Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The concentration of alpha 2HS-glycoprotein (alpha 2HS-GP), as measured by the single radial immunodiffusion technique in the sera of 52 patients with various renal diseases and varying degrees of proteinuria, was found to be significantly reduced (P less than 0.001) when compared to the control values. Out of the 52 patients examined, 34 were found to excrete alpha 2HS-GP in urine with no correlation between the serum and urine levels of this protein. Although there is a statistically significant correlation between the clearances of albumin and alpha 2HS-GP, in only six patients were the clearances of alpha 2HS-GP within +/- 25% of albumin clearance. Twelve had higher, and 16 had lower, relative clearances of alpha 2HS-GP. The relative clearance of alpha 2HS-GP had no relation to the serum levels of alpha 2HS-GP, but correlated with the degree of proteinuria and the type of histological lesion in the kidney. In conclusion, there is a quantitative reduction of serum alpha 2HS-GP in patients with renal diseases. It appears that the degree of proteinuria and the type of renal lesion influences its selective handling by the kidneys.
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PMID:Alpha 2HS-glycoprotein in the serum and urine of patients with renal diseases. 687 1

Antibodies against laminin, which is a defined glycoprotein of basement membranes, were produced in sheep and affinity purified by immunoadsorption on laminin-Sepharose (S alpha L). When injected intravenously into rats, S alpha L rapidly bound in a linear pattern to the glomerular basement membrane (GBM) in the peripheral and mesangial regions of all glomeruli, and, when greater than 0.5 mg S alpha L was injected, to some tubular BM as well. 1-2 h after the injection of conjugates of horseradish peroxidase (HRP) and S alpha L, HRP reaction product was present throughout the full thickness of the GBM and mesangial matrix. [125I]S alpha L binding to the kidney in vivo increased linearly over the dose range of 40-950 micrograms of IgG and accounted for approximately 2% of the injected dose/g kidney. When 4 mg of [125I]S alpha L was injected, 1.5% or 62 micrograms/g kidney was bound. Proteinuria did not develop within 7 wk of injection in rats that received 0.5-1.6 mg of S alpha L. In contrast, all animals that received injections of 4 mg of S alpha L gradually became proteinuric within 3-6 wk. Thickening, reduplication, and flocculent subendothelial deposits were observed in the GBM of these animals. In addition, mononuclear cells adhered to the GBM and infiltrated beneath the endothelium. However, the deposition of rat C3 was infrequently observed, and rat IgG was not seen in the glomeruli of any rat that received S alpha L. 10 wk after injection, much greater amounts of S alpha L appeared within the mesangium than the peripheral GBM. These results demonstrate that the interaction of S alpha L with the GBM, possibly in concert with infiltrating mononuclear cells, gradually altered the structure and permeability characteristics of the glomerulus independent of a host anti-S alpha L humoral response.
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PMID:Proteinuria and structural alterations in rat glomerular basement membranes induced by intravenously injected anti-laminin immunoglobulin G. 708 53

Diabetic glomerulosclerosis in man and in all spontaneous-onset and chemically induced diabetes in experimental models is characterized by diffuse increase in mesangial matrix and glomerular basement membrane thickening. The most prominent features of the biochemical changes in the glomerular basement membrane are increase in the collagen-like components, decreased sialic acid, and increased glucosylation. However, the heterogeneity of the various glycoprotein components of the glomerular basement membrane and related components of the mesangium make comparative biochemistry difficult. Increased glomerular blood flow with no apparent alterations in the glomerular filtration coefficient in diabetes may be attributed to altered vascular control mechanisms which may include both hormonal mediation as well as changes in end-organ responsiveness. Although proteinuria is a common manifestation of diabetic involvement of the glomerulus, there is little biochemical or physiologic evidence as to the specific causes of increased glomerular filtration apparatus permeability. Further information as to the pathogenesis of diabetic vascular disease of the kidney and the ability to reverse pathologic changes by correction of the metabolic milieu will require analysis of carefully selected animal models. Particular care in experimental design must include the ability to integrate pathology, physiology, and biochemistry in each model in order to relate the information to human renal diabetic complications.
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PMID:Kidney complications. 716 May 36

1. Tamm-Horsfall glycoprotein was determined, by radioimmunoassay, in samples of urine from normal individuals under a variety of physiological conditions. 2. The amount of glycoprotein excreted in 24 h by our population (39 +/- 13 mg, corrected for body surface area) was found not to be influenced by sex, age (19-60 years) or amounts of Ca2+, Mg2+ and Na+ excreted. 3. Urine samples collected at 2 h intervals over 24 h from individuals drinking in response to thirst, contained quantities of the glycoprotein which showed high positive correlations with urine volumes, but not with Ca2+, Mg2+ or Na+ excretion. 4. The amounts of urine and of the glycoprotein were correlated for individuals in antidiuresis, induced by restriction of water intake. Relatively small amounts of glycoprotein were excreted by individuals in states of water-induced diuresis. 5. The amounts of glycoprotein excreted after exercise were positively correlated with the small volumes of urine voided, but they were uninfluenced by the degree of proteinuria or of hyaline cast formation. 6. The half-life for turnover of the glycoprotein in a given individual is highly variable, from a minimum of 3-7 to a maximum of 168 h.
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PMID:Factors affecting excretion of human urinary Tamm-Horsfall glycoprotein. 719 48

We assayed plasma activities of beta-galactosidase, beta-hexosaminidase, alpha-fucosidase and alpha-galactosidase involved in degradation of the glycoprotein molecule in 110 insulin-dependent diabetics aged 3-1/2 to 19 years and compared them to a group of normal youngsters. We correlated the plasma enzyme activities with the duration, control and sequelae of insulin-dependent diabetes. Insulin-dependent diabetics had a significantly higher plasma activity of beta-hexosaminidase and alpha-mannosidase (p less than 0.01) and a significantly lower plasma activity of alpha-fucosidase and alpha-galactosidase (p less than 0.01). Of the 5 enzymes studied, only plasma beta-hexosaminidase correlated with fasting and postprandial blood sugar (p less than 0.01), cholesterol and triglycerides (p less than 0.05). Additionally, poor control of diabetes was also associated with a significantly higher plasma beta-hexosaminidase activity (p less than 0.01). Proteinuria or an abnormal Addis count suggestive of renal involvement was associated with various changes in plasma acidic hydrolases. These changes may be related to insulin deficiency rather than hyperglycemia and may be genetically determined.
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PMID:Plasma acidic glycohydrolases in insulin-dependent diabetes mellitus. 730 74

The immune nephritis antibody response against the collagen and glycoprotein portions of the glomerular basement membrane (GBM) has been monitored by using either type IV collagen prepared from pepsin digests or a collagenase digest of GBM. Sheep immunized with GBM, according to Steblay, respond by developing antibodies directed against the collagen and the glycoprotein portions, respectively. Circulating antibodies directed against sheep GBM structures were not demonstrated until overt clinical disease with high serum creatinine values and proteinuria. Such antibodies could, however, be eluted from the kidneys, where they adsorbed in a linear fashion as demonstrated by immunofluorescence microscopy. In spontaneous human nephritis in Goodpasture's syndrome, circulating antibodies were present at the time of diagnosis. These antibodies reacted only with the glycoprotein portion of the basement membrane, and not with the type IV collagen.
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PMID:Different antibody response in experimental and spontaneous glomerulonephritis. 732 28

Heymann nephritis developed in rats immunized with brush border membrane fractions isolated from rat kidney tubules. Glomerular autoantibodies eluted from cryostat sections of nephritic kidneys reacted in immunoelectron microscopy with the outer surface of isolated brush border membrane vesicles. This indicates that the autoantigens are plasma membrane components. To characterize further the chemical nature of the nephritogenic autoantigens, we treated the brush border membranes with trypsin and sodium deoxycholate, and the solubilized membranes were then fractionated by lectin affinity chromatography. The polypeptide composition of the fractions was analyzed by polyacrylamide gel electrophoresis in the presence of sodium dodecyl sulfate. The capacity of the membrane fractions to induce Heymann nephritis was assessed by observing the development of typical renal lesions, antibrush border autoantibodies, and proteinuria in rats immunized with these fractions. The results suggest that the nephritogenic autoantigen is an integral component of the brush border membrane of kidney proximal tubules and has an affinity for Lens culinaris agglutinin. This indicates that it is a glycoprotein and has mannosyl and/or glycosyl groups exposed in its oligosaccharide side chains.
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PMID:Heymann nephritis induced by kidney brush border glycoproteins. 744 31

Antiphospholipid antibodies (aPL) are associated with thrombosis, thrombocytopenia and recurrent fetal loss in humans and in some animal models. Immunization with beta 2 glycoprotein I (beta 2GPI) induced aPL production in normal rabbits and mice. However, the association of these antibodies with disease manifestations remains controversial. To determine whether induction of aPL by beta 2GPI immunization in an autoimmune strain of mice (MRL/++) would result in acceleration of clinical and serological autoimmune disease manifestations, three groups of 8-week-old female mice were studied. One group was immunized with beta 2GPI, and one with ovalbumin (OVA); the third was not immunized. After two booster injections, sera were analysed for the presence of anticardiolipin (aCL) and anti-DNA by ELISA and anti-nuclear antibody (ANA) by immunofluorescence. Mice were studied for thrombocytopenia, proteinuria, fecundity rates, litter sizes and the development of central nervous system dysfunction. Elevated levels of aCL, anti-DNA and ANA were detected in all beta 2GPI-immunized, in three OVA-immunized, and in none of the unimmunized mice. The anti-DNA antibodies were inhibited by CL micelles, suggesting cross-reactivity between aCL and anti-DNA. Platelet counts, fecundity rates and litter size were reduced in beta 2GPI-immunized but not in OVA-immunized or unimmunized mice. None of the mice developed neurological dysfunction or significant proteinuria over a 10-week period post-immunization. These findings suggest that beta 2GPI immunization induces aPL in MRL/++ mice associated with accelerated autoimmune manifestations resembling the antiphospholipid syndrome.
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PMID:Early onset of autoimmunity in MRL/++ mice following immunization with beta 2 glycoprotein I. 762 96

The immunoconjugate XMMCO-791/RTA consists of ricin A chain bound to a murine monoclonal antibody MoAb 791T. This monoclonal antibody (MoAb) binds to a glycoprotein of 72 kD, which is expressed on human colorectal carcinoma, ovarian carcinoma, and osteogenic sarcoma. XMMCO-791/RTA was tested in a Phase I trial with proposed dose escalation steps of 0.02, 0.04, 0.15, and 0.2 mg/kg per day. Twelve patients with metastatic colorectal carcinoma were treated at 0.02, 0.03, and 0.04 mg/kg per day dose levels administered over 1 hour on days 1-5. Study-related toxicities were hypotension (6 patients); greater than 10% weight gain (6 patients); peripheral edema (9 patients); fever (4 patients); confusion (3 patients); diarrhea (3 patients); proteinuria, as identified by dipstick (3 patients), greater than 0.6 mg/dl decrease in serum albumin (11 patients); greater than 25% decrease in oncotic pressure (10 patients), and a decrease in ionized calcium (8 patients). Six patients received a second course of treatment. HAMA levels developed in 9 patients and titers increased with number of courses administered. Decreased overall toxicity, in comparison to the first course, was noted, but one patient had an allergic-type response (hypotension, crushing chest pain, diaphoresis) after the test dose of the second course (HAMA level > 10,000 IgG). Life-threatening toxicity in the form of fluid shift, resulting in noncardiac pulmonary edema and third-spacing occurred after course 1 in 1 of 3 patients at the 0.04 mg/kg per day level. No further dose escalation was attempted and no antitumor activity was seen.
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PMID:Phase I study of monoclonal antibody-ricin A chain immunoconjugate Xomazyme-791 in patients with metastatic colon cancer. 762 72

A series of recent observations have shown raised levels of plasma fibronectin (FN), an alpha 2-glycoprotein produced by vascular endothelia, in diabetic patients with retinopathy and overt nephropathy. However, there are no available data on urinary FN and behavior of its excretion in patients affected by diabetic nephropathy characterized by the presence of microalbuminuria. The main purpose of the present study was to investigate whether the urinary excretion of FN (U-FN) is associated with early diabetic nephropathy and other diabetic complications. Fifty-nine diabetic inpatients classified as type II and 15 age-matched control subjects were included in this study. The amount of U-FN, assessed as microgram/g creatinine/24 h, was significantly greater in the patients as a group (348.1 +/- 48.3), than in the controls (108.6 +/- 22.7, p < 0.01). Although patients with overt proteinuria showed an extremely high level of U-FN (1080.5 +/- 184.0; range 216.1 +/- 1726.8), mean U-FN tended to be higher in the group with microalbuminuria (262.4 +/- 21.9; range 101.9-591.9) than in the group without it (188.1 +/- 34.3; range 19.4 +/- 582.4, p < 0.08). In patients who did not have retinopathy and neuropathy, the U-FN was significantly higher in the group with microalbuminuria (222.5 +/- 28.5) than in the group without it (116.1 +/- 22.6, p < 0.01). A highly significant negative correlation existed between endogenous creatinine clearance values and the amounts of U-FN in the patients (r = -0.642, p < 0.01), while there was no such relationship in the controls (r = 0.167, p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Increased urinary fibronectin excretion in type II diabetic patients with microalbuminuria. 766 99


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