Benign Nephrosclerosis

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Takashi Taguchi - One of the best experts 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 - One of the best experts 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 - One of the best experts 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.

Kimio Tomita - One of the best experts on this subject based on the ideXlab platform.

  • renal effects of temocapril hydrochloride cs 622 in patients with Benign Nephrosclerosis
    Nephrology, 1998
    Co-Authors: Hiroshi Nonoguchi, Akira Owada, Isao Umehara, S Kiyama, Yoshio Terada, Fumiaki Marumo, Kimio Tomita
    Abstract:

    SUMMARY: The short-term effects of temocapril, a new angiotensin-converting enzyme inhibitor (ACE-I), on renal function were investigated in 10 patients with Benign Nephrosclerosis (56.2 ± 7.2 years, mean ± SD). Renal plasma flow and glomerular filtration rate (GFR) were examined before and after 12-week administration, using 131I-hippuran and 99mTc-DTPA, respectively. Temocapril (mean 4.5 mg/day) decreased systolic and diastolic blood pressure (from 162 ± 6 to 140 ± 12 mmHg, P<0.001, and from 101 ± 5 to 89 ± 8 mmHg, P<0.001, respectively). Temocapril increased both renal plasma flow (from 323 ± 67 to 367 ± 72 mL/min/1.73 m2P<0.05) and GFR (from 74 ± 14 to 81 ± 15 mL/min/1.73 m2, P<0.05). These data show that short-term administration of temocapril improves renal function in patients with Benign Nephrosclerosis.

  • Renal effects of temocapril hydrochloride (CS‐622) in patients with Benign Nephrosclerosis
    Nephrology, 1998
    Co-Authors: Hiroshi Nonoguchi, Akira Owada, Isao Umehara, Yoshio Terada, Fumiaki Marumo, Kiyama S, Kimio Tomita
    Abstract:

    SUMMARY: The short-term effects of temocapril, a new angiotensin-converting enzyme inhibitor (ACE-I), on renal function were investigated in 10 patients with Benign Nephrosclerosis (56.2 ± 7.2 years, mean ± SD). Renal plasma flow and glomerular filtration rate (GFR) were examined before and after 12-week administration, using 131I-hippuran and 99mTc-DTPA, respectively. Temocapril (mean 4.5 mg/day) decreased systolic and diastolic blood pressure (from 162 ± 6 to 140 ± 12 mmHg, P

  • Therapeutic effect of hemodialysis on gouty arthritis and tophi in 2 patients with chronic renal failure.
    Japanese Journal of Nephrology, 1993
    Co-Authors: Osamu Matsuda, Kimio Tomita, Masakazu Otsuka, Toshio Yamada, Fumiaki Marumo
    Abstract:

    Therapeutic effect of hemodialysis on gouty arthritis and tophi in 2 patients with chronic renal failure (CRF) is described. One patient was 74-year-old man with CRF due to Benign Nephrosclerosis, and had severe secondary gout. There were many tophi in metatarsophalangeal joints of the fingers and toes. Another patient was 44-year-old man with CRF probably due to familial gout. He had many tophi in elbows, knees, wrists, fingers and toes. In both cases initiation of hemodialysis treatment, at first temporally exacerbated gouty arthritis, but thereafter gradually eliminated the tophi. From these results, dialysis treatment is considered to be quite efficient method of treatment for gouty arthritis and tophi in patient with CRF. Gouty arthritis in CRF patient, which does not respond to the conservative therapy, should be considered to be one of the indices for commencement of hemodialysis.

Clemens L Bockmeyer - One of the best experts on this subject based on the ideXlab platform.

  • arteriolar vascular smooth muscle cell differentiation in Benign Nephrosclerosis
    Nephrology Dialysis Transplantation, 2012
    Co-Authors: Clemens L Bockmeyer, David Sebastian Kern, Vinzent Forstmeier, Svjetlana Lovric, Friedrich Modde, Putri Andina Agustian, Sandra Steffens, Ingvild Birschmann, Jana Traeder, M E Dammrich
    Abstract:

    BACKGROUND: Benign Nephrosclerosis (bN) is the most prevalent form of hypertensive damage in kidney biopsies. It is defined by early hyalinosis and later fibrosis of renal arterioles. Despite its high prevalence, very little is known about the contribution of arteriolar vascular smooth muscle cells (VSMCs) to bN. We examined classical and novel candidate markers of the normal contractile and the pro-fibrotic secretory phenotype of VSMCs in arterioles in bN. METHODS: Sixty-three renal tissue specimens with bN and eight control specimens were examined by immunohistochemistry for the contractile markers caldesmon, alpha-smooth muscle actin (alpha-SMA), JunB, smoothelin and the secretory marker S100A4 and by double stains for caldesmon or smoothelin with S100A4. RESULTS: Smoothelin immunostaining showed an inverse correlation with hyalinosis and fibrosis scores, while S100A4 correlated with fibrosis scores only. Neither caldesmon, alpha-SMA nor JunB correlated with hyalinosis or fibrosis scores. Cells in the arteriolar wall were exclusively positive either for caldesmon/smoothelin or S100A4. CONCLUSIONS: This is the first systematic analysis of VSMC differentiation in bN. The results suggest that smoothelin is the most sensitive marker for the contractile phenotype and that S100A4 could be a novel marker for the secretory phenotype in vivo. The other markers did not seem to differentiate these phenotypes in bN. Thus, VSMC phenotype markers should be defined in the context of the vessel segment and disease under examination. S100A4 could not only be a marker of pro-fibrotic secretory VSMCs in bN but also an important mediator of arteriolar fibrosis.

  • Arteriolar vascular smooth muscle cell differentiation in Benign Nephrosclerosis
    Nephrology Dialysis Transplantation, 2012
    Co-Authors: Clemens L Bockmeyer, David Sebastian Kern, Vinzent Forstmeier, Svjetlana Lovric, Friedrich Modde, Putri Andina Agustian, Sandra Steffens, Ingvild Birschmann, Jana Traeder, M E Dammrich
    Abstract:

    Background. Benign Nephrosclerosis (bN) is the most prevalent form of hypertensive damage in kidney biopsies. It is defined by early hyalinosis and later fibrosis of renal arterioles. Despite its high prevalence, very little is known about the contribution of arteriolar vascular smooth muscle cells (VSMCs) to bN. We examined classical and novel candidate markers of the normal contractile and the pro-fibrotic secretory phenotype of VSMCs in arterioles in bN. Methods. Sixty-three renal tissue specimens with bN and eight control specimens were examined by immunohistochemistry for the contractile markers caldesmon, alphasmooth muscle actin (alpha-SMA), JunB, smoothelin and the secretory marker S100A4 and by double stains for caldesmon or smoothelin with S100A4. Results. Smoothelin immunostaining showed an inverse correlation with hyalinosis and fibrosis scores, while S100A4 correlated with fibrosis scores only. Neither caldesmon, alpha-SMA nor JunB correlated with hyalinosis or fibrosis scores. Cells in the arteriolar wall were exclusively positive either for caldesmon/smoothelin or S100A4. Conclusions. This is the first systematic analysis of VSMC differentiation in bN. The results suggest that smoothelin is the most sensitive marker for the contractile phenotype and that S100A4 could be a novel marker for the secretory phenotype in vivo. The other markers did not seem to differentiate these phenotypes in bN. Thus, VSMC phenotype markers should be defined in the context of the vessel segment and disease under examination. S100A4 could not only be a marker of pro-fibrotic secretory VSMCs in bN but also an important mediator of arteriolar fibrosis.

  • adamts13 marker of contractile phenotype of arterial smooth muscle cells lost in Benign Nephrosclerosis
    Nephrology Dialysis Transplantation, 2011
    Co-Authors: Clemens L Bockmeyer, Vinzent Forstmeier, Svjetlana Lovric, Friedrich Modde, Putri Andina Agustian, Ralf A Claus, Mario Schiffer, Christina Grothusen, Karsten Grote, Ingvild Birschmann
    Abstract:

    Background. Hyper tensive Nephrosclerosis alone and in combination with other renal diseases is a leading cause of terminal renal insufficiency. Histologic lesions manifest as Benign Nephrosclerosis (bN) with arteriolar hyalinosis and later fibrosis. Procoagulant micromilieus have been implicated in fibrosis. Hyalinosis is considered to consist of plasma insudation possibly containing procoagulant factors like von Willebrand factor (VWF). Therefore, it is hypothesized that VWF cleaving protease ADAMTS13 (a disintegrin-like and metalloprotease with thrombospondin type-1 motif, 13) is normally expressed by arteriolar vascular smooth muscle cells (VSMCs) and diminished in bN and that this reduction contributes to fibrosis in bN. Methods. AD AMTS13 expression was examined by immunohistochemistry and quantitative real-time polymerase chain reaction in VSMCs of various human organs. Fiftyfour specimens with and seven without bN were immunostained for ADAMTS13, VWF, CD61 and VSMC differentiation markers in arteriolar walls. Results. Ex pression of ADAMTS13 is confirmed in VSMCs. In bN, ADAMTS13 immunostaining of arterial VSMCs correlated inversely with fibrotic but not hyalinotic lesions. Smooth muscle myosin heavy chain showed an inverse correlation with hyalinotic, as opposed to fibrotic lesions of bN. Smoothelin showed an inverse correlation with both hyalinotic and fibrotic lesions of bN. VWF was absent in normal controls and hyalinotic lesions, but present exclusively in fibrotic lesions in 7/54 (13%) bN cases. CD61 was absent in all arteriolar walls. Conclusions. The present results establish ADAMTS13 as a novel marker of contractile VSMCs that is retained in early hyalinotic bN but partially lost later in fibrotic bN. Loss of ADAMTS13 and accumulation of VWF in fibrotic but not hyalinotic arteriolar walls could further propagate fibrosis in bN.

  • ADAMTS13—marker of contractile phenotype of arterial smooth muscle cells lost in Benign Nephrosclerosis
    Nephrology Dialysis Transplantation, 2010
    Co-Authors: Clemens L Bockmeyer, Vinzent Forstmeier, Svjetlana Lovric, Friedrich Modde, Putri Andina Agustian, Ralf A Claus, Mario Schiffer, Christina Grothusen, Karsten Grote, Ingvild Birschmann
    Abstract:

    Background. Hyper tensive Nephrosclerosis alone and in combination with other renal diseases is a leading cause of terminal renal insufficiency. Histologic lesions manifest as Benign Nephrosclerosis (bN) with arteriolar hyalinosis and later fibrosis. Procoagulant micromilieus have been implicated in fibrosis. Hyalinosis is considered to consist of plasma insudation possibly containing procoagulant factors like von Willebrand factor (VWF). Therefore, it is hypothesized that VWF cleaving protease ADAMTS13 (a disintegrin-like and metalloprotease with thrombospondin type-1 motif, 13) is normally expressed by arteriolar vascular smooth muscle cells (VSMCs) and diminished in bN and that this reduction contributes to fibrosis in bN. Methods. AD AMTS13 expression was examined by immunohistochemistry and quantitative real-time polymerase chain reaction in VSMCs of various human organs. Fiftyfour specimens with and seven without bN were immunostained for ADAMTS13, VWF, CD61 and VSMC differentiation markers in arteriolar walls. Results. Ex pression of ADAMTS13 is confirmed in VSMCs. In bN, ADAMTS13 immunostaining of arterial VSMCs correlated inversely with fibrotic but not hyalinotic lesions. Smooth muscle myosin heavy chain showed an inverse correlation with hyalinotic, as opposed to fibrotic lesions of bN. Smoothelin showed an inverse correlation with both hyalinotic and fibrotic lesions of bN. VWF was absent in normal controls and hyalinotic lesions, but present exclusively in fibrotic lesions in 7/54 (13%) bN cases. CD61 was absent in all arteriolar walls. Conclusions. The present results establish ADAMTS13 as a novel marker of contractile VSMCs that is retained in early hyalinotic bN but partially lost later in fibrotic bN. Loss of ADAMTS13 and accumulation of VWF in fibrotic but not hyalinotic arteriolar walls could further propagate fibrosis in bN.