Ultrastructural Lesions of Tubular Basement Membranes and Peritubular Capillaries in Hereditary Nephritis

2015 ◽  
pp. 47-55
Author(s):  
G. Battini ◽  
M. Meroni ◽  
L. Torri Tarelli ◽  
A. Sessa
Keyword(s):  
Basement Membranes ◽  
Hereditary Nephritis ◽  
Peritubular Capillaries

Physical Properties of Isolated Perfused Renal Tubular Basement Membranes

1971 ◽  
Vol 29 ◽  
pp. 390-391
Author(s):  
Jared Grantham ◽  
Larry Welling
Keyword(s):  
Basement Membrane ◽  
Basement Membranes ◽  
Transport Mechanisms ◽  
Permeability Characteristics ◽  
Peritubular Capillaries ◽  
Strategic Location ◽  
Tubular Lumen ◽  
Glomerular Filtrate ◽  
Urine Formation ◽  
Renal Tubular

In the course of urine formation in mammalian kidneys over 90% of the glomerular filtrate moves from the tubular lumen into the peritubular capillaries by both active and passive transport mechanisms. In all of the morphologically distinct segments of the renal tubule, e.g. proximal tubule, loop of Henle and distal nephron, the tubular absorbate passes through a basement membrane which rests against the basilar surface of the epithelial cells. The basement membrane is in a strategic location to affect the geometry of the tubules and to influence the movement of tubular absorbate into the renal interstitium. In the present studies we have determined directly some of the mechanical and permeability characteristics of tubular basement membranes.

scholarly journals Complement Activation in Acute Humoral Renal Allograft Rejection

1999 ◽  
Vol 10 (10) ◽  
pp. 2208-2214 ◽  
Author(s):  
A. BERNARD COLLINS ◽  
EVELINE E. SCHNEEBERGER ◽  
MANUEL A. PASCUAL ◽  
SUSAN L. SAIDMAN ◽  
WINFRED W. WILLIAMS ◽  
...  
Keyword(s):  
Cyclosporin A ◽  
Basement Membranes ◽  
Graft Dysfunction ◽  
Peritubular Capillary ◽  
Hla Antibodies ◽  
Ulex Europaeus ◽  
Classical Complement Pathway ◽  
Type Iv ◽  
Valuable Adjunct ◽  
Peritubular Capillaries

Abstract. The distinction between acute humoral rejection (AHR) and acute cellular rejection (ACR) in renal allografts is therapeutically important, but pathologically difficult. Since AHR is probably mediated by antibodies to the donor endothelium that activate the classical complement pathway, it was hypothesized that peritubular capillary C4d deposition might distinguish this group. Renal biopsies (n = 16) from 10 patients with AHR who had acute graft dysfunction, neutrophils in peritubular capillaries, and a concurrent positive crossmatch were stained for C4d by immunofluorescence. Control biopsies for comparison showed ACR (n = 14), cyclosporin A toxicity (n = 6), or no abnormality (n = 4). Peribiopsy sera were tested for anti-donor HLA antibody. C4d deposited prominently and diffusely in the peritubular capillaries in all AHR biopsies (16 of 16). IgM and/or C3 were also present in 19 and 44%, respectively. With two-color immunofluorescence, C4d was localized in basement membranes (type IV collagen+) and in the endothelium (Ulex europaeus agglutinin-I+). In ACR, no more than trace C4d was found in peritubular capillaries (P < 0.0001 versus AHR), and no patient had anti-donor HLA antibodies (0 of 8); 27% had neutrophils in peritubular capillaries. One of six biopsies with cyclosporin A toxicity had similar C4d deposits, and circulating anti-donor class I antibody was detected. Grafts with AHR were lost (40%) more often than those with ACR (0%; P < 0.02). C4d in peritubular capillary walls distinguishes AHR from ACR, is more specific and sensitive than traditional criteria, and is a potentially valuable adjunct in the diagnosis of graft dysfunction.

scholarly journals Narthecium ossifragum (L.) Huds. Causes Kidney Damage in Goats: Morphologic and Functional Effects

2003 ◽  
Vol 40 (3) ◽  
pp. 317-327 ◽  
Author(s):  
H. Wisløff ◽  
A. Flåøyen ◽  
N. Ottesen ◽  
T. Hovig
Keyword(s):  
Elevated Serum ◽  
Basement Membranes ◽  
Gamma Glutamyl Transferase ◽  
Narthecium Ossifragum ◽  
Urine Protein ◽  
Functional Changes ◽  
Ultrastructural Studies ◽  
Cytoplasmic Vacuolization ◽  
Peritubular Capillaries ◽  
Glutamyl Transferase

We studied the effects of Narthecium ossifragum on goat kidneys. Twenty-five Norwegian dairy goats, 5 weeks to 4 months of age, were orally dosed with an aqueous extract from N. ossifragum. In experiment 1, we studied microscopic and functional changes in 12 animals that were euthanatized 2, 3, 4, 5, and 6 days after treatment. In experiment 2, we included ultrastructural studies on serial renal biopsies and urine analysis from five extract-treated animals and two controls. In addition, urine samples were collected from four dosed and two control goats. Ultrasonography revealed perirenal and retroperitoneal fluids. Microscopic changes were observed after 6 hours. The findings, most obvious in the inner cortex and the outer medulla, consisted of cytoplasmic vacuolization, interstitial edema, and focal necrosis of tubular epithelial cells. Ultrastructurally, the tubules had loss of microvilli, irregular cytoplasmic vacuolization, mitochondrial swelling with loss of cristae, and irregular but continuous basement membranes even with necrosis. In the glomeruli, there were occasional endothelial damage and shortening and swelling of the foot processes. Peritubular capillaries had breaks in the vessel walls and irregular endothelial cell edema, and the interstitium had marked edema. The functional lesions included elevated serum urea, creatinine, and magnesium concentrations, a slight decrease in serum calcium concentration, elevated urine protein and urine protein-creatinine ratio, and increased activities of urine alkaline phosphatase and gamma glutamyl transferase. Our findings indicate a fast-acting toxic principle inducing damage by both direct toxic and secondary ischemic effects.

Ultrastructural appearance of renal and other basement membranes in the bull terrier model of autosomal dominant hereditary nephritis

2000 ◽  
Vol 36 (2) ◽  
pp. 378-391 ◽  
Author(s):  
Jennifer C. Hood ◽  
Judy Savige ◽  
Anthony E. Seymour ◽  
John Dowling ◽  
Paul Martinello ◽  
...  
Keyword(s):  
Autosomal Dominant ◽  
Basement Membranes ◽  
Hereditary Nephritis ◽  
Ultrastructural Appearance

P0424CLINICO-PATHOLOGICAL CHARACTERISTICS AND OUTCOMES OF PATIENTS WITH DNAJB9 POSITIVE FIBRILLARY GLOMERULONEPHRITIS

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Shaoshan Liang ◽  
Dandan Liang ◽  
Feng Xu ◽  
Mingchao Zhang ◽  
Fan Yang ◽  
...  
Keyword(s):  
Interstitial Fibrosis ◽  
Young Patients ◽  
Hashimoto Thyroiditis ◽  
Basement Membranes ◽  
Igg Subclasses ◽  
Tubular Atrophy ◽  
Fibrillary Glomerulonephritis ◽  
Peritubular Capillaries ◽  
Polyclonal Igg ◽  
Glomerular Deposits

Abstract Background and Aims To investigate the clinicopathological features and prognosis of DNAJB9 positive fibrillary glomerulonephritis (FGN) in a single center in China. Method Cases diagnosed as FGN by renal biopsy from January 2011 to December 2019 in Jinling Hospital were stained with anti-DNAJB9 by immunohistochemistry. The patients with DNAJB9 positive FGN were retrospective analyzed. Results DNAJB9 staining of glomerular deposits was seen in 6 cases of FGN. 1 man and 5 women with a median age of 26 years (range, 21 to 49 years) were studied. Underlying autoimmune disease of Sjogren's syndrome and Hashimoto thyroiditis was in 1 case. None of them had dysproteinemia, malignancy, hepatitis C, hepatitis B, cryoglobulinemia, or diabetes. The patients presented with hypertension and edema in 5 cases, renal insufficiency in 1 case, and proteinuria in 6 cases with the median 24-hour urine protein 2.58 g (range, 1.66 to 9.57 g), nephrotic syndrome in 3 cases, and microscopic hematuria in 2 cases. The histologic pattern was mesangial proliferative glomerulonephritis (GN) and membranoproliferative GN. A mean of 9.7% of glomeruli were globally sclerotic. Crescents were present in 1 case (10%). The degree of tubular atrophy and interstitial fibrosis were absent (2 cases) and mild (4 cases), and severe acute tubular injury was in 1 case. All 6 cases showed glomerular positivity for IgG, C3 and C1q, 5 of which were positive for IgM, and 4 of which were positive for IgA. The glomerular deposits stained for polyclonal IgG subclasses and both kappa and lambda light chains in 3 cases. In 1 case, it stained for polyclonal IgG subclasses without kappa or lambda. IgG subclasses were IgG4 dominant in 3 cases and IgG1 dominant in 1 case. In 2 cases, they stained for monoclonal IgG1-kappa and IgG1-lambda. On electron microscopy (EM), the fibrillary deposits were seen infiltrating the mesangium, subendothelial, subepithelial area in all 6 cases, and the lamina densa of the GBMs in 5 cases with diameter of 7-40nm. Combined with observation of DNAJB9 staining, immunofluorescence microscopy and EM, extraglomerular deposits were identified in vessel walls in 5 cases, tubular basement membranes in 3 cases, peritubular capillaries in 3 cases. Congo red positivity was in 4 cases. At a median time of 32.9 months (range, 1 to 68.3 months) after biopsy, 3 cases were stable, 1 case had partial renal function recovery, and 2 cases had partial remission of proteinuria. Conclusion DNAJB9 immunohistochemistry is sensitive and specific for FGN. Monoclonal IgG and light chain was observed in young patients. Extraglomerular deposits were common. Prognosis was good in this young patient’s series.

scholarly journals Alport’s syndrome and benign familial haematuria: Light and electron microscopic studies of the kidney

2008 ◽  
Vol 136 (Suppl. 4) ◽  
pp. 275-281
Author(s):  
Jovan Dimitrijevic ◽  
Vera Todorovic ◽  
Anastasija Aleksic ◽  
Dijana Jovanovic ◽  
Dijana Pilcevic ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Light Microscopy ◽  
Light And Electron Microscopy ◽  
Definitive Diagnosis ◽  
Basement Membranes ◽  
Tissue Slices ◽  
Electron Microscopic ◽  
Tissue Samples ◽  
Hereditary Nephritis ◽  
Hereditary Nephropathy

INTRODUCTION. Hereditary nephropathy is clinically characterized by the familial occurrence in successive generations of progressive haematuric nephritis and neural hearing loss. Hereditary nephropathy of Alport?s syndrome (AS) and benign familial (recurrent) haematuria (BFH) are morphologically characterized by specific and diagnostically important thickening and splitting of lamina densa of the glomerular basement membranes. Those lesions can be recognized only by electron microscopy. Hereditary nephritis is usually present clinically with haematuria, and new mutations without a family history of haematuria. It is therefore important to differentiate hereditary nephritis from BFH and no familial haematuria. Thus, electron microscopy is essential in diagnosis of haematuria. OBJECTIVE. The aim of this study was to describe, by light microscopy, constellation of renal alterations by which hereditary nephropathy can be recognized with high probability as well as to compare the diagnostic validity of the findings observed by light and electron microscopy in AS and BFH. METHOD. We examined 48 renal biopsies of the patients with hereditary nephoropathies by light and electron microscopy. Tissue samples were fixed in buffered paraformaldehyde and embedded in paraffin for long-term preservation. For the electron microscopy analysis, the following fixation in 4% glutaraldehyde tissue was postfixed in 1% osmium tetroxide. Thereafter, the following dehydration procedure tissue slices were embedded in epon. RESULTS. Our results demonstrated that the interstitial foam cells, foetal-like glomeruli, minimal glomerular abnormalities with stain less intense in basement membranes, mild irregular mesangial widening, focal thickening of Bowman?s capsule, foci of dilatation tubules, tubular ectasia and atrophy, erythrocyte tubules casts were present in hereditary nephritis. Additionally, light microscopic biopsy findings in patients with BFH were either normal or revealed minor changes (e.g. increased mesangial matrix). All biopsies were reevaluated by electron microscopy and ultrastructural findings confirmed the diagnosis of hereditary nephropathies. CONCLUSION. The findings observed by light microscopy represent an important step that leads to a definitive diagnosis of AS and BFH. The definitive diagnosis, however, depends on electron microscopy.

A web-like network of type vi collagen in human skin is revealed by immuno-electron microscopy

1988 ◽  
Vol 46 ◽  
pp. 382-383
Author(s):  
Douglas R. Keene ◽  
Robert W. Glanville ◽  
Eva Engvall
Keyword(s):  
Electron Microscopy ◽  
Monoclonal Antibody ◽  
Human Skin ◽  
Basement Membranes ◽  
Primary Antibody ◽  
Fat Cells ◽  
Secondary Antibody ◽  
Type Vi Collagen ◽  
Dermal Matrix ◽  
Immuno Electron Microscopy

A mouse monoclonal antibody (5C6) prepared against human type VI collagen (1) has been used in this study to immunolocalize type VI collagen in human skin. The enbloc method used involves exposing whole tissue pieces to primary antibody and 5 nm gold conjugated secondary antibody before fixation, and has been described in detail elsewhere (2).Biopsies were taken from individuals ranging in age from neonate to 65 years old. By immuno-electron microscopy, type VI collagen is found to be distributed as a fine branching network closely associated with (but not attached to) banded collagen fibrils containing types I and III collagen (Fig. 1). It appears to enwrap fibers, to weave between individual fibrils within a fiber, and to span the distance separating fibers, creating a “web-like network” which entraps fibers within deep papillary and reticular dermal layers (Fig. 2). Relative to that in the dermal matrix, the concentration of type VI collagen is higher around endothelial basement membranes limiting the outer boundaries of nerves, capillaries, and fat cells (Fig. 3).

Localization of cell-surface and basement-membrane heparan-sulfate proteoglycans using the malaria circumsporozoite protein

1994 ◽  
Vol 52 ◽  
pp. 294-295
Author(s):  
U. Frevert ◽  
S. Sinnis ◽  
C. Cerami ◽  
V. Nussenzweig
Keyword(s):  
Heparan Sulfate ◽  
Protein A ◽  
Kidney Tissue ◽  
Plasmodium Species ◽  
Its Region ◽  
Basement Membranes ◽  
Heparan Sulfate Proteoglycans ◽  
Infected Mosquito ◽  
Complement Components ◽  
Region Ii

Malaria sporozoites, which invade hepatocytes within minutes after transmission by an infected mosquito, are covered with the circumsporozoite (CS) protein, which in all Plasmodium species contains the conserved region II-plus. This region is also found as a cell-adhesive motif in a variety of host proteins like thrombospondin, properdin and the terminal complement components.The CS protein with its region II-plus specifically binds to heparan sulfate proteoglycans (HSPG) on the basolateral surface of hepatocytes in the space of Disse (FIG. 1), to certain basolateral cell membranes and basement membranes of the kidney (FIG. 2) as well as to heparin in the granules of connective tissue mast cells. The distribution of the HSPG receptors for the CS protein was examined by incubation of Lowicryl K4M or LR White sections of liver and kidney tissue with the recombinant CS ligand, whose binding sites were detected with a monoclonal anti-CS antibody and protein A gold.

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