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N Hinglais

Publications and source records attributed to N Hinglais.

At least 55 records · Page 3Linked to original sources
PubMed1986

Role of amount and nature of carbohydrates in the course of experimental renal failure.

The renal effects of carbohydrates (CHO) were studied in two experiments. 1) The effects of CHO-energy restriction was evaluated by comparing uremic growing rats (initial weight: 80 g) fed "ad lib" (L rats) or CHO-restricted (starch and glucose) but receiving identical amounts of all other nutrients (R rats). R rats showed reduced growth, slower increase in plasma creatinine, lower mortality rate, and less histological renal damage than L rats. 2) Two types of CHO restriction, low glucose (R1 rats) or low starch (R2 rats) were compared to "ad lib" feeding (L1 rats) in adult rats (initial weight: 130 g). Growth was identically reduced in R1 and R2 rats. Mean plasma creatinine levels at week four was lower in R1 than in L1 rats. The overall rate mortality was higher for L1 and R2 than in R1 rats (79%, 81%, 53%) but included deaths from other causes than renal failure. Actuarial survival excluding these deaths was 27%, 83% and 10% in L1, R1 and R2 rats, respectively. Diffuse renal lesions were found in 25 of 30 L1, 5 of 15 R1, and 12 of 15 R2 rats (R1 vs. R1 and R2, P less than 0.01). The results show that CHO restriction may preserve the renal parenchyma, and suggest that restriction of "simple" rather than "complex" CHO restriction may be beneficial, a finding which could be of clinical importance if confirmed by further investigations.

Animals↗
PubMed1986

Immunohistochemical analysis of C3 cleavage fragments, factor H, and the C5b-9 terminal complex of complement in de novo membranous glomerulonephritis occurring in patients with renal transplant.

Fifteen renal biopsies from 13 transplanted patients with de novo membranous nephropathy (DNMN) were investigated by immunofluorescence for the presence of C5b-9 neoantigens of the terminal sequence of complement and for antigens expressed by C3 cleavage fragments. DNMN lesions were classified as stage I, II or III upon light and electron microscopy examination. Seven biopsies were classified as stage I DNMN and 8 stage II-III. All patients were proteinuric. In six biopsies with stage I DNMN, staining for C5b-9 neoantigens was restricted to a fine granular labeling in mesangial areas which was analogous to that seen in normal kidneys in contrast with extensive parietal labeling for IgG, C3d and factor H antigens. In eight biopsies with stage II-III DNMN, the pattern of staining with anti-C5b-9 neoantigens antibodies was similar to that obtained with anti-IgG, anti-C3d and anti-factor H antibodies. These results suggest that in situ activation of the whole complement sequence throughout C5b-9 only occurs on large immune deposits (stage II-III DNMN).

Adolescent↗
PubMed1986

De novo focal glomerular sclerosis in preeclampsia.

Eleven women were selected on the presence, in postpartum renal biopsies, of focal glomerulosclerosis (FGS) superimposed to glomerular lesions of typical pregnancy-induced nephropathy. Ten out of them presented with severe preeclampsia. The renal specimens were examined by light and/or electron and/or immunofluorescence microscopy. The present study gathered clinical and morphological data suggesting that FGS might develop during preeclampsia. In these renal biopsies with FGS and lesions of pregnancy-induced nephropathy a sparse detachment of podocyte was observed at a distance from the segmental lesions by electron microscopy. The latter has also been observed in experimental models of FGS in which FGS is dependent on glomerular hemodynamic alterations. We think that the mechanism of the development of FGS in these pathological pregnancies may be analogous to these experimental models of FGS with hyperfiltration.

Adolescent↗
PubMed1984

Renin storage and cell differentiation in juxtaglomerular cell tumors: an immunohistochemical and ultrastructural study of three cases.

Three renin-secreting juxtaglomerular cell tumors were studied by ultrastructural and immunocytochemical methods. Both active and inactive renins were identified in tumor extracts. By immunofluorescence and the peroxidase-antiperoxidase (PAP) method with antirenin antiserum, immunolabeling was intracytoplasmic and irregularly distributed throughout the tumor tissue. Electron microscopic examination revealed various types of secretory granules, including atypical giant crystalloid protogranules in one case, and the postembedding PAP procedure showed labeling of all types of granules. Acid phosphatase staining was observed within secretory granules and autophagic vacuoles. The process of renin storage and release is discussed. The presence in one case of a neural component and a distal tubular structure supports the view of a hamartomatous lesion.

Adult↗
PubMed1984

Immunohistochemical study of Ia antigen in the normal and diseased human kidney.

The presence and distribution of Ia antigen in normal human kidneys and biopsy specimens from patients with renal disease were investigated by immunohistochemical techniques using two monoclonal antibodies to the nonpolymorphic determinants of human HLA-DR molecules. Ia antigen was found on the endothelium of glomerular and peritubular capillaries and of veins and vasa recta. Loss of endothelial staining was found in necrotic and sclerotic glomerular and tubulointerstitial lesions. Staining or decreased staining was also not found in the severe proliferative nephritis of systemic lupus erythematosus although endothelial cells could still be identified upon light microscopic examination of the same biopsy specimen. Resting and proliferating cells in mesangial areas did not stain with anti-Ia antibody and extracapillary proliferating cells did not express Ia antigen except for occasional cells in anti-GBM crescentic glomerulonephritis, suggesting that Ia-bearing cells are not involved in mesangial and most extracapillary proliferations in human glomerulonephritis. All clustered mononuclear cells infiltrating the renal interstitium stained with anti-Ia antibody regardless of the type of nephritis where infiltrates occurred.

Antibodies, Monoclonal↗
PubMed1983

Immunoelectron microscopic study of plasma protein pathways through the abnormal intestinal vasculature of HgCl2 induced immune disease in brown Norway rats.

Localization of immune deposits (ID) and the pathway of circulating serum proteins through the intestinal vasculature have been studied in 40 Brown Norway (BN) rats poisoned by mercuric chloride, using anti-peroxidase IgG as tracer. ID were found in all vessels but were initially detected along the epithelial basement membrane of villi and in pericytic venules and veins. ID were found in all the layers of the vessel walls. In pericytic or myocytic vessels, no ID were detected outside the adventitial lamina densa. ID trapped non immune IgG. Abnormal pathways were only found in venular capillaries and in pericytic venules with large gaps between endothelial junctions. ID were particularly abundant in these vessels.

Animals↗
PubMed1983

Glomerular and vascular IgG deposits in HgCl2 nephritis: role of circulating antibodies and of immune complexes.

The respective roles of circulating anti-glomerular basement membrane antibodies and of circulating immune complexes in the appearance of glomerular linear and granular IgG deposition during HgCl2-induced glomerulonephritis in the Brown-Norway rat has been studied. Syngeneic kidney transplantations have been performed at various phases of the disease. Results show that circulating antibodies are responsible for linear IgG deposition which did not change to granular deposits during the course of the disease. Electron-dense subepithelial deposits occurred only when circulating immune complexes were detected. These experiments strongly suggest that, in the mercury model, circulating immune complexes are responsible for granular IgG deposits observed in arteries and in the subepithelial space of glomeruli.

Animals↗
PubMed1983

Immunohistochemistry of renin in human diseased kidney.

The distribution of renin in human kidney was investigated by immunofluorescence and the peroxidase-antiperoxidase (PAP) procedure at the light and ultrastructural level. In three cases of juxtaglomerular renin-secreting tumors, renin was localized within the cytoplasm of tumor cells. In kidney biopsies, a semi-quantitative assessment was carried out, taking into account the size and the number of immunostained juxtaglomerular apparatuses. In 12 cases of ischemic kidneys and 8 cases of segmental renal hypoplasia, the increase in immunostaining for renin was striking in altered areas, while spared areas remained negative. In 2 cases of Bartter's syndrome, the pattern was similar to that found in ischemic kidneys. The study was extended to a series of 133 needle kidney biopsies from patients with various glomerular and vascular diseases; the immunomorphological parameters were correlated with serum creatinine levels but not with blood pressure values. Post-embedding immunoelectronmicroscopy using the PAP procedure performed on two of the cases of renin-secreting tumors, showed renin in all types of secretory granules.

Bartter Syndrome↗
PubMed1982

Immunoelectron microscopic study of plasma protein pathways through the different segments of the rat intestinal vasculature.

Nineteen Brown-Norway (BN) rats received intravenous injections of sheep anti-peroxidase (HRP) antibodies. Four BN rats were immunized to HRP. The anti-HRP antibodies were used to trace permeability pathways of large physiological molecules across different vessels of the small intestine. This organ was chosen because of the possibility of convenient "in situ" fixation and for the diversity of vessel types it contains. It was shown that: 1) There were no obvious transendothelial pathways in arteries with an elastic lamina. 2) The antibodies readily crossed fenestrated capillaries through the fenestrae. 3) There were two possible pathways through muscle capillaries and pericytic venules, namely transcytoplasmic vesicular "cactus-like" channels and interendothelial junctions. 4) Interendothelial permeability was a possible factor in veins with an elastic lamina. 5) Lymphatics were readily permeable through intercellular junctions and cytoplasmic vesicles.

Animals↗
PubMed1982

Effects of decomplementation on mercuric chloride-induced glomerulonephritis in Brown-Norway rats.

The course of mercuric chloride-induced immune glomerulonephritis is characterized by complement activation, intensive proteinuria, linear and then granular IgG and C3 deposits in the glomeruli. To assess the role of complement activation in the occurrence of the disease, decomplementation was achieved by intravenous injections of cobra venom factor in rats injected with mercuric chloride. In these animals, proteinuria still appeared while rats were decomplemented by cobra venom factor through the alternative pathway. These rats exhibited linear IgG deposits without detectable C3 deposits. In the rats injected with cobra venom factor alone, no proteinuria, no classical pathway complement activation and no renal IgG or C3 deposits were observed. Therefore, in Brown-Norway rats intoxicated with mercuric chloride, proteinuria appears to be at least in part complement independent.

Animals↗
PubMed1982

Alport's syndrome: experience at Hôpital Necker.

We review the characteristic morphologic features identifiable by electron microscopy that have been described in patients presenting with Alport's syndrome. They are diffuse thickening and splitting of the glomerular basement membrane (GBM), which are either isolated or associated with thinning. In occasional cases, only diffuse thinning can be seen. Our study of 100 families followed in Necker's hospital, of which 60 patients have had electron microscopic examination of their renal parenchyma, demonstrates that these GBM changes are highly suggestive of Alport's syndrome. All the patients included in the study fulfilled the following clinical criteria: familial incidence, nerve deafness in the propositus or in another member of the family, renal disease with progression to renal failure in the proband or in another member of the kindred. Although a failure in the proband or in another member of the kindred. Although a normal GBM was found in five patients, the GBM changes should be one of the criteria for the definition of the syndrome. Results dealing with a few other problems raised by this syndrome are reported. They concern the antigenicity and the biochemical composition of the GBM, the incidence of macular and perimacular changes, and the genetic transmission of the disease. It is concluded that Alport's syndrome is genetically heterogeneous and that the GBM ultrastructural changes are observed in most patients whatever the type of genetic transmission.

Adolescent↗
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↗
PubMed1980

Distribution of blood group antigen A in normal and pathologic human kidneys.

We tested this distribution with an indirect immunofluorescent technique using purified rabbit anti-A antiserum on 21 whole normal kidneys (a group, N equal to 18; AB group, N equal to 1; O group, N equal to 2) and on 349 kidney biopsy samples (A group, N equal to 140; AB group, N equal to 14; O or B group, N equal to 195) representing a large spectrum of renal diseases. In normal kidneys from A and AB groups, the A antigen was detected in the whole vascular endothelium and in the convoluted distal tubules. In secretors, collecting tubules were brightly positive. Epithelial staining was more diffuse in the inner part than it was in the outer part of the medulla. The basement membrane of the inner collecting tubules was positive in frozen sections but not in paraffin sections. In pathologic kidneys, modifications were obvious: (1) The thickened basement membrane of atrophic convoluted distal tubules was brightly stained. (2) Endothelial staining allowed a precise appreciation of the glomerular and interstitial vasculature. (3) In proliferative changes such as arterial intimal proliferation, proliferative glomerulonephritis, and interstitial cell infiltration, endothelial cells do not proliferate. This routine staining technique of endothelial cells by anti-A antiserum provide information not obtainable with light microscopy.

ABO Blood-Group System↗
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↗