Über die experimentelle Glomerulonephritis durch das spezifische Antinierenserum

Masugi, Matazo

doi:10.1016/s0005-8165(76)80081-9

Cited by 22 publications

(19 citation statements)

References 5 publications

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“…In this regard it is a well-known, highly reproducible model. Also according to other authors (3,4,(20)(21)(22)(23)(24) proteinuria started already within few hours after the injection of the antiserum ( fig. 1), although the absolute amount of proteinuria at a given time varied significantly from animal to animal (fig.…”

Section: Discussionsupporting

confidence: 69%

Glomerular Protein Filtration in Normal and Nephritic Rats1,2

et al.

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Section: Discussionsupporting

confidence: 69%

Glomerular Protein Filtration in Normal and Nephritic Rats1,2

et al.

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“…Hematuria and R B C casts were first described by Masugi [11] in the original study o f rabbit Masugi nephri tis. However, since then no researchers have paid atten tion to hematuria.…”

Section: Discussionmentioning

confidence: 99%

Mechanism of Hematuria

Makino

Nishimura

Takaoka

et al. 1988

Nephron

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A model of hematuria was established in rabbits. An accelerated form of unilateral Masugi nephritis was induced in 10 New Zealand white rabbits by an intravenous injection of duck antirabbit kidney serum and by ligating the left renal artery immediately after the injection of the antibody. All 10 rabbits became hematuric 1–2 weeks after the injection of the antibody and red blood cell (RBC) casts were found in the urinary sediment of all these animals. An ultrastructural examination of renal glomeruli by transmission electron microscopy revealed the transcapillary passage of polymorphonuclear leukocytes through the gaps of the glomerular basement membrane (GBM). RBC were found in the urinary space in 50% of the glomeruli observed by scanning electron microscopy (SEM) and the passage of leukocytes and RBCs through the glomerular capillary wall was also observed. Gaps in the GBM became clearer after the removal of cellular components by detergents. In control rabbits, no RBCs could be observed in the urinary space, and isolated GBM were intact by SEM. These data further support the hypothesis that in rabbit Masugi nephritis hematuria is a result of the passage of RBCs through gaps in the GBM.

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“…The modified technique of Masugi [ 10] described by Feldman cl al. [ 11 ] was used to induce GN in female Spraguc-Dawley rats.…”

Section: Preparation O F Animalsmentioning

confidence: 99%

Impaired Sodium Excretion in Experimental Glomerulonephritis: an Explanation for the Controversies in the Literature

Chachati¹,

Godon²

1985

Kidney Blood Press Res

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Considerable discrepancies exist in the literature concerning Na excretion by the rat kidney in experimental antiglomerular basement membrane (GBM) glomerulonephritis (GN). Previous studies in our laboratories demonstrated a disturbance in Na excretion with an impaired absolute (UNa × V) and fractional (FENa) excretion of Na after saline loading. However, most of the other authors in the literature failed to observe similar findings. The present study was undertaken to elucidate some of these controversies: We showed that a difference in Na excretion between anesthetized GN and normal rats might not be detected after a volume expansion if the latter is small or slow (FENa in GN 2 ± 0.1%, in normals 2 ± 0.2%; not significant). Only a rapid and important volume expansion is sufficient to unmask such a difference between the two groups (FENa 3 ± 0.3 and 6 ± 1%, respectively, p < 0.001), and detect an impaired Na excretion in GN animals. The same amount of NaCl was nevertheless administered during slow and rapid volume expansion. Similarly, in GN conscious rats only after a saline load or repeated water loads did we observe a significantly smaller UNa × V compared to normals while no difference was present between the two groups after a single water load. In the literature, all the authors, that failed to demonstrate a disturbance in Na excretion in anti-GBM GN, administered slow and small isotonic saline loads to their rats. The hypothesis we formulate to explain these controversies is that the nonobserved disturbance in sodium excretion in most of these studies is probably secondary to insufficient natriuretic stimuli.

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Über die experimentelle Glomerulonephritis durch das spezifische Antinierenserum

Cited by 22 publications

References 5 publications

Glomerular Protein Filtration in Normal and Nephritic Rats1,2

Glomerular Protein Filtration in Normal and Nephritic Rats1,2

Mechanism of Hematuria

Impaired Sodium Excretion in Experimental Glomerulonephritis: an Explanation for the Controversies in the Literature

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