of renal tubular epithelial cells and leads to reduced renal injury in cisplatin-induced acute renal failure in mice.

Acute Kidney Injury↗
PubMed2003

Renal tubular regeneration by bone marrow-derived cells in a girl after bone marrow transplantation.

Recent studies have indicated that bone marrow cells can contribute to regeneration of the kidney in experimental models. However, renal regeneration by apparent bone marrow-derived cells has not been shown previously in humans. The authors here report on a 7-year-old girl who received whole bone marrow transplantation from a male donor, and the contribution of bone marrow cells to the regeneration after renal damage was shown by in situ hybridization for the Y chromosome on autopsy specimens of the kidney. This observation suggests the clinical potential of bone marrow cells as a therapeutic option for renal injury.

Bone Marrow Transplantation↗
PubMed2003

Role of hydrogen peroxide in cyclosporine-induced renal tubular cell (LLC-PK1) injury.

We examined the role of hydrogen peroxide production in cyclosporine A (CsA)-induced LLC-PK1 injury. After exposure to CsA (0.1 microM - 100 microM), cytotoxicity assessed by lactate dehydrogenase release to the media increased dose-dependently. LLC-PK1 cells produced hydrogen peroxide, visualized by 2,7-dichlorodihydrofluorescein assay by the treatment with 100 microM CsA, that was blocked by the treatment with catalase. The cytotoxicity of CsA significantly decreased either by the treatment with catalase, mannitol, or deferoxamine, but not with superoxide dismutase. These results suggest the role of hydrogen peroxide as the source of hydroxyl radical, which mainly contributes to CsA-induced LLC-PK1 injury.

Animals↗
PubMed2002

Absence of angiotensin II type 1 receptor in bone marrow-derived cells is detrimental in the evolution of renal fibrosis.

We examined the in vivo function of the angiotensin II type 1 receptor (Agtr1) on macrophages in renal fibrosis. Fourteen days after the induction of unilateral ureteral obstruction (UUO), wild-type mice reconstituted with marrow lacking the Agtr1 gene (Agtr1(-/-)) developed more severe interstitial fibrosis with fewer interstitial macrophages than those in mice reconstituted with Agtr1(+/+) marrow. These differences were not observed at day 5 of UUO. The expression of profibrotic genes - including TGF-beta1, alpha1(I) collagen, and alpha1(III) collagen - was substantially higher in the obstructed kidneys of mice with Agtr1(-/-) marrow than in those with Agtr1(+/+) marrow at day 14 but not at day 5 of UUO. Mice with Agtr1(-/-) marrow were characterized by reduced numbers of peripheral-blood monocytes and macrophage progenitors in bone marrow. In vivo assays revealed a significantly impaired phagocytic capability in Agtr1(-/-) macrophages. In vivo treatment of Agtr1(+/+) mice with losartan reduced phagocytic capability of Agtr1(+/+) macrophages to a level comparable to that of Agtr1(-/-) macrophages. Thus, during urinary tract obstruction, the Agtr1 on bone marrow-derived macrophages functions to preserve the renal parenchymal architecture, and this function depends in part on its modulatory effect on phagocytosis.

Animals↗
PubMed2002

Highly selective transport of a uranyl ion through a liquid membrane containing a lipophilic ion-associate of methyltrioctylammonium and hydroxycalix[n]arene-p-sulfonates (n = 6, 8) as metal carriers.

Uranyl ion, UO2(2+), in an aqueous sodium hydrogen carbonate solution of pH 4-8 (source phase) was simultaneously and selectively transported into a dilute sulfuric acid solution (receiving phase) through a membrane (chloroform, bulk) containing a lipophilic ion-associate of methyltrioctylammonium ion and hydroxycalix[n]arene-p-sulfonate ion, 2n (n = 6, 8), MTA+-2n, as a metal carrier. The rate of transport increased in proportion to the concentrations of UO2(2+) in the source phase and carrier in the membrane and along with an increase in the temperature of the system. The rate was also increased along with an increase in the pH of the source phase. None of the other metal ions were transported, or obstructed the transport of UO2(2+), while the presence of large amounts of sodium hydrogencarbonate and sodium chloride in the source phase interfered with the transport by causing a delay in the start of transport.

Journal Article↗