Benign Nephrosclerosis - Explore the Science & Experts | ideXlab

Scan Science and Technology

Contact Leading Edge Experts & Companies

Benign Nephrosclerosis

The Experts below are selected from a list of 267 Experts worldwide ranked by ideXlab platform

Takashi Taguchi – 1st expert on this subject based on the ideXlab platform

  • Pathological influence of obesity on renal structural changes in chronic kidney disease
    Clinical and Experimental Nephrology, 2009
    Co-Authors: Shigeko Kato, Arifa Nazneen, Yumiko Nakashima, Mohammed S. Razzaque, Tomoya Nishino, Akira Furusu, Noriaki Yorioka, Takashi Taguchi

    Abstract:

    Background Role of obesity in renal pathological and structural changes remains poorly investigated, and this study was designed to examine the pathological effects of obesity on renal structural components in patients with chronic kidney diseases (CKD). Methods The study subjects were obese (body mass index, BMI ≥ 25 kg/m^2) patients with nonglomerulonephritis (non-GN, n  = 26), IgA nephropathy (IgAN, n  = 19), Benign Nephrosclerosis (BNS, n  = 15), and thin basement membrane disease (TMD, n  = 6), and 65 nonobese controls ( n  = 20, 20, 10, and 15, respectively). Patients were evaluated for glomerular lesions (mesangial proliferation and focal segmental/global glomerulosclerosis), glomerular size, and thickness of glomerular basement membrane (GBM). Results Urinary protein was higher in obese non-GN, IgAN, and BNS groups than in the respective controls. Focal segmental glomerulosclerosis (FSGS) lesions were noted in all obesity groups. The glomeruli were larger in size in obese than in nonobese patients of the non-GN and IgAN groups. The glomeruli of nonobese TMD and BNS patients were significantly larger in size than those of nonobese non-GN patients. GBM were thicker in obese than in nonobese patients irrespective of types of glomerular diseases, but only significantly so in non-GN and BNS groups. Conclusion In non-GN, IgAN, and BNS, obesity worsens proteinuria and is associated with structural changes such as glomerulomegaly and GBM thickening, similar to changes observed in obesity-related nephropathy. Obesity seems to worsen the renopathological state in CKD.

  • immunohistochemical analysis of type iii and iv collagens in tubulointerstitial damage in human Benign Nephrosclerosis
    Journal of International Medical Research, 1995
    Co-Authors: M S Razzaque, M Cheng, Yoshio Horita, Minoru Nishihara, Takashi Harada, Takashi Taguchi

    Abstract:

    Prolonged hypertension causes structural changes including glomerulosclerosis and tubulointerstitial damage of the kidney, termed Benign Nephrosclerosis. It is generally accepted that, in Benign Nephrosclerosis, increased accumulation of extracellular matrix in the glomeruli results in glomerulosclerosis. Little is known, however, about the possible role of the extracellular matrix in the tubulointerstitial damage in Benign Nephrosclerosis. In this study, the possible roles of type IV basement-membrane collagen and type III interstitial collagen in tubulointerstitial damage caused by hypertension were explored. Immunohistochemical techniques were used to investigate the distribution of type III and type IV collagens in the kidney sections of 15 patients with Benign Nephrosclerosis with tubulointerstitial damage and in 10 controls. In the control renal sections strong immunostaining for type III collagen was found in the interstitium and immunostaining for type IV collagen was present in the tubular basement membrane and weakly in the interstitium. In the patients with tubulointerstitial damage there was increased immunostaining for both type III and type IV collagens in the expanded interstitium and damaged tubules than was found in the control kidney sections. These findings indicate that increased accumulation of both type III and type IV collagens might play a significant role in the tubulointerstitial damage in Benign Nephrosclerosis.

  • glomerular expression of type iii and type iv collagens in Benign Nephrosclerosis immunohistochemical and in situ hybridization study
    Pathology Research and Practice, 1994
    Co-Authors: M S Razzaque, Takashi Harada, Takehiko Koji, H Kawano, Paul K Nakane, Takashi Taguchi

    Abstract:

    Summary The development of glomerular sclerosis in Benign Nephrosclerosis (BNS) was studied. We investigated the intraglomerular expression of type III and IV collagens and their mRNAs by immunohistochemistry and by the in situ hybridization method. Formalin-fixed paraffin sections from 28 patients with BNS and 10 control cases were stained by the avidin-biotin complex (ABC) method using monoclonal antibodies for human type III and IV collagens. In the course of the sclerotic process of the glomerulus in BNS, the glomerular staining intensity of type IV collagen increased. The strongest staining was observed in the glomerulus at the early sclerotic stage, and intensity decreased slightly at the later stages. Although type III collagen was absent in normal and nonsclerotic glomeruli, peripheral regions of the sclerotic glomeruli were positive at the early sclerotic stage. Later, type III collagen was diffusely observed in the completely hyalinized glomeruli. The expression of type III and type IV collagen mRNAs was detected in the glomeruli of BNS by the non-radioactive in situ hybridization method using thymine-thymine (T-T) dimerized synthetic oligonucleotides. The number of mRNA positive cells for type III and type IV collagens increased at the presclerotic and early sclerotic stages. But these cells gradually decreased in number as glomerular sclerosis developed. We concluded that type III collagen was presumably synthesized by the intraglomerular cells and may contribute to the development of glomerular sclerosis in BNS along with type IV collagen.

Takashi Yokoo – 2nd expert on this subject based on the ideXlab platform

  • Time-averaged proteinuria during follow-up and renal prognosis in patients with biopsy-proven Benign Nephrosclerosis
    Clinical and Experimental Nephrology, 2020
    Co-Authors: Hoichi Amano, Kentaro Koike, Kotaro Haruhara, Nobuo Tsuboi, Makoto Ogura, Takashi Yokoo

    Abstract:

    Background Heavy proteinuria at diagnostic renal biopsy has been reported as an independent risk factor for deteriorating renal function in Benign Nephrosclerosis (BNS). However, studies investigating the relationship between the amount of proteinuria during follow-up and long-term renal prognosis in BNS are limited. This study aimed to assess the relationship between time-averaged proteinuria (TAP) and renal prognosis in BNS. Methods The study participants included 98 patients with biopsy-proven BNS (average age 52 ± 13 years, estimated glomerular filtration rate (eGFR) 53 ± 25 ml/min/1.73 m^2, urine protein excretion at baseline 1.34 ± 1.30 g/gCr) from the Jikei University Hospital. Multivariate analysis was used to investigate the effects of TAP and other clinicopathological findings on the risk for renal outcome in biopsy-proven BNS (a 30% decline in eGFR from baseline or end-stage renal disease). Proteinuria was measured every 6 months and the mean value was used as an indicator of TAP. Results The average observation period was 56 ± 43 months. In the unadjusted model, higher levels of TAP and urinary protein at baseline, glomerulosclerosis, and tubulointerstitial damage were associated with renal prognosis. The adjusted model demonstrated a significant association between TAP and renal outcomes (hazard ratio 5.45, 95% confidence interval 3.02–10.7), which was independent of higher baseline proteinuria, glomerulosclerosis, and tubulointerstitial damage. Conclusions TAP is an independent risk factor for renal prognosis in patients with BNS, indicating the significance of urinary protein excretion during follow-up for the progression of BNS. Clinicians should understand the importance of follow-up evaluation for proteinuria in patients with BNS.

  • time averaged proteinuria during follow up and renal prognosis in patients with biopsy proven Benign Nephrosclerosis
    Clinical and Experimental Nephrology, 2020
    Co-Authors: Hoichi Amano, Kentaro Koike, Kotaro Haruhara, Nobuo Tsuboi, Makoto Ogura, Takashi Yokoo

    Abstract:

    BACKGROUND: Heavy proteinuria at diagnostic renal biopsy has been reported as an independent risk factor for deteriorating renal function in Benign Nephrosclerosis (BNS). However, studies investigating the relationship between the amount of proteinuria during follow-up and long-term renal prognosis in BNS are limited. This study aimed to assess the relationship between time-averaged proteinuria (TAP) and renal prognosis in BNS. METHODS: The study participants included 98 patients with biopsy-proven BNS (average age 52 +/- 13 years, estimated glomerular filtration rate (eGFR) 53 +/- 25 ml/min/1.73 m(2), urine protein excretion at baseline 1.34 +/- 1.30 g/gCr) from the Jikei University Hospital. Multivariate analysis was used to investigate the effects of TAP and other clinicopathological findings on the risk for renal outcome in biopsy-proven BNS (a 30% decline in eGFR from baseline or end-stage renal disease). Proteinuria was measured every 6 months and the mean value was used as an indicator of TAP. RESULTS: The average observation period was 56 +/- 43 months. In the unadjusted model, higher levels of TAP and urinary protein at baseline, glomerulosclerosis, and tubulointerstitial damage were associated with renal prognosis. The adjusted model demonstrated a significant association between TAP and renal outcomes (hazard ratio 5.45, 95% confidence interval 3.02-10.7), which was independent of higher baseline proteinuria, glomerulosclerosis, and tubulointerstitial damage. CONCLUSIONS: TAP is an independent risk factor for renal prognosis in patients with BNS, indicating the significance of urinary protein excretion during follow-up for the progression of BNS. Clinicians should understand the importance of follow-up evaluation for proteinuria in patients with BNS.

Hoichi Amano – 3rd expert on this subject based on the ideXlab platform

  • Time-averaged proteinuria during follow-up and renal prognosis in patients with biopsy-proven Benign Nephrosclerosis
    Clinical and Experimental Nephrology, 2020
    Co-Authors: Hoichi Amano, Kentaro Koike, Kotaro Haruhara, Nobuo Tsuboi, Makoto Ogura, Takashi Yokoo

    Abstract:

    Background Heavy proteinuria at diagnostic renal biopsy has been reported as an independent risk factor for deteriorating renal function in Benign Nephrosclerosis (BNS). However, studies investigating the relationship between the amount of proteinuria during follow-up and long-term renal prognosis in BNS are limited. This study aimed to assess the relationship between time-averaged proteinuria (TAP) and renal prognosis in BNS. Methods The study participants included 98 patients with biopsy-proven BNS (average age 52 ± 13 years, estimated glomerular filtration rate (eGFR) 53 ± 25 ml/min/1.73 m^2, urine protein excretion at baseline 1.34 ± 1.30 g/gCr) from the Jikei University Hospital. Multivariate analysis was used to investigate the effects of TAP and other clinicopathological findings on the risk for renal outcome in biopsy-proven BNS (a 30% decline in eGFR from baseline or end-stage renal disease). Proteinuria was measured every 6 months and the mean value was used as an indicator of TAP. Results The average observation period was 56 ± 43 months. In the unadjusted model, higher levels of TAP and urinary protein at baseline, glomerulosclerosis, and tubulointerstitial damage were associated with renal prognosis. The adjusted model demonstrated a significant association between TAP and renal outcomes (hazard ratio 5.45, 95% confidence interval 3.02–10.7), which was independent of higher baseline proteinuria, glomerulosclerosis, and tubulointerstitial damage. Conclusions TAP is an independent risk factor for renal prognosis in patients with BNS, indicating the significance of urinary protein excretion during follow-up for the progression of BNS. Clinicians should understand the importance of follow-up evaluation for proteinuria in patients with BNS.

  • time averaged proteinuria during follow up and renal prognosis in patients with biopsy proven Benign Nephrosclerosis
    Clinical and Experimental Nephrology, 2020
    Co-Authors: Hoichi Amano, Kentaro Koike, Kotaro Haruhara, Nobuo Tsuboi, Makoto Ogura, Takashi Yokoo

    Abstract:

    BACKGROUND: Heavy proteinuria at diagnostic renal biopsy has been reported as an independent risk factor for deteriorating renal function in Benign Nephrosclerosis (BNS). However, studies investigating the relationship between the amount of proteinuria during follow-up and long-term renal prognosis in BNS are limited. This study aimed to assess the relationship between time-averaged proteinuria (TAP) and renal prognosis in BNS. METHODS: The study participants included 98 patients with biopsy-proven BNS (average age 52 +/- 13 years, estimated glomerular filtration rate (eGFR) 53 +/- 25 ml/min/1.73 m(2), urine protein excretion at baseline 1.34 +/- 1.30 g/gCr) from the Jikei University Hospital. Multivariate analysis was used to investigate the effects of TAP and other clinicopathological findings on the risk for renal outcome in biopsy-proven BNS (a 30% decline in eGFR from baseline or end-stage renal disease). Proteinuria was measured every 6 months and the mean value was used as an indicator of TAP. RESULTS: The average observation period was 56 +/- 43 months. In the unadjusted model, higher levels of TAP and urinary protein at baseline, glomerulosclerosis, and tubulointerstitial damage were associated with renal prognosis. The adjusted model demonstrated a significant association between TAP and renal outcomes (hazard ratio 5.45, 95% confidence interval 3.02-10.7), which was independent of higher baseline proteinuria, glomerulosclerosis, and tubulointerstitial damage. CONCLUSIONS: TAP is an independent risk factor for renal prognosis in patients with BNS, indicating the significance of urinary protein excretion during follow-up for the progression of BNS. Clinicians should understand the importance of follow-up evaluation for proteinuria in patients with BNS.