PubMed Health⌕ Search

Biomedical subjects

L Allegri

Publications and source records attributed to L Allegri.

At least 37 records · Page 2Linked to original sources
PubMed1989

Antigenic targets in epimembranous glomerulonephritis. Experimental data and potential application in human pathology.

Although membranous glomerulonephritis (MGN) has been long considered as a prototype of glomerulonephritis (GN) due to the deposition of circulating immune complexes (CIC), a growing body of evidence indicates that immune deposits can also be formed in situ and implicate antigens expressed by glomerular epithelial cells (GEC). Some of these antigens have recently been identified. The first one, gp330 - a 330-kd glycoprotein restricted to the coated pits of GEC and renal brush border (BB) - is responsible for Heymann nephritis, a rat model of MGN. However, it is absent in the human glomerulus and is therefore probably not involved in human cases of MGN, at least in those due to in situ formation of CIC. In addition, by raising monoclonal antibodies against rat and rabbit BB, we have isolated two other BB proteins also expressed on GEC. The latter, respectively identified as dipeptidyl peptidase IV (90 kd) and enkephalinase (85 kd), can serve as targets for the formation of short-lived immune deposits. Since they are also detected on human GEC, they might play a role in the pathogenesis of MGN in man.

Animals↗
PubMed1989

[The physiopathologic bases of the neurotoxicity of phosphorus chelating agents containing soluble aluminum salts in patients with renal insufficiency].

To what extent can damage to the central and peripheral nervous systems be ascribed to chronic aluminum (Al) intoxication taken as a chelating agent for phosphorus, to limit hyperphosphatemia in uremic patients? Since Al is normally eliminated by the renal route, its accumulation in uremia has to be ascribed to a reduced or abolished renal clearance of the metal, which results in preferential toxicity for certain tissues, especially nervous tissue, which shows difficulty in eliminating Al, even after intake has been stopped. This review discusses, on the basis of toxicologic, experimental and clinical data, the possible pathogenic steps of Al neurotoxicity in uremia, considering: the damage to axonal transport in which Al intoxication tends to affect the components of the cytoskeleton, the polymerization phase of the alpha and beta tubulin constituents of neurotubules, and the normal translocation of neurofilaments from the perikaryon to more distal positions of the axon; the abnormalities in the brain pool of adrenergic, cholinergic and GABA neurotransmitters; the increase in permeability and changes in perm-selectivity of the blood-brain-barrier, with further loss of neurotransmitters and with acquisition, from the systemic circulation, of neurotransmitter-like substances such as hormones, monoamines and peptides, which may adversely modulate synaptic and membrane functions; the cerebral energy metabolism and particularly the hexokinase reaction, by Al replacement of the Mg-ion in the Mg-ATP complex, so that phosphorylation of glucose to G6P is blocked; the interaction of Al with calmodulin by displacement of the Ca-ion and subsequent formation of a stable Al-calmodulin complex with a cytotoxic effect due to the increase in the intracellular calcium concentration.(ABSTRACT TRUNCATED AT 250 WORDS)

Aluminum↗
PubMed1988

Detection of cell surface antigens in tissue sections by means of pre-embedding immunogold staining.

The immunogold technique has been used in electron microscopy to detect cytoplasmic and extracellular antigens by postembedding techniques. It has also been used to detect plasma-membrane-associated molecules on suspended cells and, recently, to visualize cell surface antigens in ultrathin sections of Lowicryl embedded specimens. In the present study, cell surface antigens of rat kidney and human skin were identified in tissue sections by using pre-embedding immunogold labeling. Brush border microvillar antigens and dermal lymphocyte antigens both bound numerous gold particles. The immunogold staining described here has the advantage over immunoperoxidase procedures that is not subject to diffusion or reabsorption artifacts, and allows estimation of the antigen density on labeled cells. Furthermore, this pre-embedding immunogold technique is ideally suited to detecting cell surface-associated antigens since it preserves antigenicity, allows gold particle penetration and enhances cell membrane profiles.

Animals↗
PubMed1986

Polyvalent antigen-antibody interactions are required for the formation of electron-dense immune deposits in passive Heymann's nephritis.

In order to analyze the initial steps involved in the formation of subepithelial electron-dense immune deposits, the authors induced passive Heymann's nephritis in rats by intravenous injection of monoclonal or polyclonal antibodies to the relevant antigen, a 330,000-dalton brush border protein also expressed within coated pits of glomerular epithelial cells. Whereas both mono- and polyclonal antibodies induced deposits detectable by indirect immunofluorescence, electron-dense deposits were only found in glomerular capillary walls of rats injected with polyclonal antibodies. Immunoultrastructural analysis confirmed the subepithelial location of heterologous IgG: monoclonal antibodies were essentially confined to the coated pits of glomerular epithelial cells, whereas polyclonal antibodies were detected in coated pits and in the subepithelial electron-dense deposits. In the face of an excess of circulating antibody, gp 330 was not detectable in the deposits, but a striking increase in the number of endoplasmic reticula positive for gp 330 was found. The results indicate that highly cross-linked immune complexes formed by polyvalent antibodies on the epithelial cell surface are necessary for the induction of subepithelial electron-dense deposits.

Animals↗
PubMed1984

A monoclonal antibody to brush border and passive Heymann nephritis.

An IgG2a monoclonal antibody (MoAb) reacting with the brush border of the renal proximal tubule and glomerular capillary wall was produced by fusion of NS1 myeloma cells with spleen cells from BALB/c mice immunized with renal brush border preparations from rat kidney cortex. This antibody reacts with a 90,000 mol. wt protein which can be isolated by immunoprecipitation of radiolabelled brush border or glomerular preparations and localized on these structures by immunoperoxidase electron microscopy, thus demonstrating the presence of common antigenic determinants. Survey of various organs showed that the MoAb reacted with the brush border of the gut, but also with antigens associated with the distal vascular system. In the liver antigenic determinants were located along the sinusoid walls but mainly on bile canaliculi. Specific glomerular binding could be demonstrated in vivo by immunofluorescence after an intravenous injection of 2 mg of antibody or by paired label methodology using tracer amounts. Kinetics however were dramatically different from those observed in classical passive Heymann nephritis since glomerular binding was transient during the first hours after injection. Binding was also found in tubular structures, as well as in lung, liver, spleen and heart. These results identify a well defined antigen-antibody system responsible for the formation of transient extramembranous glomerular deposits and may be relevant to some human cases of glomerulonephritis. They may also provide new models to study glomerular and tubular transfer of membrane bound antibodies.

Animals↗
PubMed1980

Sarcoid granulomatous nephritis with isolated and reversible renal failure. A case report.

A case of reversible renal failure due to sarcoid granulomatous nephritis is described. The patient, a 21-year-old student, was admitted with renal insuffciency (GFR = 25 ml/min); no damage was found in any organ except for slightly enlarged pulmonary hilar lymph nodes. Repeated percutaneous renal biopsies showed an interstitial noncaseating granulomatous nephritis. Steroid therapy provided rapid improvement and the diagnosis of sarcoidosis was established. Complete recovery of renal function with normal urinalyses was seen.

Acute Kidney Injury↗
PubMed1980

Mesangioproliferative glomerulonephritis.

UNLABELLED: The clinical and bioptic aspects of 211 cases of primary mesangioproliferative glomerulonephritis with urinary abnormalities lasting mre than 1 year were reviewed. We observed the following clinical syndromes: 1) Persistent proteinuria, isolated or with microhematuria: - a) with latent onset: 39% with hypertension (H); 10% with renal failure (RF); - b) with acute nephritic syndrome at onset: 31% with H; 6% with RF; 2) Recurrent macroscopic hematuria: 26% with H; 10% with RF; 3) Nephrotic syndrome: 70% with H; 29% with RF. The histological lesions, diffuse in all cases, appeared unrelated to the clinical syndromes and/or immunofluorescent patterns. In 65 cases with prevalent mesangial deposits of IgA, 46% showed persistent proteinuria with latent onset, 23% persistent proteinuria with acute nephritic syndrome at onset, 28% recurrent hematuria and 3% nephrotic syndrome. 37% of such patients developed H, 14% RF and 6% remission (R). On the other hand in 65 patients with other deposits the clinical aspects were as follows: persistent proteinuria with latent onset: 46%; persistent proteinuria with acute nephritic syndrome at onset: 31%; recurrent hematuria: 17%; nephrotic syndrome: 6%. 35% of these cases displayed H; 9% RF and 8% R. CONCLUSION: primary mesangioproliferative glomerulonephritis appears to represent a heterogeneous group with only the morphological aspects in common and associated with one of the three above-mentioned clinical syndromes. Immunohistology shows different Ig and/or complement which bear no specific relationship with clinical courses. In particular IgA deposits are present in 50% of the cases and are only related to higher incidence of recurrent hematuria and abnormal IgA serum levels.

Adolescent↗
PubMed1975

Studies on tryptophan metabolism in ethylism.

The urinary excretion of the metabolites "via kynurenine" was studied in a group of patients with chronic alcoholism after a L-tryptophan loading (100 mg/kg body-weight) with or without simultaneous administration of vitamin B6 or nicotinamide or both. In these subjects an abnormal tryptophan metabolism was obtained with excretion total mean values of 9 metabolites of 15.34% against 6.86% in healthy controls. The treatment with vitamin B6 or nicotinamide in 5 patients decreased the total average excretion from 14.41% to 9.47% and to 9.92% respectively without normalizing, however, the excretory pattern produced from the aminoacid loading. The simultaneous administration of these two vitamins in 9 chronic alcoholic men corrected completely the metabolic defect (from 15.34% to 6.55%).

Adult↗