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)

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

S-(1,2-dichlorovinyl)-L-cysteine (DCVC)-induced nephrotoxicity in vivo was investigated in New Zealand White rabbits. A primary emphasis in these studies was further characterization of DCVC-induced nephrotoxicity using a variety of serum and urinary analytes, including sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). Additionally, the role of oxidative injury was assessed to address the dichotomy between reports indicating that such a mechanism is important in vivo and those indicating that such mechanisms do not contribute substantially to the mechanism of effects observed in vitro. Urine was collected prior to and at 8 and 24 hr after iv administration of DCVC. Serum was collected 15 min prior to and 24 hr after DCVC administration. Rabbits were euthanized 24 hr post-DCVC administration, and kidneys were fixed in formalin and further processed for light microscopic examination. DCVC (10 mg/kg, iv) induced a 45-50-fold increase in total urinary protein excretion, a 10-15-fold increase in urinary N-acetyl-beta-D-glucosaminidase concentration, plus a marked glucosuria by 24 hr postadministration. Additionally, DCVC increased serum creatinine levels by about 2-fold, with a trend toward increased blood urea nitrogen. SDS-PAGE analysis of rabbit urine confirmed the clinical finding of marked proteinuria in DCVC-treated animals, which in contrast to previously reported data was due to the presence of both low and high molecular weight proteins. Antioxidants had no significant effect on DCVC-dependent renal injury, nor was there evidence for DCVC-induced lipid peroxidation, as measured by either thiobarbituric acid-reactive substances or a commercial assay for malondialdehyde and hydroxalkenals.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:S-(1,2-dichlorovinyl)-L-cysteine-induced nephrotoxicity in the New Zealand white rabbit: characterization of proteinuria and examination of the potential role of oxidative injury. 750 60

To characterize the defect in glomerular permselectivity responsible for proteinuria after renal transplantation, we studied 10 patients with moderate proteinuria (median 0.37 g/d, range 0.20-0.79), 16 patients with the nephrotic syndrome (6.73 g/d, 3.9-14.6), 8 living related donor transplant recipients without any history of rejection (median proteinuria 0.26 g/d, 0.06-0.58), and 12 healthy volunteers. The fractional clearance of neutral dextrans > 54 A was significantly higher in nephrotic patients, demonstrating a defect in glomerular size selectivity. Using a log-normal model of glomerular pore size distribution, r*(5%) and r*(1%), indices for the presence of large pores, were increased in the nephrotic patients. The fractional clearance of negatively charged dextran sulfate was significantly higher in all patient groups, indicating a loss of glomerular charge selectivity. Biopsy findings showed more prominent glomerular lesions in the nephrotic group compared with the moderately proteinuric group. We conclude that mild proteinuria late after renal transplantation is associated with a defect in glomerular charge selectivity. The development of nephrotic range proteinuria is associated also with a defect of glomerular size selectivity, which correlates with prominent glomerular pathology.
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PMID:Glomerular permselectivity in proteinuric patients after kidney transplantation. 761 91

We have studied the effect of peripheral blood mononuclear cells (PBMC) from renal transplant patients on 35sulfate uptake by rat glomerular basement membrane (GBM). Nine patients were included in the study; six were studied during an episode of acute allograft rejection and seven while not undergoing acute rejection. The sulfate uptake index, calculated as the ratio between uptake by GBM from rat glomeruli cocultured with PBMC and 35sulfate incorporation by GBM from glomeruli cultured alone, was significantly higher when glomeruli were cocultured with PBMC from patients undergoing an acute rejection (3.26 +/- 1.18, mean +/- SEM) than it when glomeruli were cocultured with PBMC from nonrejecting transplant patients not showing proteinuria (0.81 +/- 0.11) (P = 0.0053). After reversing the acute allograft rejection with resolution of proteinuria, the sulfate uptake index returned to normal in four of five patients. The fifth patient had persistent nephrotic syndrome and his sulfate uptake index remained elevated. These findings are similar to those observed in idiopathic minimal lesion nephrotic syndrome patients in relapse. Because the GBM sulfated compounds may play a role in glomerular permeability to plasma proteins, by acting on these compounds PBMC may be a common mechanism for proteinuria.
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PMID:The effect of lymphocytes from renal transplant patients on glomerular basement membrane sulfate uptake. 763 21

This study examined the mechanisms by which angiotensin II (Ang II) receptor blockade improves glomerular barrier function in rats with reduced nephron number. Proteinuria was measured at four weeks after 5/6 renal ablation, and rats were then divided into a group which received the Ang II receptor blocker MK954 and a group which received no treatment. Studies performed one week later showed that Ang II receptor blockade reduced proteinuria without altering GFR in renal ablated rats. Micropuncture studies showed that Ang II blockade reduced both mean arterial pressure (142 +/- 7 mm Hg, ablation without treatment; 105 +/- 2 mm Hg, ablation with treatment) and glomerular transcapillary pressure (54 +/- 3 mm Hg, ablation without treatment; 43 +/- 1 mm Hg, ablation with treatment). Dextran sieving studies showed that untreated rats developed a size-selective defect characterized by increased transglomerular passage of neutral dextrans with radii 54 to 76 A and a charge-selective defect characterized by an increased transglomerular passage of anionic dextran sulfate with a radius of approximately 18 A. Ang II blockade reduced fractional clearance values for large neutral dextrans near to values observed in normal rats but had no effect on the fractional clearance of dextran sulfate (0.68 +/- 0.11, ablation without treatment; 0.66 +/- 0.08, ablation with treatment; 0.46 +/- 0.05, normal rats). These findings indicate that reducing Ang II activity improves size-selectivity without affecting charge-selectivity in injured remnant glomeruli.
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PMID:Effects of angiotensin II receptor blockade on remnant glomerular permselectivity. 768 77

We measured plasma endogenous digitalis-like substances (EDLS), angiotensin II concentrations and plasma renin activity (PRA) by radioimmunoassay in 30 patients with pregnancy-induced hypertension (PIH), 30 normal pregnant women during the third trimester, and 23 non-pregnant women. Compared to the normal pregnant women, the concentration of plasma EDLS was significantly increased in patients with PIH (P < 0.05). There were significant positive correlations among plasma EDLS level, mean arterial pressure (r = 0.615; P < 0.01), the score index of PIH patients (r = 0.818; P < 0.01), hematocrit (r = 0.853; P < 0.01) and uric gravity (r = 0.764; P < 0.01). There was a significant negative correlation between plasma EDLS level and PRA in patients with PIH (r = -0.718; P < 0.01). Severe proteinuria and edema were related to a significant higher plasma EDLS level than the mild in patients with PIH (P < 0.001). After magnesium sulfate was administered in 9 severe patients of PIH, plasma EDLS levels were decreased (P > 0.05). These findings suggest that EDLS may play an important role in the pathogenesis of PIH and severe as an indicator of the severity of PIH. Its secretion may not be influenced after the administration of magnesium sulfate. There may be a close relationship between EDLS and renin-angiotensin system. When the medicine of digitalis type was administered in patients with PIH, the influence of EDLS must be considered to prevent digitalism.
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PMID:[Clinical significance of endogenous digitalis-like substances in patients with pregnancy-induced hypertension]. 795 23

We optimized the electrophoretic separation using sodium dodecyl sulfate-polyacrylamide gel (SDS-PAGE) and silver staining to detect small peptides in serum, without extraction of major proteins and applied this method to the search for specific peptides that may be used as early markers of preeclampsia during pregnancy. Appropriate separation of peptides was possible by modifying several parameters: increasing total proportion of monomers (%T) from 3 to 5% in the stacking gel; decreasing total proportion of crosslinker (%C) from 2.7 to 1.5% in the separating gel; selecting alkaline stacking gel buffer (pH 8.8) and alkaline sample buffer (pH 8.0); adding glycerol to both gels; and processing with weak current (15 mA). Silver nitrate staining was improved by using glutaraldehyde as the fixing agent, by reducing cross-linker concentration and by eliminating oxidizing and reducing agents. Sensitivity of the improved silver nitrate staining was 50 ng. We compared the electrophoretic pattern of serum peptides in the range of 2-14 kDa of 20 preeclamptic women with and without proteinuria and of 25 women in their third trimester who later developed preeclampsia to that of 24 normal pregnant women at term. No differences were found in the electrophoretic patterns among the groups and there was no correlation between the intensity of the bands and the severity of preeclampsia. We conclude that there is no characteristic electrophoretic pattern associated with preeclampsia.
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PMID:Electrophoretic method for separating small peptides in serum without extraction of macromolecules: application to the detection of preeclampsia. 807 74

Puromycin aminonucleoside (PA) and Adriamycin (ADR) cause glomerular proteinuria associated with degenerative alterations of glomerular visceral epithelial cells (GVEC) and detachment from the glomerular basement membrane when administered to rats. This in vitro study was performed to define, in detail, the quantitative and qualitative changes of a number of adhesion-associated proteins (cytoskeletal, extracellular matrix and integrin proteins) upon exposure to PA and ADR. By immunofluorescence we observed: (1) dose- and incubation-time-dependent filament pattern changes and decreased staining of the cytoskeletal proteins actin, vimentin, keratin, and beta-tubulin; (2) an altered distribution, and decreased expression of the extracellular matrix proteins laminin and heparan sulfate and (3) a loss of the beta 1-integrin focal adhesions upon exposure to PA and ADR. Using an ELISA, a concentration-dependent decrease was found (a 50% reduction with 50 micrograms/ml PA for 48 h and with 2 micrograms/ml ADR for 24 h) in the production of cytoskeletal and extracellular matrix proteins per cell. These general effects were suggestive of a disturbance of protein synthesis but, by metabolic labelling studies, no reduction in overall protein synthesis was found. Using two-dimensional PAGE on 35S-methionine steady-state labeled cells, no changes were found in intracellular protein patterns of PA- and ADR-treated cells (pH 5-7.5, MW 110-20 kD). We hypothesize that exposure of GVEC in vitro to PA and ADR might result, directly or indirectly, in perturbation of the macromolecular organization of cytoskeletal and extracellular matrix proteins with loss of GVEC adhesion.
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PMID:Puromycin aminonucleoside and adriamycin disturb cytoskeletal and extracellular matrix protein organization, but not protein synthesis of cultured glomerular epithelial cells. 808 96

Preeclampsia is a major cause of maternal and fetal morbidity and mortality. It remains a management challenge despite recent advances in the understanding of the pathophysiology of this condition and its prevention, and it remains a major cause of maternal and fetal morbidity and mortality. The hallmarks of preeclampsia are proteinuria and edema in a woman who is hypertensive. Current theories suggest altered prostaglandin synthesis, inappropriate sensitivity to angiotensin II and immunologic factors as etiologies of preeclampsia. Low-dose aspirin therapy and high-dose calcium supplementation show promise in preventing preeclampsia and reducing its severity when it occurs. However, aggressive antenatal maternal and fetal assessment, magnesium sulfate therapy and early delivery are the standards of preeclampsia management.
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PMID:Preeclampsia: progress and puzzle. 811 19

Overall, the goal of the emergency physician is proper recognition of the gravid woman whose pregnancy is complicated by hypertensive disease, particularly preeclampsia-eclampsia. As the classic triad of hypertension, proteinuria, and edema does not always occur simultaneously, supporting signs and symptoms as well as laboratory data may be necessary to support the diagnosis. Once the diagnosis is established, drug therapy aimed at the prevention of seizures and emergent control of blood pressure should be instituted to stop progression of the disease. Although many agents are undergoing investigation, magnesium sulfate and hydralazine remain the drugs of choice for anticonvulsant and antihypertensive therapy, respectively. Early consultation with an obstetrician should facilitate timely termination of the pregnancy with the least possible trauma to the mother and infant.
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PMID:Hypertensive disorders of pregnancy. 830 38


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