ovalbumin and Proteinuria

Topics: Adrenocorticotropic Hormone; Alpha-Globulins; Androgens; Animals; Apolipoproteins; Estrogens; Female; Fructose-Bisphosphate Aldolase; Glucocorticoids; Glutamate-Ammonia Ligase; Growth Hormone; Hormones; Humans; Male; Ovalbumin; Phosphoenolpyruvate Carboxykinase (GTP); Progesterone; Prolactin; Proteinuria; RNA, Viral; Steroids; Transcription, Genetic; Tryptophan Oxygenase; Tyrosine Transaminase; Uteroglobin; Vitellogenins

In our clinical work, some patients with type I hypersensitivity could be detected protein in their urine. This study focused on the early renal injury in patients with type I hypersensitivity.. From 43 type I hypersensitivity patients with proteinuria, 10 patients were randomly selected for mass spectrometry analysis of 24-h urine together with 5 healthy volunteers. Mice were vaccinated with Dermatophagoides farina (Der f) and ovalbumin (OVA) were used as antigen to establish the type I hypersensitivity animal models.. The urine protein of hypersensitivity patients was significantly increased in the alpha-1-microglobulin/ bikunin precursor (Protein AMBP) (t = 3.140, P = 0.008), retinol binding protein 4 (RBP4) (t = 2.426, P = 0.031), kininogen-1 (t = 2.501, P = 0.027), and transferrin appeared only in patients' urine. After immunizing mice with antigens, significant increases of the total serum immunoglobulin E (IgE) were observed in both Der f (86.92 ± 36.01 U/mL, t = 5.231, P = 0.0004) and OVA group (34.65 ± 24.72 U/mL, t = 2.891, P = 0.0161) compared with the negative control group (2.68 ± 0.47 U/mL). Meanwhile, definite eosinophil infiltration around the impaired renal tubules as well as the bronchus in Der f mice were observed, and urine protein appeared. After stopping the allergen stimulation, proteinuria disappeared. Instead, when the mice were treated with the antigen again, proteinuria reappeared.. Our findings suggest that renal tubular damage in patients with type I hypersensitivity is reversible, and proteinuria disappears with allergy symptoms remission.

Topics: Allergens; Animals; Humans; Hypersensitivity; Hypersensitivity, Immediate; Immunoglobulin E; Kidney; Mice; Ovalbumin; Proteinuria; Retinol-Binding Proteins, Plasma

Lysosomal membrane permeabilization (LMP) has been shown to cause the release of cathepsins and other hydrolases from the lysosomal lumen to the cytosol and initiate a cell death pathway. Whether proteinuria triggers LMP in renal tubular epithelial cells (TECs) to accelerate the progression of renal tubulointerstitial injury remains unclear. In the present study, we evaluated TEC injury as well as changes in lysosomal number, volume, activity, and membrane integrity after urinary protein overload in vivo and in vitro. Our results revealed that neutrophil gelatinase-associated lipocalin and kidney injury molecule-1 levels were significantly increased in the urine of patients with minimal change nephrotic syndrome (MCNS) and the culture supernatant of HK-2 cells treated by urinary proteins extracted from MCNS patients. Urinary protein overload also induced apoptotic cell death in HK-2 cells. Importantly, we found that lysosomal volume and number were markedly increased in TECs of patients with MCNS and HK-2 cells overloaded with urinary proteins. However, lysosome function, as assessed by proteolytic degradation of DQ-ovalbumin and cathepsin-B and cathepsin-L activities, was decreased in HK-2 cells overloaded with urinary proteins. Furthermore, urinary protein overload led to a diffuse cytoplasmic immunostaining pattern of cathepsin-B and irregular immunostaining of lysosome-associated membrane protein-1, accompanying a reduction in intracellular acidic components, which could be improved by pretreatment with antioxidant. Taken together, our results indicate that overloading of urinary proteins caused LMP and lysosomal dysfunction at least partly via oxidative stress in TECs.

Topics: Adolescent; Adult; Cathepsins; Cell Line; Epithelial Cells; Female; Humans; Intracellular Membranes; Kidney Tubules; Lysosomes; Male; Ovalbumin; Oxidative Stress; Permeability; Proteinuria; Young Adult

Munchausen syndrome is a factitious disorder with predominantly physical signs and symptoms, resulting from the patient's high motivation for assuming a sick role, without any external incentives or boundaries. We report the case of a young female patient with factitious proteinuria in the nephrotic range and a fairly eventful medical history. After performing many expensive and unnecessary investigations and procedures,the real origin of the proteinuria was determined;it was found to be caused by the patient carefully adding calibrated egg albumin to her urine samples. This discovery roused suspicions about multiple, non-corroborated conditions from her history (e.g., multiple miscarriages, breast cancer, and thyroid disorders).The diversity of diseases presented by a single Munchausen patient tends to be bizarre,and thus is a challenge for health care providers to diagnose the condition. Teamwork is therefore of the utmost necessity to diagnose Munchausen syndrome.

Topics: Adult; Diagnosis, Differential; Female; Humans; Kidney Glomerulus; Munchausen Syndrome; Ovalbumin; Proteinuria

The association of allergic diseases and disease activity in systemic lupus erythematosus (SLE, lupus) is controversial. The study investigates lupus activity-related differences in the induction of late allergic rhinitis (LAR) in the female NZB×NZW(B/W)F(1) mouse model for lupus. The LAR, which is induced by ovalbumin, was examined during the preactive (before clinical onset) and active (after clinical onset) phases in mice. Induction of LAR was less severe in mice with active lupus in contrast to clinically healthy lupus mice that developed a more severe allergic rhinitis. Inhibition of the development of LAR may be due to reduced eosinophilia and local interleukin-4 secretion during active autoimmune disease. In addition, systemic interferon-γ, but not IL-4, production increased during the active phase, but not the preactive phase. This suggests that the predominating Th1 lineage commitment in mice with active lupus may be responsible for the inhibition of the allergic Th2 response. The present study may shed some light on the controversy of the prevalence of allergic diseases in SLE patients.

Topics: Animals; Antibodies, Antinuclear; Blood Urea Nitrogen; Creatinine; Eosinophilia; Eosinophils; Female; Inflammation; Interferon-gamma; Interleukin-4; Leukocytes; Lupus Erythematosus, Systemic; Lymphocyte Count; Mice; Mice, Inbred BALB C; Mice, Inbred NZB; Nasal Lavage Fluid; Neutrophils; Ovalbumin; Proteinuria; Rhinitis, Allergic; Rhinitis, Allergic, Perennial; Spleen; Th1 Cells; Th2 Cells

To investigate, whether T lymphocytes alone are sufficient to induce glomerulonephritis, a model in SCID mice was developed. Conditions for the generation and exclusive glomerular targeting of crosslinked ovalbumin (OVA) polymers and a series of OVA-specific T-cell clones and lines were established. Only a well-defined subfraction of OVA polymers exclusively targeted to the glomerular mesangium without causing local alteration in the absence of IgG. From numerous T-cell preparations spanning different Th-1/-2 profiles one T-helper cell clone characterized by ELISPOT assay as pure Th-1 (IFN-gamma and IL-2) induced nephritislike pathology. Histological examination at days 1, 2, 5, and 21 showed major infiltrates in proximal tubular regions (PTR) at day 5 accompanied by significant proteinuria. No injury was observed after deposition of irrelevant antigen or injection of other T-cell preparations. Detailed histological analysis revealed that Th-1 cell numbers peaked early in glomeruli (2.1 +/- 0.6 vs 0/gcs). Macrophages, however, were hardly detectable in glomeruli (0.5 +/- 0.3/gcs) at this time, while they formed the major constituent of the PTR infiltrates at day 5 (83 +/- 1). These data in a new SCID nephritis model indicate that memory Th-1 cells together with localized antigen presenting cells trigger nephritis.

Topics: Adoptive Transfer; Animals; Antigens; CD4-Positive T-Lymphocytes; Disease Models, Animal; Female; Glomerular Mesangium; Glomerulonephritis; Immunologic Memory; Kidney Glomerulus; Kidney Tubules, Proximal; Macrophages; Mice; Mice, Inbred BALB C; Mice, SCID; Ovalbumin; Proteinuria; Th1 Cells; Time Factors

Treatment with cyclosporin A (CsA) improves proteinuria and reduces renal cellular infiltration in chronic serum sickness (CSS). We examined if these effects were associated with a reduced renal expression of CD54 and its ligands, interferon-gamma (IFN-gamma), tumour necrosis factor-alpha (TNF-alpha) and MHC class II molecules. We studied two groups of rats in which CSS was induced by daily injections of ovalbumin (OVA): a group treated with CsA (OVA.CsA group, n = 11) and a group that received no treatment (OVA.CSS group, n = 11). An additional group of five rats (control group) received only phosphate buffer. Immunostaining techniques were used to follow CSS and to study the expression of CD54, CD18, CD11b/c, IFN-gamma, TNF-alpha and MHC class molecules. Proteinuria (mg/24 h) was reduced from 248.2 +/- 73.1 (OVA.CCS group) to 14.5 +/- 13.1 with CsA treatment (P < 0.0001). The renal expression of CD54 and its ligands (CD18 and CD11b/c) was reduced by 50% to 75%. Correspondingly, there was a 60% to 85% reduction in the number of infiltrating leucocytes. The number of cells expressing TNF-alpha, IFN-gamma and MHC II molecules was also reduced. CsA reduces expression of CD54 and its ligands. This effect is associated with a reduction of cellular infiltration, IFN-gamma, TNF-alpha-producing cells and with MHC II expression in the kidney. These findings suggest that expression of adhesion molecules plays a critical role in CSS and underline the importance of cellular immunity in this experimental model.

Topics: Animals; Cell Adhesion Molecules; Chemotaxis, Leukocyte; Chronic Disease; Creatinine; Cyclosporine; Disease Models, Animal; Gene Expression Regulation; Histocompatibility Antigens; Immune Complex Diseases; Immunization; Immunosuppressive Agents; Intercellular Adhesion Molecule-1; Interferon-gamma; Kidney; Kidney Glomerulus; Male; Microscopy, Fluorescence; Nephritis; Ovalbumin; Proteinuria; Rats; Rats, Sprague-Dawley; Serum Sickness; T-Lymphocytes; Tumor Necrosis Factor-alpha

Differential glomerular permeability to macromolecules as a function of their size (size permselectivity) is altered in experimental models of proteinuric renal disease. Size permselectivity during protein overload proteinuria was examined using urinary clearances of neutral dextrans in anesthetized Wistar-Furth rats. The animals were studied 3-4 h after the last of six twice-a-day intraperitoneal injections of either bovine serum albumin (BSA) or ovalbumin (OA) or of vehicle alone (controls). Glomerular filtration rates did not differ significantly among the three groups. OA-treated (n = 4) and control (n = 5) rats had virtually identical fractional dextran clearances over almost the entire molecular size range from 18 to 58 A Stokes-Einstein radius. In contrast, BSA-treated rats (n = 5) had elevated fractional clearances for medium-sized dextrans with the increases reaching statistical significance at radii of 40 A (+22.7% vs. control) and 44 A (+20.4%). Fractional clearances for BSA-treated rats returned to control values for larger dextrans. These findings demonstrate a significant size permselectivity defect in BSA overload, although not in OA overload.

Topics: Animals; Circadian Rhythm; Dextrans; Kidney Glomerulus; Male; Ovalbumin; Permeability; Plasma Volume; Proteinuria; Rats; Rats, Inbred WF; Serum Albumin

The effects of hyperfiltration induced due to unilateral nephrectomy on immunologically induced glomerular injuries were studied. Glomerulonephritis was induced in rats by sensitizing them with egg albumin as an antigen. Unilateral nephrectomy did not affect the removal rate of the antigen from the glomeruli in the rats, but accelerated the rate of the glomerular injuries after cessation of the immunologically induced glomerular inflammation. The histopathological features were characterized by sclero-adhesive lesions with aneurysmal dilatation and hyalinosis of the glomerular capillaries. The parietal epithelial cells extended from the Bowman's capsule with matrices to cover the denuded basement membrane and formed adhesions. The neighboring capillaries collapsed, and the sclero-adhesive lesions progressed. These findings indicate that hyperfiltration at the capillary level did not accelerate the recovery from glomerulonephritis, but induced glomerular sclerosis with adhesions and deteriorated the trivial glomerular injuries to produce similar focal segmental lesions.

Topics: Animals; Complement C3; Glomerular Filtration Rate; Glomerulonephritis; Immunoglobulin G; Immunohistochemistry; Kidney Glomerulus; Male; Microscopy, Electron; Microscopy, Immunoelectron; Nephrectomy; Ovalbumin; Proteinuria; Rats; Serum Sickness

Topics: Animals; Female; Kidney Glomerulus; Ovalbumin; Proteinuria; Rats; Serum Albumin, Bovine

The intraperitoneal injection of 1 g of bovine serum albumin daily for 5 days was shown by electron-microscope morphometry to cause swelling of the glomerular epithelial cells and very severe loss of foot processes. However, these changes were found in only 70 per cent. of glomeruli and the other 30 per cent. remained normal. After 7 days' recovery following five daily injections of 1 g of bovine serum albumin, the swelling of the glomerular epithelial cells had subsided and the foot process reappeared. These changes were accompanied by severe proteinuria which resolved only slowly when the injections were stopped. After daily injections of 0-8 g of egg albumin for 5 days there was no swelling of the glomerular epithelial cells and only very slight loss of foot processes detectable only by morphometry. There was a less severe proteinuria than after injections of bovine serum albumin and it resolved more rapidly when injections were stopped. It is suggested that these differences arise from the fact that bovine serum albumin is reabsorbed by the glomerular epithelial cell but egg albumin is not. Two of four rats allowed to recover for 7 days after five daily injections of 1 g of bovine serum albumin had unusual glomerular lesions.

Topics: Animals; Female; Kidney Glomerulus; Ovalbumin; Proteinuria; Rats; Serum Albumin, Bovine; Time Factors

Normal rats were injected with guinea pig anti-rat glomerular basement membrane antibodies of the IgG1 or IgG2 class or with their F (ab') 2 fragments, in order to study which antibody site triggers the alternate complement pathway in vivo. Both IgG classes were able to induce a heavy proteinuria and led to C3 deposition in the glomeruli in a pattern similar to their own distribution along the glomerular basement membrane, as shown by the immunofluorescence technique. The Fab(ab')2 fragment of IgG2 did not produce C3 binding or proteinuria. The F(ab')2 fragment of IgG1 was difficult to obtain devoid of Fc determinants. A F(ab')2 fragment of IgG1 still bearing Fc determinants led to C3 binding and proteinuria, whereas the true F(ab')2 fragment of IgG1 had none of these effects in two out of three animals.

Topics: Animals; Antibodies; Basement Membrane; Complement C3; Complement System Proteins; Epitopes; Fluorescent Antibody Technique; Goats; Guinea Pigs; Hemolysis; Immune Sera; Immunoglobulin Fab Fragments; Immunoglobulin Fc Fragments; Immunoglobulin G; Kidney Glomerulus; Male; Ovalbumin; Proteinuria; Rabbits; Rats; Ultrafiltration; Zymosan

Topics: Animals; Antigen-Antibody Complex; Basement Membrane; Binding Sites, Antibody; Complement System Proteins; Female; Glomerulonephritis; Immunization; Immunoglobulin G; Iodine Isotopes; Kidney Glomerulus; Male; Microscopy, Electron; Ovalbumin; Proteinuria; Rabbits

Topics: Albuminuria; Bence Jones Protein; Blood Proteins; Chromatography, Gel; Electrophoresis, Disc; Fructose-Bisphosphate Aldolase; gamma-Globulins; Humans; Kidney Diseases; Kidney Glomerulus; Kidney Tubules; L-Lactate Dehydrogenase; Methods; Molecular Weight; Muramidase; Ovalbumin; Pepsin A; Protein Binding; Proteinuria; Sodium Dodecyl Sulfate

Topics: Animals; Antibody Formation; Arteritis; Cattle; Complement Fixation Tests; Egg White; Histones; Hydrogen-Ion Concentration; Lung; Muramidase; Nitrogen; Ovalbumin; Pancreas; Precipitin Tests; Proteinuria; Pulmonary Artery; Rabbits; Ribonucleases; Serum Albumin; Thymus Gland

Topics: Fibrinolysis; Fibrinolytic Agents; Humans; Male; Molecular Weight; Myoglobin; Ovalbumin; Plasminogen; Proteinuria; Serum Albumin

Topics: Chromatography, Gel; Chymotrypsin; gamma-Globulins; Humans; Molecular Weight; Myoglobin; Ovalbumin; Proteinuria; Serum Albumin; Ultracentrifugation; Urine

Topics: Animals; Antigen-Antibody Reactions; Complement System Proteins; gamma-Globulins; Glomerulonephritis; Kidney; Metabolism; Nephritis; Ovalbumin; Pepsin A; Proteinuria; Rabbits; Rats; Research; Tissue Extracts