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)

Canine transitional cell carcinoma (TCC) carries a poor prognosis in part due to late disease detection. The measurement of specific tumor markers shed in the urine may aid in sensitive, early disease detection and therefore improved prognosis. A 1-year prospective clinical trial was designed to assess the efficacy, sensitivity and specificity of the first generation Bard BTA test to diagnose TCC in dogs. This test is a qualitative, rapid, latex agglutination, dipstick test run on voided urine, which measures a glycoprotein antigen complex associated with bladder cancer in human patients. Sixty-five dogs were entered in the study: 20 TCC confirmed patients, 19 healthy controls and 26 urologic controls with a variety of conditions including urinary tract infection, crystalluria and proteinuria. Overall test sensitivity was 90% and specificity was 78%. False positive test results were noted in the presence of significant glucosuria (4+), proteinuria (4+), and pyuria or hematuria (> 30-40 WBC or RBC per hpf). Urine parameters that had no effect on efficacy included collection method (cystocentesis or free catch), pH, specific gravity, crystalluria, bilirubinuria, bacteriuria and casts. These data indicated that the Bard BTA test was sensitive for the detection of the bladder tumor-associated antigen complex in canine TCC. As evaluated, this test may serve as a useful adjunct to diagnosis, especially when cytology or biopsy is questionable or impractical. Furthermore, because of the high sensitivity of the test, it may be a practical screening test to rule out TCC in geriatric patients or patients with clinical signs related to the lower urinary tract, particularly before pyuria and hematuria develop which may interfere with test results.
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PMID:Detection of canine transitional cell carcinoma using a bladder tumor antigen urine dipstick test. 1207 35

Transforming growth factor (TGF)-beta1 is important in fibrogenesis and has been involved in the pathogenesis of chronic allograft nephropathy (CAN). The angiotensinogen (AGT) gene encodes the only glycoprotein known to be a precursor of the vasopressor angiotensin II. Angiotensin II is also a growth factor and a profibrogenic cytokine. It mediates the induction of TGF-beta1. We studied the relationship among the intragraft expression of AGT, TGF-beta1, and CAN in stable renal transplant patients (RTP). We used a competitive quantitative reverse transcriptase-polymerase chain reaction (RT-PCR)-ELISA assay to identify intragraft amounts of AGT expression in RTP and correlated it with TGF-beta1 mRNA expression. We studied and performed kidney biopsies on 12 RTP with long-functioning grafts and 6 RTP in the immediate posttransplantation period (7 days) who had acute tubular necrosis as control. Histology was based on Banff working classification criteria. Total RNA was isolated from biopsy specimens. For RT-PCR-ELISA, we created heterologous RNA competitors that coamplified with the same primers as AGT and TGF-beta1. Six of 12 long RTP had proteinuria >1000 mg/24 hr and 6 had proteinuria <1000 mg/24 hr. The differences between Banff grades (P =0.03), AGT, and TGF-beta1 levels by RT-PCR-ELISA were statistically significant between both groups (106.2+/-60.7 vs. 34.1+/-11.9 pg/microg total RNA [P =0.01] and 5954+/-5612 vs. 436+/-517 transcripts/microg total RNA [P =0.01], respectively). The control group showed AGT levels of 25+/-12.2 pg/microg total RNA and TGF-beta1 levels of 228+/-111 transcripts/microg total RNA, significant only for the higher proteinuria group (P=0.01 and P=0.04, respectively). There was a correlation between AGT and TGF-beta1 in both groups (r=0.96, P=0.001). We showed a relationship between mRNA expression of AGT and TGF-beta1 in kidney transplant patients with different grades of CAN and proteinuria.
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PMID:Intragraft messenger RNA expression of angiotensinogen: relationship with transforming growth factor beta-1 and chronic allograft nephropathy in kidney transplant patients. 1235 92

Thrombin Activatable Fibrinolysis Inhibitor (TAFI) is a relatively recently described glycoprotein (MM 55 KDa) that can be converted into its active form by the thrombin/thrombomodulin complex and potentially inhibits fibrinolysis. Since it represents a link between coagulation and fibrinolysis, TAFI can be expected to play a part in various clinical conditions associated with a thrombotic tendency. Preeclampsia (PE) and intrauterine fetal growth retardation (IUFGR) are fairly common complications of pregnancy that are characterized by hemostatic abnormalities. TAFI antigen and its influence on hemostasis was investigated in 46 women with PE and/or IUFGR and in 16 normal pregnancies. We found a significant decrease of TAFI antigen in the patient group. Using the recently described method Overall Hemostatic Potential (OHP) in plasma we measured clot lysis time (CLT) and overall fibrinolytic potential (OFP). We found that CLT is prolonged and OFP decreased in patients with PE and/or IUFGR. Since OFP did not increase after addition of the specific inhibitor of TAFI (potato tuber carboxypeptidase inhibitor), it seems that TAFI does not contribute to the impairment of fibrinolysis in these patients. Since serum albumin was decreased together with presence of proteinuria and aminotransferases were increased in the patients, it seems that one explanation for the decrease in TAFI could be reduced hepatic synthesis and an increased loss in urine. It an be speculated that this mechanism can prevent more serious thrombotic complications in patients with PE and/or IUFGR.
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PMID:Does thrombin activatable fibrinolysis inhibitor (TAFI) contribute to impairment of fibrinolysis in patients with preeclampsia and/or intrauterine fetal growth retardation? 1236 37

Normal mammals generally excrete only small amounts of protein in the urine, thus avoiding major leakage of proteins from the body. Proteinuria is the most commonly recognized abnormality in renal disease. However, healthy domestic cats ( Felis catus ) excrete proteins at high concentrations (about 0.5 mg/ml) in their urine. We investigated the possible cause of proteinuria in healthy cats, and discovered a 70 kDa glycoprotein, which was excreted as a major urinary protein in cat urine, irrespective of gender. To elucidate the biochemical functions and the excretion mechanism of this protein, we cloned the cDNA for this protein from a cat kidney cDNA library. The deduced amino acid sequence shared 47% identity with the rat liver carboxylesterase (EC 3.1.1.1), and both the serine hydrolase active site and the carboxylesterase-specific sequence were conserved. Therefore we named this protein cauxin (carboxylesterase-like urinary excreted protein). In contrast to the mammalian carboxylesterases, most of which are localized within the cells of various organs, cauxin was expressed specifically in the epithelial cells of the distal tubules, and was secreted efficiently into the urine, probably because it lacked the endoplasmic reticulum retention sequence (HDEL). Based on our finding that cauxin is not expressed in the immature cat kidney, we conclude that cauxin is involved in physiological functions that are specific for mature cats. Recently, cauxin-like cDNAs were found from human brain and teratocarcinoma cells. These data suggest that cauxin and cauxin-like human proteins are categorized as a novel group of carboxylesterase multigene family.
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PMID:Molecular cloning and characterization of a novel carboxylesterase-like protein that is physiologically present at high concentrations in the urine of domestic cats (Felis catus). 1240 Nov 31

Fibronectin, a large adhesive glycoprotein, is a prominent constituent of the extracellular matrix. Abnormalities in fibronectin homeostasis occur in numerous disease states, ranging from primary fibrosing conditions to neoplastic transformation. We demonstrate that fibronectin is a target protein substrate for ubiquitin-dependent degradation. Coimmunoprecipitation experiments and confocal microscopy demonstrated ubiquitin-fibronectin interaction. In an in vitro model of renal fibrosis, relaxin, an insulin-like growth factor, increased ubiquitin-dependent fibronectin degradation. Relaxin also was evaluated in an anti-glomerular basement membrane model of renal fibrosis. Animals treated with relaxin experienced renoprotection, manifested by decreased serum creatinine and proteinuria. Histological evaluation of kidney sections from animals treated with relaxin showed decreased glomerulosclerosis and interstitial fibrosis. We conclude that relaxin might be developed as a useful agent for the treatment of renal fibrosis.
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PMID:Relaxin increases ubiquitin-dependent degradation of fibronectin in vitro and ameliorates renal fibrosis in vivo. 1282 Jun 41

Hashimoto's thyroiditis and membranous nephropathy are believed to be mediated by immune mechanisms. A 12 year-old patient is reported who presented with fatigue, dislike of cold, pallor and growth retardation. Initial laboratory assessment showed moderate proteinuria and impaired renal function (serum creatinine 2.3 mg/dl), and hypothyroidism due to autoimmune thyroiditis. Light, immunofluorescence and electron microscopy of the renal biopsy showed membranous nephropathy. The patient recovered from nephropathy after substitution of thyroid hormone and therapy with prednisone. Megalin can be envisaged as a potential pathogenetic link between the two disease entities. The glycoprotein megalin is expressed on thyroid cells in a TSH-dependent manner and may have a crucial role in the immunopathogenesis of glomerular injury in membranous nephropathy. For similar cases, we want to encourage colleagues to consider this hypothesis and to examine blood and renal biopsy specimens for the presence of megalin and antibodies against it.
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PMID:Autoimmune thyroiditis in association with membranous nephropathy. 1496 28

Tamm-Horsfall (TH) is a large glycoprotein which originates in the kidney and is very abundant in the urine. This protein has been measured mainly by immunoassays. Here we describe a different approach for its measurement based on high-performance liquid chromatography (HPLC) using a molecular exclusion column with native fluorescence detection in the ultraviolet range. This method in addition to measuring the level of the protein has the advantage of detecting changes in size or aggregation. Urine, 1 ml was mixed with 100 microl of 30% NaCl and left at 37 degrees C for 30 min. The urine was centrifuged at 12000 rpm for 20 s. The precipitate was vortex-mixed and dissolved in a triethanolamine buffer. A 20 microl aliquot was injected on a Macrosphere GPC column which was eluted with phosphate buffer and the effluent was detected by a fluorometer set at 280 nm for excitation and 325 nm for emission. Since the protein has a very large molecular mass compared to other urinary and serum proteins we did not experience any interference. It elutes as the first peak (in approximately 2.5 min on a 500 A and 2.7 min on 1000 A). The protein precipitates rapidly < 60 min at 37 degrees C. The detection in the UV is sensitive for this protein down to 1 mg/l in absence of any concentration steps. The method was linear between 1 and 100 mg/l. The R.S.D. was 10.4% (mean 62, n = 10). The mean level in 42 normal individuals was 31 mg/g creatinine and in 30 patients with proteinuria (different renal disorders) was 23 mg/g creatinine.
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PMID:Analysis of Tamm-Horsfall protein by high-performance liquid chromatography with native fluorescence. 1497 98

All-trans-retinoic acid (ATRA), a vitamin A derivative, was reported to suppress the interleukin-6 (IL-6) production and to downregulate the IL-6 receptor (IL-6R) and/or its signal transducer glycoprotein 130. We investigated the in vivo antinephritic effect of ATRA on IL-6 transgenic mice which had developed mesangial proliferative glomerulonephritis (PGN) as well as its in vitro inhibitory effect on the proliferation of rat mesangial cells. In vivo experiments on IL-6 transgenic mice showed that ATRA administration suppressed proteinuria and hematuria and reduced the IL-6 concentrations; furthermore, histological examination demonstrated that it improved PGN. In vitro experiments using rat mesangial cells demonstrated that ATRA inhibited cell growth in a dose-dependent manner within a range from 10(-4) to 10(-6) M. This inhibition by ATRA was partially counteracted by the addition of IL-6. RT-PCR assay results showed that ATRA also reduced IL-6R, but not the glycoprotein 130 expression in mesangial cells. These findings indicate that, by blocking of the IL-6 function, ATRA may be therapeutically effective in PGN.
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PMID:All-trans-retinoic acid inhibits the development of mesangial proliferative glomerulonephritis in interleukin-6 transgenic mice. 1579 17

Acquired deficiency of anticoagulant proteins, due to loss in the urine, has been proposed as one of the major thrombogenic alterations in nephrotic syndrome (NS). Protein Z (PZ) is a single-chain vitamin K-dependent glycoprotein. Low PZ levels are reported to be a risk factor for thrombosis. The aim of this study was to investigate protein Z and other natural anticoagulant levels in children with NS. Thirty children aged between 1.5 and 12 years with NS (Groups I and II) and 19 age-and-sex-matched healthy controls (Group III) were enrolled into the study. Patients were divided into two groups: Group I (proteinuria >40 mg/m2/hr) and Group II (patients in remission). Plasma PZ levels in Group I were significantly lower than Group II (p=0.009) and group III (p=0.018). Plasma levels of AT III for Group I were significantly lower than for Groups II and III (p=0.009, p=0.005, respectively). Protein C levels in Group I were higher than in Group II and Group III (p=0.002, p=0.000, respectively). Protein Z levels positively correlated with serum total protein and albumin levels (p=0.003, p=0.003, respectively) and negatively with the degree of proteinuria (p=0.000). Protein Z levels were positively correlated with AT III (r=0.037, p=0.04). Along with the other coagulation abnormalities, decreased protein Z may contribute to increased risk of thromboembolic complications in children with NS. The negative correlation between proteinuria and PZ level suggests the possibility of renal PZ loss. Further studies are needed to investigate the mechanism and role of decreased PZ in NS.
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PMID:Low protein Z levels in children with nephrotic syndrome. 1681 May 11

The normal values for orosomucoid and the alpha(1) acid glycoprotein of Schultze in young adults are reported, specifically estimated by an immunological technique. The use of purified orosomucoid as a standard allowed of absolute estimation of this protein. The alpha(1) acid glycoprotein is estimated relative to a standard normal serum. These proteins were estimated in the serum of eight patients after surgery. Both proteins rise markedly in the serum, the alpha(1) acid glycoprotein reaching peak concentration in two to three days, and falling again equally rapidly, the orosomucoid rising more slowly to reach a peak after four to seven days, and returning to normal values in 10 to 14 days. Estimations of serum levels in 24 patients with a variety of diseases show that the two proteins can vary independently; values as high as eight times normal were found for orosomucoid in Crohn's disease. In patients with proteinuria, orosomucoid is preferentially excreted in the urine. The losses of alpha(1) acid glycoprotein are, however, anomalous, being proportionately less than those of albumin, relative to the serum levels. The significance of these preliminary findings is discussed.
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PMID:The estimation of two alpha(1) glycoproteins (orosomucoid and another alpha(1) acid glycoprotein) in health and disease. 1681 Sep 92


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