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Biomedical subjects

J Bariety

Publications and source records attributed to J Bariety.

At least 109 records · Page 6Linked to original sources
PubMed1982

Phagocytosis of heat-aggregated immunoglobulins by mesangial cells: an immunoperoxidase and acid phosphatase study.

It has been demonstrated previously that mesangial cells (MC) phagocytose particulate material and nonimmune proteins, but that cells are able to engulf aggregated immunoglobulins (Igs) has not been proven so far. To investigate this cell function, heat-aggregated antiperoxidase (HRP) Igs were injected intravenously into Lewis rats. Sequential immunoelectron microscopic studies revealed that the injected material accumulates progressively in the extracellular compartment from 10 minutes to 5 hours and disappear afterward. This disappearance was related in part to the incorporation of aggregated anti-HRP Igs within phagosomes and phagolysosomes by MC. Quantitation of the phagocytic process showed that it starts as early as 10 minutes after injection and reaches its peak at 2.5 hours. Endocytosis seems to be associated with the sequestration of injected Igs within large cytoplasmic invaginations and with micropinocytosis. To further support these observations, ultrastructural cytochemistry for acid phosphatase activity was performed. Quantitative studies showed that the number of acid phosphatase-labeled lysosomes in MC was up to 7-fold greater in rats receiving aggregated anti-HRP Igs than in noninjected ones. In conclusion, our combined immunoperoxidase and acid phosphatase studies show that MC possess a vacuolar (lysosomal) apparatus capable of handling heat-aggregated Igs. Whether these cells are also operational in the disposal of soluble immune complexes in spontaneous and experimental conditions remains to be proven. In addition, observations suggesting the drainage of macromolecules from mesangium to the juxtaglomerular apparatus and from mesangium to the urinary space are presented.

Acid Phosphatase↗
PubMed1981

[Dramatic aggravation of renal amyloidosis after surgery. Three cases (author's transl)].

A few cases of improvement in secondary renal amyloidosis following surgery (in particular, removal of the amylogenic foci) have been published, but cases of aggravation are much more numerous. The authors report on three patients whose renal function deteriorated dramatically after extra-renal surgery (pneumonectomy, aortic valve replacement, mitral valve replacement). None of the usual precipitating factors, such as DIC, cardiovascular collapse, sepsis or renal vein thrombosis, could be detected, but two patients had been under extracorporeal circulation. Such accidents appear to be unpredictable and irreversible. They can be seen in primary or secondary amyloidosis and whether or not surgery involves an amylogenic focus. Indeed, in two of their patients the diagnosis of amyloidosis was unknown before the operation. This suggests that in patients with suspected amyloidosis no major surgical operation should be undertaken without prior renal biopsy.

Adult↗
PubMed1981

Renin localization in segmental renal hypoplasia. Immunohistochemical demonstration in two cases.

The distribution of renin in two cases of segmental renal hypoplasia was investigated by immunofluorescence and the peroxidase anti-peroxidase (PAP) method using an anti-human renin antiserum. Renin-containing cells were found only in hypoplasic segments in the vicinity of altered glomeruli and small arteries. Well-preserved renal cortex and areas of chronic atrophic pyelonephritis failed to show any demonstrable site of renin production. Whatever is the mechanism of the disease, the characterization of large numbers of renin-containing cells in the affected kidney support a role for the renin-angiotensin system stimulation in this form of hypertension.

Adolescent↗
PubMed1981

Investigation of the mechanism of action of prostaglandin synthesis inhibitors on renin and aldosterone secretion and sodium excretion.

Mean blood pressure (MBP) was found to be lower, while renal plasma flow (RPF), glomerular filtration rats (GFR), sodium excretion rate (U(Na)V), potassium excretion rate (U(k)V) and urinary prostaglandin E (PGE) concentration were higher in 15 normotensive subjects (15NS) compared with the values obtained in 15 essential hypertensive patients (15EHP) of the same mean age. After volume expansion of the 15HP with isotonic saline infusion, RPF, U(Na)V, U(k)V, urine volume (UV) and urinary PGE increased significantly while plasma renin activity (PRA) decreased significantly. Urinary aldosterone concentration and MBP decreased also but not significantly. After oral administration of 75 mg of indomethacin, in the same loaded group of 15 EHP, urinary PGE, urinary aldosterone and PRA decreased significantly while RPF, GRF, U(Na)V remained unaltered and MBP increased. When these values obtained in saline loaded and indomethacin treated 15EHP were compared to those obtained in the same group before volume expansion, it was found that RPF, U(NaV, U(k)V and UV were higher after indomethacin-saline administration while MBP, GRF and urinary PGE did not differ significantly and PRA and urinary aldosterone were significantly lower. These findings argue against the suggestion that PGE increases sodium reabsorption at the distal tubule and indicate that the unaltered sodium excretion rate in saline loaded and indomethacin treated unanaesthetized subjects, results from the simultaneous decrease of renomedullary PGE, Renin and aldosterone secretion.

Adult↗
PubMed1981

Immunoenzymatic study of the protein pathway through the glomerular barrier in rat glomerulonephritides.

Circulating anti-horseradish peroxidase (HRP) IgG antibodies were used in the rat to study the glomerular leakage of proteins in glomerulonephritis (GN) induced by aminonucleoside (AN) and in glomerulonephritis induced by mercuric chloride to produce anti-glomerular basement membrane (GBM) antibodies. In ANGN, autologous albumin and fibrinogen were also detected by immunoperoxidase techniques. In both types of GN, the proteins studied were observed in the glomerular urinary space and proximal tubular cells. No channels were visible in the lamina densa. No accumulation of proteins was seen under the epithelial slits that were not closed. In ANGN, accumulation of proteins was observed in the subepithelial space where the podocytes act as a barrier (closed slits, subepithelial blind pockets, areas covered by broad sheets of cytoplasm), but no accumulation was seen in the lamina rara externa under normal or enlarged slits and areas of large epithelial cytoplasm detachment. Statistical analysis showed that in ANGN, at the time of maximal proteinuria, the number of "micropinocytotic" vesicles in the GBM-embedded part of podocytes was not increased as compared with controls. Such vesicles were not labeled. We conclude that in both types of GN, the permeability of the GBM is diffusely increased and that the plasma proteins pass into the urinary space via an extracellular pathway.

Animals↗
PubMed1981

Demonstration of a passive Heymann nephritis-like mechanism in a human kidney transplant.

The underlying mechanism of human extramembranous glomerulonephritis (EMGN) is generally thought to involve circulating immune complexes. Data presented here suggest that "in situ" formation of immune deposits may also be important in the pathogenesis of EMGN. We describe a patient with a "de novo" EMGN in a kidney transplant a few months after the graft placement. Before transplantation, the patient's serum contained antibodies reacting in vitro with rat kidney brush-border, but serum concentration of these antibodies rapidly decreased prior to the onset of proteinuria. No circulating immune complexes were detected on serial serum samples from the patients. Antibodies which were eluted from the kidney transplant biopsy were shown to react with the brush-border of the proximal convoluted tubule of rat kidney. We postulate that "in situ" formation of immune complexes within the glomerular capillary walls, and not circulating immune complexes, is the pathogenic mechanism responsible for the glomerular lesions of this case of EMGN.

Adult↗
PubMed1981

Immunohistochemical characterization of renin-containing cells in the human juxtaglomerular apparatus during embryonal and fetal development.

Thirty kidneys from nine embryos, 20 fetuses, and one full-term baby were examined for their renin content by immunofluorescence and the peroxidase antiperoxidase method, using an antihuman renin antiserum. Renin-containing cells were found in the early metanephros (5-week-old fetuses). Most of them were located in the wall of well-developed renal arteries in the vicinity of the prospective vascular pole of the glomeruli. In the poorly differentiated peripheral renal cortex, intracellular fluorescence was seen in nearby arterioles of pocket-like s-shaped tubules. Rarely, labeled cells were found in the wall of major branches of renal arteries. In all locations, the renin-containing cells appear to be clearly linked to the development of the renal vascular system.

Cell Differentiation↗
PubMed1981

Nephrotic syndrome, linear glomerular IgG deposits, and minimal glomerular changes. Report of a case.

A young adult patient had an unusual acute idiopathic nephrotic syndrome. This nephrotic syndrome was remarkable for (1) association with acute renal failure and hypertension, (2) finding of minimal glomerular changes with a linear fixation of the anti-human IgG conjugate along the glomerular capillary wall without demonstrable antiglomerular basement membrane antibodies, and (3) complete recovery, including disappearance of the linear staining, after treatment with prednisone, cyclophosphamide, and plasmapheresis.

Acute Disease↗
PubMed1980

Use of a specific antiserum for renin detection in human kidney.

The use of anti-human renin antibodies made possible the intrarenal localization of renin in human kidney by immunofluorescence. In normal kidney, only some juxtaglomerular apparatus (JGA) were fluorescent. In these JGA, granular or diffuse fluorescence was only seen in afferent arterioles and was not present in all cells. In the ischemic areas of partially infarcted kidney, fluorescence was seen in all JGA and in interlobular arteries. In these arteries the most eccentric cells were often the most positive. In the nonischemic areas of the same kidneys, fluorescence was not seen in JGA, but was observed in proximal tubular cells, suggesting the reabsorption of filtered renin at this site.

Antibodies↗
PubMed1980

Characterization by immunoperoxidase of the lymphocytes with bundle-shaped tubular (BST) inclusions in human normal peripheral blood.

In six normal subjects, no surface immunoglobulins were detected on blood lymphocytes containing bundle-shaped tubular (BST) inclusions, after incubation with anti-human IgM peroxidase-labeled Fab'2 fragments. These Fab'2 fragments from pepsin-digested sheep anti-human immunoglobulins revealed human mu kappa, and lambda chains. These results suggest that the BST inclusions do not belong to B lymphocytes but belong to T cells and/or a third lymphocyte population, including K cells and precursors of T and B cells.

Animals↗
PubMed1980

Renal lesions in the hypertensive syndromes of pregnancy: immunomorphological and ultrastructural studies in 114 cases.

One hundred and fourteen women presenting during pregnancy with an abnormally high blood pressure and/or proteinuria had a renal biopsy usually on the 8th day following delivery. The pathological specimens were examined by light and/or electron and/or immunofluorescence microscopy. Forty-one cases were studied with all three techniques. The patients could be allocated to six groups on the basis of clinical criteria. The first two groups (52 patients) showed the typical clinical and pathological features of classical preeclampsia. The remaining 62 women (four groups) had isolated hypertension, and, of these, 42 had a renal pathological pattern similar to that of preeclampsia. These 42 patients also had persistent hyperuricemia. Thus in pregnancy, hypertension and persistently elevated uric acid levels are indicative of glomerular lesions of "pregnancy induced nephropathy".

Adult↗
PubMed1979

Urinary prostaglandins in kidney disease.

Substances having the chromatographic behaviour and the bioassay properties of prostaglandins (PGE and PGF) were detected in the urine of 30 patients with kidney disease and 15 healthy subjects. The mean urinary PGE and PGF values in 15 patients with chronic glomerular disease or nephrosclerosis were significantly lower than those of 15 patients with chronic pyelonephritis and other forms of chronic interstitial nephritis, polycystic kidney disease, obstructive nephropathy or diuretic phase of acute renal failure, and of the mean PGE and PGF values found in the healthy subjects. It was suggested that in contrast to disease affecting primarily the renal medulla, chronic glomerular disease and nephrosclerosis are accompanied by a decrease of renal prostaglandin synthesis and/or release.

Glomerulonephritis↗
PubMed1979

Direct radioimmunoassay and immunocytochemical localization of renin in human kidneys.

1. Highly specific antibodies to human renin were prepared in rabbits and used for the preparation of a renin-free substrate, the direct radioimmunoassay of renin in plasma and kidneys, and the localization of renin with fluoresceinated antibodies. 2. In a patient with a partially infarcted kidney, plasma renin activity was increased, and could be activated by acid. The direct measurement of plasma renin by radioimmunoassay gave identical values before and after acidification. 3. In the ischaemic part of the kidney, renin content was high, both by the enzymatic and the direct method of measurement. It was low in the non-ischaemic part of the kidney. 4. All afferent and some interlobular arteries of the obsolescent glomeruli were stained with fluoresceinated anti-renin antibodies. In the non-ischaemic area, the juxtaglomerular appratus did not stain. 5. Renin can now be measured in human plasma and kidney as an entity, by a specific radioimmunoassay. A direct investigation of this intrarenal hormone is now possible at the renal tissue level.

Animals↗
PubMed1979

Podocytes in aminonucleoside glomerulonephritis investigated ultrastructurally with concanavalin A.

Peroxidase labeled concanavalin A (Con A) permits the detection of some saccharide determinants. This histochemical technique permits the visualization of cellular pathological modifications not observed with other methods. Its use in an ultrastructural study of nephritis induced by a single injection of aminonucleoside demonstrated the following in podocytes. The Con A positive endoplasmic reticulum (ER), essentially the rough ER, lost its normal linear and network appearance to take on a dot dash pattern. ER contents but not attached ribosomes and membranes were Con A positive. The dot dash pattern, due to a fragmentation of the ER, appeared prior to the onset of proteinuria and was attenuated before the disappearance of proteinuria. These changes of the ER were not observed in other proteinuric states. This suggests that aminonucleoside can damage the synthesis apparatus of podocytes, revealed by the Con A method.

Animals↗
PubMed1979

[Arterial subendothelial structures: anatomy, biochemistry, functions].

This review summarizes the main structural and biochemical features of the fibrillar constituents of the subendothelial layers of the arterial wall. Several constituents are directly identified by various histochemical methods and electron-microscopic studies. (1) The microfibrils (MF), stained by tannic acid, cationic stains such as ruthenium red, and various peroxidase-labeled lectins are mostly found in association with elastin within the internal elastic lamina (IEL). They have been characterized by chemical analysis as acidic glycoproteins, hydrolyzed by a variety of proteases, but resistant to collagenases. The endothelial cells seem to participate in their biosynthesis. (2) Elastin (El), which is the main constituent of the IEL, forms a wide, concentric, electron-lucent, tannic-acid-stainable zone. Fibrous El results from the association of tropoelastin (or proelastin) molecules by intermolecular cross-linkage. During the elastigenesis, this cross-linkage occurs directly between tropoelastin molecules which have been previously sterically oriented by the MF probably synthetized by the same cells (smooth muscle cells and possibly endothelial cells). (3) Interstitial collagen forms sparse fibers characterized by their cross-striation (with a periodicity of 640 A). They are relatively resistant to most proteolytic enzymes, except collagenases. They result from the intermolecular cross-linkage of rigid molecules, resulting themselves from the intramolecular cross-linkage of three helical alpha chains as a triple helix. The interstitial subendothelial collagen has been identified by indirect immunofluorescence as a type III collagen. The same technique has also been used to detect type IV collagen and fibronectin. This glycoprotein could play a role in the attachment of the endothelial cells to the fibrillar network of the subendothelium, despite an affinity which is greater toward denatured collagen than toward native collagen. One of the most important functions of the subendothelium is its role in thrombogenesis, in which both MF and collagen are involved. In type III collagen, this property is linked to the preservation of an ordered structure in which a 9-amino acids fragment, localized in the central part of each chain, could bear an adhesion site.

Animals↗