Glomerular Permeability

Venkatachalam, M. A.; Karnovsky, Morris J.; Cotran, Ramzi S.

doi:10.1084/jem.130.2.381

Cited by 80 publications

(44 citation statements)

References 9 publications

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“…11,16,17 Changes in the state of cytoskeletal aggregation are associated with decreased fibrillar attachment of the epithelium to the GBM and with the onset of massive proteinuria. 16,18,19 Our results reproduced these abnormal features and provided evidence for a toxic effect of B. moojeni venom on visceral epithelial cells.…”

Section: Discussionsupporting

confidence: 76%

Bothrops moojeni snake venom-induced renal glomeruli changes in rat.

Bôer

Gontijo²,

Cruz‐Höfling³

2002

The American Journal of Tropical Medicine and Hygiene

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Abstract. The venom of Bothrops moojeni has potent proteolytic and phospholipase A 2 activities. In previous work, we showed that intravenous injection of this venom in rats decreased creatinine clearance and caused tubular dysfunction and histopathological changes with no alterations in blood pressure. The current study used scanning and transmission electron microscopy to assess the ultrastructural changes caused by B. moojeni venom (0.4 mg/kg i.v.) in rat renal glomeruli and correlated these alterations with the severity of proteinuria 5 hours, 16 hours, and 48 hours after venom injection. The changes included mesangiolysis, glomerular microaneurysms, and glomerular basement membrane (GBM) abnormalities. In addition, there was a reduction in the number and width of podocyte pedicels, which caused a reduction in the number of filtration slits. Electron-dense amorphous material, which may be proteinaceous in origin, was found in the pedicels. The severity of the ultrastructural abnormalities correlated with the level of proteinuria. These morphophysiological changes were attributed to biochemical and physiological disturbances in the components of the GBM and mesangial matrix as well as in cytoskeleton-associated proteins of podocytic processes, and could account for the breakdown of optimal glomerular filtration barrier functioning. These results, together with the absence of appreciable glomerular fibrin deposits, support the hypothesis of a direct activity of B. moojeni venom on rat kidneys. Proteolytic activity of the venom on renal glomeruli could then contribute to the onset of acute renal failure, and would explain the clinical manifestations of renal injury after bites by this and other Bothrops species.

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Section: Discussionsupporting

confidence: 76%

Bothrops moojeni snake venom-induced renal glomeruli changes in rat.

Bôer

Gontijo²,

Cruz‐Höfling³

2002

The American Journal of Tropical Medicine and Hygiene

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“…In aminonucleoside nephrosis, evidence has been obtained indicating transport of tracers by large vacuoles which originate on the GBM side and which open into the urinary space (12,13). In AIC nephritis, in contrast, only rare subepithelial pockets containing tracer were observed.…”

Section: Comparison To Other Experimental Models Characterized By Promentioning

confidence: 93%

“…Functional studies have shown that differential protein clearance is more slective in aminonucleoside nephrosis than in AIC nephritis (38). These functional data cannot be explained on the basis of presently available morphological observations (12,13).…”

Section: Comparison To Other Experimental Models Characterized By Promentioning

confidence: 95%

Altered Functional Properties of the Renal Glomerulus in Autologous Immune Complex Nephritis

Schneeberger

Leber

Karnovsky

et al. 1974

The Journal of Experimental Medicine

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The present study was undertaken in order to investigate the nature of the glomerular damage in a form of experimental immune complex nephritis. The model of autologous immune complex nephritis (AIC) 1 (Heymann's nephritis) (1) was chosen for several reasons. First, the model bears a remarkable resemblance, in terms of ultrastructural and immunofluorescence features, to an important renal disease in man, membranous glomerulonephritis. Furthermore, the model is highly reproducible. In addition, the basic pathogenetic mechanism has been thoroughly documented (2-4). Briefly, the disease is produced in rats by immunization with homologous kidney preparations, which results in the formation of autoantibodies against a renal antigen, normally found in the brush border of proximal tubules. This antigen is presumed to enter the circulation in small amounts and combine with autoantibody to form complexes which deposit in glomeruli. 2 The complexes are detected as granular deposits of immunoglobulin and complement along the epithelial side of the glomerular basement membrane. The disease, like its human counterpart, is manifested by proteinuria, which is often heavy.Our approach was to use the enzymatic tracers horseradish peroxidase (HRP) (40,000 daltons) and catalase (240,000 daltons), and the electronopaque tracer ferritin (ca. 500,000 daltons) as probe molecules with which to assess the altered functional properties of the glomerular capillary wall. These ultrastructural tracers can be directly visualized, and their location within the glomerular capillary wall can be followed at sequential intervals after intravenous injection. Such protein tracers have been extensively used to identify * This study was supported by U.S. Public Health Service grants no. AM 16392 and AM 13132.1Abbreviations used in this paper: AIC, autologous immune complex; CFA, complete Freund's adjuvant; CL, capillary lumen; DAB, 3,3' diaminobenzidine-tetra-HC1; GBM, glomerniar basement membrane; HRP, horseradish peroxidase; US, urinary space.It is of interest that a related pathogenetic mechanism may operate in man. It has recently been reported that a tubular-derived antigen may be present in the glomerular immune deposits in some cases of human membranous glomerulonephritis (5).

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“…It has been suggested that increased glomerular filtration of protein is the initiating lesion in the nephrotic syndrome [3,5,6,9,15,20,21], but direct evidence for this has been lacking. In a recent study of the ultrastructure of the glomerulus in aminonucleoside nephrosis, Venkatachalam and coworkers [21] have reported that horseradish peroxidase (molecular weight 40,000) crosses the glomerular capillary barrier into the urinary space in nephrotic rats.…”

Section: Discussionmentioning

confidence: 99%

Micropuncture Study of Albumin Transfer in Aminonucleoside Nephrosis in the Rat

Lewy

Pesce

1973

Pediatr Res

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ExtractAlbumin concentration in the proximal tubules of normal rats and rats with aminonucleoside nephrosis (AMN) was estimated by means of a sensitive radioimmunoassay. Nephrotic animals were studied at the onset of proteinuria and when the nephrotic syndrome was fully established. Albumin concentration in the proximal tubule of normal male rats averaged 2.5 ± 0.3 mg/100 ml, whereas in early nephrotic rats it averaged 4.9 ± 1.3 mg/100 ml and in normal sized tubules of heavily proteinuric rats, 15.7 ± 3.3 mg/100 ml. Control and early AMN animals appeared to have a relatively homogeneous population of surface convolutions, whereas the fully nephrotic rats had markedly increased heterogeneity. A population of dilated proximal tubules with an albumin concentration of 233.8 ± 35.4 mg/100 ml was found in this group. Albumin concentrations were randomly distributed throughout the proximal convolution of all three groups with no clear pattern of changing concentration along the nephron. The data demonstrate that enhanced glomerular permeability to albumin occurs in the experimental nephrotic syndrome in the rat. Speculation

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Glomerular Permeability

Cited by 80 publications

References 9 publications

Bothrops moojeni snake venom-induced renal glomeruli changes in rat.

Bothrops moojeni snake venom-induced renal glomeruli changes in rat.

Altered Functional Properties of the Renal Glomerulus in Autologous Immune Complex Nephritis

Micropuncture Study of Albumin Transfer in Aminonucleoside Nephrosis in the Rat

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