Search PubMed⌕ Search

Biomedical subjects

Sonoo Mizuiri

Publications and source records attributed to Sonoo Mizuiri.

10 recordsLinked to original sources

Significance of subclinical rejection in early renal allograft biopsies for chronic allograft dysfunction.

To determine the significance of early subclinical rejection of renal allografts, we reviewed 127 biopsy specimens obtained soon after transplantation. Histological finding was categorized according to a modification of the Banff scheme as: acute rejection (AR), borderline changes (BL); non-specific inflammatory changes, (NI) and no rejection (NR). Subclinical rejection was defined as AR, BL or NI. Patients with BL or NI were divided into two groups; one was treated with high-dose methylprednisolone (MP), the other remained untreated. Freedom from chronic allograft dysfunction (defined as non-doubling of serum creatinine 5 yr after transplantation) was significantly more frequent in the NR group (89%) than in the BL (70%) and AR (64%) groups. At 1 yr after transplantation, mean serum creatinine had increased significantly only in the untreated group (p < 0.05), and re-biopsy showed that interstitial fibrosis had developed to a significantly greater extent in the untreated group than in the treated group (p < 0.01). Subclinical rejection in the early protocol biopsies correlated closely with subsequent allograft dysfunction. High-dose MP treatment for early subclinical rejection may be effective in suppressing the development of interstitial fibrosis at 1 yr after transplantation.

Adult↗

Post-transplant early recurrent proteinuria in patients with focal glomerulosclerosis--angiotensin II immunostaining and treatment outcome.

We reviewed the transplantation data and results of histopathological studies with additional angiotensin II (AII) immunostaining of renal graft biopsies of nine cases (10 grafts) with recurrent proteinuria and three controls without recurrent proteinuria that received renal transplantation for primary focal segmental glomerulosclerosis (FSGS) between 1986 and 2002. Recurrent FSGS was confirmed in six grafts from nine cases by light microscopy. In cases with recurrent proteinuria, loss of graft function was noted in all six renal grafts received between 1986 and early 1992 but in none of four grafts received between late 1992 and 2002. Two of four patients of the late group but none of those of the early group received angiotensin converting enzyme (ACEI) or angiotensin II receptor blocker (ARB) with plasma exchange (PE). In control cases without proteinuria, AII immunostaining was detected in tubules but not in glomeruli in 1-hour biopsies as well as later on. In cases with recurrent proteinuria, AII immunostaining was detected in both tubules and glomeruli, although glomerular AII staining was not observed in 1-hour biopsies. Our results suggest that effective treatment of post-transplantation recurrent FSGS requires ACEI or ARB with PE in the absence of another etiology.

Adolescent↗

Nuclear factor-kappaB activation in diabetic rat kidney: evidence for involvement of P-selectin in diabetic nephropathy.

Activation of a transcription factor, nuclear factor-kappaB (NF-kappaB), is a key step in the pathogenesis of diabetic nephropathy. In this study, we investigated the role of P-selectin, a platelet-derived adhesion molecule, in diabetic nephropathy by examining the activation status of NF-kappaB in the renal cortex of streptozotocin (STZ)-treated rats. The STZ treatment induced pathogenetic parameters such as increased creatinine clearance, increased blood glucose and massive albuminuria in a time-dependent manner. Electrophoretic mobility shift assays (EMSAs) with a specific probe, representing the P-selectin gene promoter, revealed the activation status of NF-kappaB in the STZ-treated rats, as judged by the time-dependent increase in the formation of the specific protein-DNA complexes. This increase was associated with the increased pathogenetic parameters. Supershift assays with specific antibodies revealed that p50, but not p52, p65, Rel B, or c-Rel, may be involved in the activation of NF-kappaB, though the component primarily responsible for the increase could not be determined. Western blot analysis confirmed an increase in P-selectin in STZ-treated rats. Notably, treatment with ammonium pyrrolidinedithiocarbamate, an antioxidant and inhibitor of NF-kappaB, inhibited the activation of NF-kappaB in STZ-treated rats and decreased P-selectin in the renal cortical tissue. Our results indicate that expression of the P-selectin gene is induced through the activation of NF-kappaB and that P-selectin may be involved in the pathogenesis of diabetic nephropathy.

Animals↗

[Recurrence of sarcoidosis in a hemodialysis patient confirmed by abnormal calcium metabolism].

28-year-old man hospitalized for a fever of unknown origin. This patient was already diagnosed as neurosarcoidosis proven by brain biopsy in 1997, then entered chronic hemodialysis therapy in 2002. The data showed hypercalcemia without taking any calcium agent and vitamin D, also showed suppressed intact-parathyroid hormone and normalized 1,25-dihydroxyvitamin D even the condition of end stage renal failure. Recurrence of sarcoidosis was made in this hospitalization. The laboratory data as well as symptom improved after taking oral prednisolone. We reported the case of recurrent sarcoidosis in a hemodialysis patient confirmed by abnormal calcium metabolism.

Adult↗

A male patient with steroid-dependent nephrotic syndrome for 25 years and obesity-associated focal segmental glomerulosclerosis.

An obese male patient with steroid-dependent nephrotic syndrome since age 6 years had a thirty-third relapse at the age of 29 years. Renal biopsy showed focal segmental glomerulosclerosis. Proteinuria disappeared after treatment with prednisolone. He went into complete remission and renal function remained normal at the age of 31 years. Focal segmental glomerulosclerosis associated with obesity was suspected. Long-term follow-up with renal biopsy is necessary in obese children with steroid-dependent nephrotic syndrome.

Aging↗

Activation of nuclear factor-kappa B and macrophage invasion in cyclosporin A-and tacrolimus-treated renal transplants.

This retrospective study was designed to compare the efficacy of cyclosporin A (CyA) and tacrolimus (FK506) on chronic rejection (CR) associated with nuclear factor-kappa B (NF-kappaB) activation and macrophage invasion. Non-episodic day 50 protocol renal biopsy was performed in 63 consecutive patients with renal transplants from living donors, treated with either CyA or FK506. Southwestern histochemistry for NF-kappaB, immunostaining for CD68, and Banff classification were performed, and these findings were compared with outcome over 34 +/- 13 months. Compared with specimens from FK506-treated patients (n = 20), specimens from CyA-treated patients (n = 43) showed a significant increase in tubulointerstitial CD68-positive cells (1.5 +/- 0.9 vs. 0.9 +/- 0.8, p < 0.01), although no significant differences were observed in NF-kappaB activation. Specimens with Banff acute rejection (AR) grade > or = 1A (n = 20) showed increased macrophages (p < 0.01) compared with specimens with AR < 1A (n = 43). Specimens from patients with clinical AR prior to day 50 biopsy (n = 23) also showed increased macrophage invasion (p < 0.01) compared with specimens from patients without prior clinical AR (n = 40). The cumulative well-functioning (serum creatinine < 1.5 mg/dL) graft survival rate was significantly lower in patients with increased tubulointerstitial CD68-positive cells (n = 63, p < 0.05). Our findings suggest that tacrolimus is more effective than CyA against CR with respect to macrophage invasion and AR.

Adult↗

Estimation of damaged tubular epithelium in renal allografts by determination of vimentin expression.

BACKGROUND: Various invasive and non-invasive methods have been investigated for their prognostic value in predicting the outcome of renal allografts. In the present study, vimentin expression in tubular epithelial cells (TEC) was determined by the immunohistochemical examination of biopsy specimens and the prognostic value of this method was assessed. METHODS: Ninety-two renal transplant recipients were recruited for the present study. Protocol biopsy of the renal graft was performed 1, 3 and 5 years after transplantation in each case. All biopsy specimens were treated with conventional stains and immunostained with an antivimentin antibody. The correlation between vimentin expression and glomerular filtration rate (GFR) and the association between vimentin expression and histopathological findings were determined. RESULTS: Vimentin was localized in TEC adjacent to interstitial lesions with lymphocyte infiltration and also in TEC with tubulitis or in atrophic tubules. Vimentin positivity significantly correlated with GFR and both vimentin positivity and GFR were significantly associated with the extent of chronic allograft nephropathy, but not with acute rejection. Additionally, vimentin expression and GFR 3 and 5 years after transplantation were higher in cases where graft loss occurred between 5 and 7 years after transplantation compared with graft survival cases. CONCLUSIONS: These results suggest that immunohistochemistry using antivimentin antibodies on protocol biopsy specimens is useful for the detection of injured TEC and as a predictor of allograft outcome.

Adult↗

Living related kidney transplantation in a patient with autosomal-recessive Alport syndrome.

We discuss a patient with Alport syndrome who received a renal transplant from a donor with thin basement membrane disease. A 30-year-old woman, diagnosed with Alport syndrome on the basis of sensorineural hearing loss, characteristic renal biopsy findings and a family history of microhaematuria, entered chronic haemodialysis therapy. She then received a renal transplant donated from her father, who had sensorineural hearing loss and persistent microhaematuria. On the day of renal transplantation, a 1-h graft biopsy after reperfusion showed thin basement membrane disease. We re-tested the patient's native kidney biopsy specimen by immunohistochemical staining using alpha-chain-specific collagen type IV monoclonal antibodies. There was no expression of collagen type IV alpha3-, alpha4- and alpha5-chain on glomerular basement membrane, but positive staining of alpha5-chain on Bowman's capsular basement membrane was noted. A diagnosis of autosomal-recessive Alport syndrome was made. We concluded that this family might display different phenotypic expressions of the same genotype: one suffered end-stage renal disease and the other thin basement membrane disease.

Adult↗

[Not Available].

Explore the source record for details and available documents.

Journal Article↗