Glomerular Permeability

1980 ◽  
Vol 3 (1-6) ◽  
pp. 250-256
Author(s):  
Tito Cavallo
Keyword(s):  
Glomerular Permeability

Ficoll and dextran vs. globular proteins as probes for testing glomerular permselectivity: effects of molecular size, shape, charge, and deformability

2005 ◽  
Vol 288 (4) ◽  
pp. F605-F613 ◽  
Author(s):  
Daniele Venturoli ◽  
Bengt Rippe
Keyword(s):  
Hard Spheres ◽  
Molecular Size ◽  
Globular Proteins ◽  
Molecular Probes ◽  
Glomerular Permeability ◽  
Ample Evidence ◽  
Deformable Structure ◽  
Glomerular Barrier ◽  
Size Asymmetry

Polydisperse mixtures of dextran or Ficoll have been frequently used as molecular probes for studies of glomerular permselectivity because they are largely inert and not processed (reabsorbed) by the proximal tubules. However, dextrans are linear, flexible molecules, which apparently are hyperpermeable across the glomerular barrier. By contrast, the Ficoll molecule is almost spherical. Still, there is ample evidence that Ficoll fractional clearances (sieving coefficients) across the glomerular capillary wall (GCW) are markedly higher than those for neutral globular proteins of an equivalent in vitro Stokes-Einstein (SE) radius. Physical data, obtained by “crowding” experiments or measurements of intrinsic viscosity, suggest that the Ficoll molecule exhibits a rather open, deformable structure and thus deviates from an ideally hard sphere. This is also indicated from the relationship between (log) in vitro SE radius and (log) molecular weight (MW). Whereas globular proteins seem to behave in a way similar to hydrated hard spheres, polydisperse dextran and Ficoll exhibit in vitro SE radii that are much larger than those for compact spherical molecules of equivalent MW. For dextran, this can be partially explained by a high-molecular-size asymmetry. However, for Ficoll the explanation may be that the Ficoll molecule is more flexible (deformable) than are globular proteins. An increased compressibility of Ficoll and an increased deformability and size asymmetry for dextran may be the explanation for the fact that the permeability of the GCW is significantly higher when assessed using polysaccharides such as Ficoll or dextran compared with that obtained using globular proteins as molecular size probes. We suggest that molecular deformability, besides molecular size, shape, and charge, plays a crucial role in determining the glomerular permeability to molecules of different species.

In progressive nephropathies, overload of tubular cells with filtered proteins translates glomerular permeability dysfunction into cellular signals of interstitial inflammation.

1998 ◽  
Vol 9 (7) ◽  
pp. 1213-1224 ◽  
Author(s):  
M Abbate ◽  
C Zoja ◽  
D Corna ◽  
M Capitanio ◽  
T Bertani ◽  
...  
Keyword(s):  
Time Course ◽  
Early Stage ◽  
Protein Accumulation ◽  
Glomerular Injury ◽  
Cellular Mechanisms ◽  
Proinflammatory Response ◽  
Glomerular Permeability ◽  
Tubular Cells ◽  
Interstitial Inflammation ◽  
Tubulointerstitial Lesions

Progression to end-stage renal failure is the final common pathway of many forms of glomerular disease, independent of the type of initial insult. Progressive glomerulopathies have in common persistently high levels of urinary protein excretion and tubulointerstitial lesions at biopsy. Among the cellular mechanisms that may determine progression regardless of etiology, the traffic of excess proteins filtered from glomerulus in renal tubule may have functional importance by initiating interstitial inflammation in the early phase of parenchymal injury. This study analyzes the time course and sites of protein accumulation and interstitial cellular infiltration in two different models of proteinuric nephropathies. In remnant kidneys after 5/6 renal mass ablation, albumin and IgG accumulation by proximal tubular cells was visualized in the early stage, preceding interstitial infiltration of MHC-II-positive cells and macrophages. By double-staining, infiltrates developed at or near tubules containing intracellular IgG or luminal casts. This relationship persisted thereafter despite more irregular distribution of infiltrate. Similar patterns were found in an immune model (passive Heymann nephritis), indicating that the interstitial inflammatory reaction develops at the sites of protein overload, regardless of the type of glomerular injury. Osteopontin was detectable in cells of proximal tubules congested with protein in both models at sites of interstitial infiltration, and by virtue of its chemoattractive action this is likely mediator of a proximal tubule-dependent inflammatory pathway in response to protein load. Protein overload of tubules is a key candidate process translating glomerular protein leakage into cellular signals of interstitial inflammation. Mechanisms underlying the proinflammatory response of tubular cells to protein challenge in diseased kidney should be explored, as well as ways of limiting protein reabsorption/deposition to prevent consequent inflammation and progressive disease.

Intravital multiphoton microscopy of dynamic renal processes

2005 ◽  
Vol 288 (6) ◽  
pp. F1084-F1089 ◽  
Author(s):  
Bruce A. Molitoris ◽  
Ruben M. Sandoval
Keyword(s):  
Proximal Tubule ◽  
Multiphoton Microscopy ◽  
Field Of View ◽  
Glomerular Permeability ◽  
Structural Alterations ◽  
Two Photon Microscopy ◽  
Two Photon ◽  
Dynamic Events ◽  
Subcellular Resolution ◽  
Functioning Kidney

Recent advances in microscopy and optics, computer sciences, and the available fluorophores used to label molecules of interest have empowered investigators to utilize intravital two-photon microscopy to study the dynamic events within the functioning kidney. This emerging technique enables investigators to follow functional and structural alterations with subcellular resolution within the same field of view over seconds to weeks. This approach invigorates the validity of data and facilitates analysis and interpretation as trends are more readily determined when one is more closely monitoring indicative physiological parameters. Therefore, in this review we emphasize how specific approaches will enable studies into glomerular permeability, proximal tubule endocytosis, and microvascular function within the kidney. We attempt to show how visual data can be quantified, thus allowing enhanced understanding of the process under study. Finally, emphasis is given to the possible future opportunities of this technology and its present limitations.

Nephroimmunopathology and pathophysiology

1985 ◽  
Vol 248 (3) ◽  
pp. F319-F331
Author(s):  
C. B. Wilson ◽  
R. C. Blantz
Keyword(s):  
Renal Function ◽  
Transport Systems ◽  
Complex Materials ◽  
Glomerular Permeability ◽  
Immune Mediator ◽  
Mediator Systems ◽  
Single Nephron Filtration Rate ◽  
Single Nephron ◽  
Collaborative Interaction ◽  
Scientific Value

Immunologic models of renal injury are useful in the study of pathophysiology. Some of these models have already been used in glomerular micropuncture studies and were shown to be approachable with the same techniques that were developed to study normal renal function. The typical decrease in the glomerular permeability coefficient found in such studies is countered by an increase in the hydrostatic pressure gradient, minimizing decreases in single nephron filtration rate. Antibody mechanisms involving either direct glomerular (and tubular) fixation of antibody or accumulation of immune complex materials provide an array of acute and chronic lesions for evaluation with relevance to the bulk of immune glomerular and tubular lesions in humans. The influences of varied and overlapping immune mediator systems are also useful areas for physiologic assessment. The tools of the renal immunopathologist may be useful to the physiologist in identifying and localizing the effects of transport systems central to renal function. The collaborative interaction of investigators skilled in immunology, pathology, and physiology is necessary to achieve optimum scientific value.

PLATELET ACTIVATING FACTOR (PAF) AS A MEDIATOR OF PROTEINURIA IN ISOLATED PERFUSED KIDNEY (IPK).

1987 ◽  
Author(s):  
F Delani ◽  
M Tagliaferri ◽  
D Macconi ◽  
C Lupini ◽  
N Perico ◽  
...  
Keyword(s):  
Platelet Activating Factor ◽  
Sprague Dawley ◽  
Cationic Protein ◽  
Glomerular Permeability ◽  
Urine Protein Excretion ◽  
Protein Excretion ◽  
Sprague Dawley Rats ◽  
Vehicle Injection ◽  
Stabilization Period ◽  
Krebs Henseleit Buffer

PAF amplifies tissue damage in glomerulonephritis and can promote proteinuria stimulating platelet and neutrophil cationic protein release. We used IPK to establish whether PAF directly causes proteinuria. Kidneys were isolated from male Sprague-Dawley rats and perfused at constant pressure (100 mmHg) in a closed circuit with a Krebs-Henseleit buffer containing glucose urea creatinine, BSA (1%), Ficoll 70 (3.5%) and amino acids. After 25 min stabilization period, a basal 10 min clearance period was followed by PAF (1.8 nM f.c. n = 6) or vehicle (n = 5) injection into the renal artery. As seen in the figure PAF but not vehicle significantly (p<0.01) increased urine protein excretion. No significant changes in GFR (as creatinine clearance) were observed after PAF or vehicle injection (Basal: 0.786 ± 0.075 PAF: 0.658 ± 0.070. Basal 0.653 ± 0.081, vehicle 0.639 ± 0.074 ml/min/g kidney). The data indicate that PAF may directly increase glomerular permeability to proteins.

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