Alteration of glomerular anionic sites by the development of subepithelial deposits in experimental glomerulonephritis in the rat

Suzuki, Yasuhito; Maesawa, Akira; Matsui, Katsuyuki; Oite, Takashi; Koda, Yutaka; Arakawa, Masaaki

doi:10.1007/bf02890171

Cited by 22 publications

(17 citation statements)

References 30 publications

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“…Thus, the proteinuria we observed in this study was associated with a decrease in ASs in GBM, as has been noted in other renal disease (1,11,13,15,19,20,26,28,30). In contrast, in animal models, including puromycin aminonucleoside nephrosis, AS distributions in GBM did not change significantly (4,9,22).…”

Section: Ultrastructural Study For Asssupporting

confidence: 87%

Alterations in Glomerular Anionic Sites in the Autologous Phase of Canine Anti-Glomerular Basement Membrane Nephritis

et al. 1996

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There have been a few studies on canine nephrotoxic glomerulonephritis produced by anti-glomerular basement membrane serum (AGBM), but these reports have not focused on an alteration in the charge properties of glomerular basement membrane (GBM). In this study, rabbit AGBM or normal rabbit serum (NRS) was given intravenously (2 ml/kg body weight) to 16 male beagle dogs. An alteration of anionic sites (ASs) of GBM was studied quantitatively using polyethyleneimine as a cationic probe by electron microscopy at weeks 1, 2, 4, and 8 postinjection. In AGBM-treated dogs, severe or mild proteinuria continued until week 2. At weeks 4 and 8, there was no significant difference in the intensity of proteinuria between AGBM-and NRS-treated groups. Until week 2 postinjection, there were significantly fewer ASs of GBM in AGBM-treated dogs than in NRS-treated dogs. At week 8, however, there was no difference in ASs of GBM between AGBM-and NRS-treated dogs. The fact that a reduction of glomerular AS occurred in AGBMtreated dogs with severe or mild proteinuria and the recovery of AS in the GBM coincided with an improvement of proteinuria suggested that alteration of the glomerular ASs might play an important role in the pathogenesis of proteinuria in canine anti-GBM nephritis.

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Section: Ultrastructural Study For Asssupporting

confidence: 87%

Alterations in Glomerular Anionic Sites in the Autologous Phase of Canine Anti-Glomerular Basement Membrane Nephritis

et al. 1996

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“…Distinct decrease in ASs was evidenced in LRE of GBM in the portions with subepithelial electron-dense deposits in this study. Experimental studies have suggested that subepithelial immune deposits were closely related to the disturbance of ASs and to the development of proteinuria [1,5,15,21]. A localized loss of ASs was often associated with subepithelial deposits in the patients with membranous nephropathy [27].…”

Section: Discussionmentioning

confidence: 99%

“…Rabbits received a single intravenous injection of cationized protein developed a transient interaction of the protein with fixed ASs in the glomerular basement membrane (GBM) resulting in loss of negative charge and concomitant proteinuria [2]. Recent studies have shown that the number of ASs in the GBM decreases in some human glomerulonephropathies [4,11,24,27,28] and experimental nephropathies [1,8,13,20,21,25,26]. It is interesting to note that in experimentally induced acute serum sickness of rabbits, cationic proteins derived from platelets and neutrophils may bind to glomerular capillary walls and possibly contribute to the neutralization of glomerular polyanions [3].…”

Section: Histopathologymentioning

confidence: 99%

Alteration of Anionic Sites in Renal Glomerular Basement Membrane of Pigs.

Shirota

Tanaka

Sugimoto

et al. 1997

The Journal of Veterinary Medical Science

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ABSTRACT. Ultrastructural alteration of anionic sites (ASs) in the glomerular basement membrane (GBM) was studied in 10 cases of swine mesangial proliferative glomerulonephritis using a cationic ultrastructural tracer, 0.5% polyethyleneimine (M.W.= 1,800). Glomerular ASs were seen as discrete electron-dense particles in the GBM, mesangial matrix and epithelial cell surfaces by electron microscopy. In the lamina rara externa (LRE) of the normal GBM, ASs were distributed regularly in a single layer. In those areas of the LRE that contained electron dense deposits or clusters of spherical microparticles (SMPs), however, a distinct reduction or loss of ASs was observed in all the pigs. Quantitative assessment of ASs in the LRE over 1,000 nm of the GBM revealed a significant reduction in ASs in one case with diffuse global thickening of the GBM as compared with the remaining nine pigs without GBM thickening (P<0.001, MannWhitney's U-test). There were no ASs in the lamina densa (LD) of the normal GBM, but an irregular distribution of ASs was seen within the LD of the pig showing diffuse global thickening of the GBM. These results suggest that a disturbance of the charge-selective barrier in the GBM may be induced by electron-dense deposits or SMPs in the LRE as well as thickening of the GBM in swine glomerulonephritis. -KEY WORDS: anionic site, glomerular basement membrane, glomerulonephritis, kidney, swine.

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“…Loss of glomerular anionic sites has been documented in PHN using various cationic probes [1,[21][22][23] . In the study by Arai et al [21] , anionic charge of the GBM in the heterologous phase of PHN was examined by measurements of ruthenium red binding to the GBM.…”

Section: Discussionmentioning

confidence: 99%

“…Profuse proteinuria is a common finding and loss of glomerular anionic sites has been presented and postulated as a cause of proteinuria in PHN [1] . The time sequence of glomerular anionic site depletion is not known.…”

Section: Introductionmentioning

confidence: 99%

Glomerular Charge Barrier and Development of Proteinuria in Passive Heymann Nephritis

Christiansen

Kolmannskog²,

Leh³

et al. 2008

Kidney Blood Press Res

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Background/Aim: Passive Heymann nephritis (PHN) in rats is a commonly used model of membranous glomerulonephritis in man where the cause of proteinuria is not fully resolved. This study was designed to investigate the role of the glomerular charge barrier in development of PHN proteinuria. Methods: We studied female Sprague-Dawley rats (n = 33) at days 0, 2, 5 and 14 after induction of PHN by injection of antiserum against renal tubular epithelial antigens (anti-Fx1A). Measuring clearance of chymotrypsinogen A (Chym, MW 25,000, 21 Å) and similar sized anionic chymotrypsinogen (aChym), together with ⁵¹Cr-EDTA, we hypothesized an increased sieving coefficient (θ) of aChym in the early phase of PHN due to impairment of the glomerular charge barrier. Results: No proteinuria was seen at day 2 (5.8 ± 1.4 mg/ 24 h, p > 0.05), while protein excretion increased to 23.2 ± 2.9 mg/24 h (p < 0.05) at day 5 (84 ± 2% albumin) and further to 544.3 ± 51.1 mg/24 h (p < 0.01) at day 14 (60 ± 1% albumin; p < 0.01, day 5 vs. day 14). θ aChym was similar to control at day 2 (0.49 ± 0.03, p > 0.05), increased at day 5 to 0.62 ± 0.02 (p < 0.01) but decreased at day 14 to 0.39 ± 0.02 (p < 0.01). The sieving coefficient of Chym (θ Chym) was decreased at day 14 (p < 0.05). The ratio of θ aChym to θ Chym was increased at day 5 (p < 0.01) but was elsewhere similar to control. Conclusion: The increased ratio of θ aChym to θ Chym and selective albuminuria at day 5 indicates an initial impairment of the glomerular charge barrier in PHN.

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Alteration of glomerular anionic sites by the development of subepithelial deposits in experimental glomerulonephritis in the rat

Cited by 22 publications

References 30 publications

Alterations in Glomerular Anionic Sites in the Autologous Phase of Canine Anti-Glomerular Basement Membrane Nephritis

Alterations in Glomerular Anionic Sites in the Autologous Phase of Canine Anti-Glomerular Basement Membrane Nephritis

Alteration of Anionic Sites in Renal Glomerular Basement Membrane of Pigs.

Glomerular Charge Barrier and Development of Proteinuria in Passive Heymann Nephritis

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