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)

Dipeptidyl peptidase IV (EC 3.4.14.5) and angiotensinase A (EC 4.4.11.7) were purified to homogeneity from pooled urine concentrate of patients with renal damage, using ultrafiltration, ammonium sulphate precipitation, lectin affinity chromatography, FPLC-ion-exchange(Mono-Q-)chromatography, and FPLC-gel filtration (Superdex). Based on the specific enzyme activity of the starting material, dipeptidyl peptidase IV was enriched 1629 fold, angiotensinase A 1183 fold. The relative molecular masses, Michaelis constants and isoelectric points were determined. Negative staining of the purified enzymes revealed globular proteins (5-7 nm). Antisera raised against dipeptidyl peptidase IV and angiotensinase A reacted specifically with tubular and, in the case of anti-angiotensinase A sera, with tubular and glomerular structures. In addition, urinary membrane vesicles of proximal tubule origin were eluted with the void volume (Superdex-gel filtration), indicating heavy epithelial cell disintegration. Both soluble tissue enzymes (dipeptidyl peptidase IV, angiotensinase A) and vacuolar blebs shed from epithelia contribute to proteinuria, as was shown in patients with glomerulonephritis, interstitial nephritis, diabetic nephropathy and, for angiotensinase A, in patients with essential arterial hypertension.
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PMID:Biochemical and immunological properties of urinary angiotensinase A and dipeptidylaminopeptidase IV. Their use as markers in patients with renal cell injury. 136 94

Enzymuria is a frequent finding in patients suffering from various kidney diseases. The present study was undertaken to evaluate the clinical value of the determination of tubule-brush-border-associated dipeptidyl aminopeptidase IV (DAP IV) in the urine of patients with acute and chronic tubulointerstitial nephritis (n = 12), chronic glomerulonephritis (n = 15), essential arterial hypertension (n = 30), after kidney transplantation (n = 20), and of healthy control persons (n = 68). DAP IV was measured in spontaneously voided mid-stream morning urine ("second morning urine"), and was expressed as enzyme activity in units/liter. In order to account for variations due to urine concentration without collecting 24-hour specimens, a urinary DAP IV/creatinine ratio (DCR) was calculated. Furthermore, patterns of proteinuria were assayed by SDS-polyacrylamide gel electrophoresis. Urinary DAP IV activity of healthy controls was 4.94 +/- 0.12 U/l (DCR: 0.46 +/- 0.30 U/mmol creatinine) with only small day to day variations. Urinary DAP IV activity in patients with tubulointerstitial nephritis was significantly higher (15.5 +/- 15.6 U/l, p less than 0.05 vs controls; DCR: 1.67 +/- 0.97 U/mmol creatinine, p less than 0.001 vs controls). In patients with chronic glomerulonephritis urinary DAP IV activity was 9.6 +/- 5.6 U/l, p less than 0.05 (DCR: 1.22 +/- 0.75 U/mmol creatinine, p less than 0.05 vs controls). Increased urinary DAP IV activity in patients with chronic glomerulonephritis was associated with a mixed glomerulo-tubular pattern of proteinuria (as determined by SDS-PAGE).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Urinary excretion of dipeptidyl aminopeptidase i.v. in patients with renal diseases. 232 11

The present studies dealt with the pathogenesis of renal involvement in murine chronic graft-versus-host disease, which is a model for human systemic lupus erythematosus. The disease was induced in (C57BL10xDBA/2)F1 hybrids by injection of DBA/2 lymphocytes. The animals developed systemic disease accompanied by deposition of autoantibodies in the glomeruli and a lupus type of nephritis. Antibodies were eluted from glomeruli isolated during various stages of the disease by magnetic extraction from iron-perfused kidneys. For assessment of the specificity of the antibodies, we used indirect immunofluorescence, an enzyme-linked immunosorbent assay, and immunoblotting. In glomeruli from week 4, autoantibodies were found to be directed against several antigens, among which were the glomerular basement membrane component laminin and the glomerular enzyme dipeptidyl peptidase IV, whereas week 8 glomeruli also showed antibodies directed against nuclear antigens. Both laminin and dipeptidyl peptidase IV are known nephritogenic antigens occurring in renal tubular epithelial brush border preparations. Antibodies eluted from isolated glomeruli of diseased animals bound in a granular pattern along the glomerular capillary wall after in vivo transfer. Anti-renal tubular epithelial antibodies in the sera of diseased animals were affinity purified and injected into naive mice, which induced immune complex glomerulonephritis and proteinuria, thus confirming the nephritogenic role of these autoantibodies in this model.
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PMID:Characterization and in vivo transfer of nephritogenic autoantibodies directed against dipeptidyl peptidase IV and laminin in experimental lupus nephritis. 239 30

Injection of antibodies to renal tubular membrane (Fx1A) into Lewis rats induces granular deposits of IgG in glomeruli and proteinuria (passive Heymann nephritis, PHN), and similar lesions are also induced by antibody to one of the antigens in Fx1A, dipeptidyl peptidase IV (DPP IV, gp 108). In this study, the role of DPP IV in PHN was investigated using DPP IV-deficient F344 rats. The amount of DPP IV found in F344 rat kidneys was less than 0.05% of that present in Wistar rats, and injection of anti-DPP IV antibody into F344 rats did not induce proteinuria. Injection of anti-F344 Fx1A rabbit antibodies that contain no detectable anti-DPP IV antibody into Lewis or F344 rats induced PHN, characterized by granular deposits of rabbit IgG in glomeruli and massive proteinuria, although the appearance of proteinuria was delayed in comparison with that occurring in response to injection of anti-Wistar Fx1A antibodies. These results indicate that DPP IV may contribute to, but is not essential for, the induction of PHN.
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PMID:Role of dipeptidyl peptidase IV (gp 108) in passive Heymann nephritis. Use of dipeptidyl peptidase IV-deficient rats. 256 37

Our previous paper showed that the glycoprotein of Mr 108,000 (gp108) is one of the major components of rat renal tubular brush border antigens and that an injection of anti-gp108 antiserum in rats induces passive Heymann nephritis with acute and severe proteinuria. In this study, gp108 was identified as a monomer of dipeptidyl peptidase IV (DPP IV). The anti-gp108 antibody was shown to immunoprecipitate DPP IV from Triton-extract of renal tubular membrane fractions. DPP IV was co-purified with gp108 from the Triton-extract by columns of DEAE-cellulose and Bio-gel A-1.5 m. The ratio of DPP IV activity and gp108 content was nearly constant throughout the purification steps. The final purified gp108 showed a high specific activity of DPP IV, comparable to that reported for purified rat DPP IV. These results indicate that gp108 is a monomer of DPP IV.
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PMID:Identification of gp108, a pathogenic antigen of passive Heymann nephritis, as dipeptidyl peptidase IV. 289 1

Angiotensin I converting enzyme (ACE) activity was measured in serum, urine, and tissues of rats with acute renal failure (ARF) induced by glycerol. Glycerol-injected rats were subdivided in three groups according to the urinary volume: oliguric, nonoliguric, and polyuric. The damage to the proximal tubule was evident by (a) the histological analysis at light and electron microscopy level, (b) the augmented urinary excretion of the enzymes dipeptidyl aminopeptidase IV and N-acetyl-beta-D-glucosaminidase, and (c) the low molecular weight proteinuria pattern. On the other hand, the appearance of the glomeruli at the ultrastructural level was normal. These data suggest that the increased urinary excretion of enzymes and proteins in these rats is a consequence of the tubular injury. ARF was markedly higher in the oliguric rats. Urine ACE activity increased in the rats of the three groups, but statistical significance was reached only in the oliguric rats. Serum ACE activity increased in the oliguric rats and tissue ACE activity did not change. It is concluded that the high urinary ACE in glycerol-treated rats is associated with the damage to the kidney tubules. These data support the contention that urinary ACE may be another marker of injury to the proximal tubule.
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PMID:Angiotensin I converting enzyme in glycerol-induced acute renal failure in rats. 756 9

Angiotensin I converting enzyme (ACE) was measured in urine, serum, and tissues from rats with acute renal failure (ARF) induced by a single subcutaneous injection (15 mg/kg BW) of uranyl nitrate (UN). Urine was collected daily until day 5, when rats were sacrificed by decapitation for the obtention of blood serum and tissues. Other groups of rats were sacrificed on days 1 and 2. These rats showed proteinuria and polyuria. The damage to the kidney proximal tubule was shown by (a) histological analysis at light and electron microscopy levels on days 1, 2, and 5, (b) the increase in urinary excretion of dipeptidyl aminopeptidase IV and N-acetyl-beta-D-glucosaminidase on days 1-5, and (c) the low molecular weight proteinuria pattern on day 1. In addition, the histological analysis at the ultrastructural level showed normal glomeruli appearance on days 1 and 2, but structural alterations on day 5. These data suggest that the increased urinary excretion of enzymes and proteins is a consequence of the tubular injury on days 1 and 2, and of tubular and glomerular injury on day 5. ACE activity increased in urine on days 1-5 and in serum on day 5. Tissue ACE activity increased in lung, small intestine, and adrenal glands; and remained unchanged in testis, aorta, brain, kidney, heart, and liver. Our data suggest that: (a) the increase in serum ACE may be secondary to the changes in tissue ACE activity, and (b) the urine ACE increase may be due to the kidney proximal tubule damage. This work supports the contention that an increase in urine ACE may be an indicator of injury to the proximal tubule.
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PMID:Angiotensin I converting enzyme activity in uranyl nitrate induced acute renal failure in rats. 756 10

Massive proteinuria is induced in rats by administration of rabbit antibody to dipeptidyl peptidase IV (DPPIV, gp108), a glycoprotein present on glomerular cell membranes and in serum. This study was undertaken to know which antigen, glomerular or serum DPPIV, is responsible for forming immune complex in glomeruli and development of proteinuria. An i.p. injection of the antibody resulted in a rapid decrease of serum DPPIV and a gradual increase of rabbit IgG deposited along glomerular capillary wall for 4-8 h. Abnormal proteinuria appeared within 8 h, peaked on day 2 (> 200 mg/24 h) and then declined. An increase of urinary protein and glomerular deposition of IgG also occurred, when the antibody was injected into serum DPPIV-depleted rats that had received preinjection of anti-DPPIV antibody. These results suggest that proteinuria is induced by direct binding of anti-DPPIV antibody to the membrane antigen of glomerular cells.
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PMID:Proteinuria induced by anti-dipeptidyl peptidase IV (gp108); role of circulating and glomerular antigen. 790 95

The angiotensin I-converting enzyme (ACE) activity was studied in 2 experimental models of acute renal failure: (a) rats treated with a single injection of mercuric chloride (1.5 mg/kg) and (b) rats treated with a single injection of potassium dichromate (15 mg/kg). Rats were sacrificed 24 and 48 h after mercuric chloride or potassium dichromate injection. ACE activity was measured in urine, serum, and kidney. These data were compared with vehicle-treated rats. Rats with acute renal failure had proteinuria, polyuria, and decreased creatinine clearance. The damage to the kidney proximal tubule was evident by (a) the histological analysis at light and electron microscopy, (b) the augmentation in the urinary excretion of dipeptidyl aminopeptidase IV and N-acetyl-beta-D-glucosaminidase, and (c) the low molecular weight proteinuria pattern. In addition, the histological analysis at the ultrastructural level showed normal glomeruli appearance. The above data suggest that the increased urinary excretion of enzymes and proteins in rats with acute renal failure is a consequence of tubular injury. Urinary and serum ACE activities increased and kidney ACE activity decreased. Our data suggest that the increase in urine ACE activity may be due to the kidney proximal tubule damage. This work supports the contention that an increase in urine ACE may be an indicator of injury to the proximal tubule.
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PMID:Urinary angiotensin I-converting enzyme activity is increased in experimental acute renal failure. 871 86

Maleate treatment of rats induces transport defects similar to those seen in the Fanconi syndrome (glycosuria, aminoaciduria, phosphaturia, proteinuria, etc.) and causes an accumulation of apical vesicles in proximal tubule epithelial cells. Because the apical membrane glycoprotein, gp330, is a receptor associated with the apical endocytotic and recycling apparatus in these cells, we examined the effect of maleate on the distribution of this protein and other brush border markers. Rats received sodium maleate (400 mg/kg ip) and were killed at various times between 45 min and 3 h; kidneys were perfusion fixed with paraformaldehyde-lysine-periodate before processing for immunofluorescence and immunoelectron microscopy. In control rats, staining with a polyclonal or monoclonal gp330 antibody showed a uniform distribution on the brush border and in coated pits of all proximal tubule cells. In the S3 segments, the immunofluorescence labeling of the microvilli was generally uniform but at times showed spike labeling, suggesting that gp330 sheds easily from the apical membrane. After maleate treatment, the staining intensity of the brush border was decreased in all proximal tubule segments, and cytoplasmic streaks as well as an intense vacuolar staining were seen. In the S3 segment, a remarkable mosaic pattern of staining was observed, with the brush border of some cells being completely negative, while adjacent cells showed an apparently normal staining pattern. These results were confirmed at the electron microscope level, using the protein A-gold technique. Maleate had no effect on the distribution or staining intensity of four other brush border markers, dipeptidyl peptidase IV, and various lectins (Helix pomatia lectin, peanut lectin, elderberry bark lectin). The urinary excretion of gp330 occurs in normal rats and was already increased as early as 1 h after maleate injection and remained at a twofold increment between 6 and 24 h. These data suggest that the generalized membrane transport derangement seen in this experimental Fanconi syndrome could occur via a specific effect on gp330, which seems to block endocytosis and the recycling apparatus at the late endosome level and inhibits the formation of new dense apical tubules.
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PMID:Specific effect of maleate on an apical membrane glycoprotein (gp330) in proximal tubule of rat kidneys. 889 22


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