Detection of Renal Tubular Lesions after Abdominal Aortography and Selective Renal Arteriography by Quantitative Measurements of Brush-Border Enzymes in the Urine

Nephron ◽  
1985 ◽  
Vol 39 (2) ◽  
pp. 95-101 ◽  
Author(s):  
H.G. Hartmann ◽  
H.E. Braedel ◽  
G.A. Jutzler
Keyword(s):  
Brush Border ◽  
Brush Border Enzymes ◽  
Quantitative Measurements ◽  
Renal Arteriography ◽  
Renal Tubular

Different diuresis-dependent excretions of urinary enzymes: N-acetyl-beta-D-glucosaminidase, alanine aminopeptidase, alkaline phosphatase, and gamma-glutamyltransferase.

1986 ◽  
Vol 32 (3) ◽  
pp. 529-532 ◽  
Author(s):  
K Jung ◽  
G Schulze ◽  
C Reinholdt
Keyword(s):  
Alkaline Phosphatase ◽  
Brush Border ◽  
Excretion Rate ◽  
Urine Flow ◽  
High Intake ◽  
Brush Border Enzymes ◽  
Urinary Creatinine ◽  
Gamma Glutamyltransferase ◽  
Alanine Aminopeptidase ◽  
Brush Border Enzyme

Abstract We studied how much of the lysosomal enzyme N-acetyl-beta-D-glucosaminidase (EC 3.2.1.30) and of the brush-border enzymes alanine aminopeptidase (EC 3.4.11.2), alkaline phosphatase (EC 3.1.3.1), and gamma-glutamyltransferase (EC 2.3.2.2) was excreted in urine over 8 h after a high intake of fluid (22 mL per kilogram of body weight). The hourly excretion of all four enzymes increased with the increasing urine flow rate. The excretion rate of the brush-border enzymes was more markedly influenced than that of N-acetyl-beta-D-glucosaminidase. By relating the enzyme excretion to urinary creatinine we could reduce the variability of brush-border enzyme output and could completely compensate for the effect of diuresis on the excretion of N-acetyl-beta-D-glucosaminidase.

Enzymatic Cleavage of Thymopoietin Oligopeptides by Pancreatic and Intestinal Brush-Border Enzymes

Peptides ◽  
1996 ◽  
Vol 17 (7) ◽  
pp. 1083-1089 ◽  
Author(s):  
J. HEIZMANN ◽  
P. LANGGUTH ◽  
A. BIBER ◽  
R. OSCHMANN ◽  
H.P. MERKLE ◽  
...  
Keyword(s):  
Brush Border ◽  
Enzymatic Cleavage ◽  
Brush Border Enzymes ◽  
Intestinal Brush Border ◽  
Intestinal Brush Border Enzymes

scholarly journals Certain mouse strains are deficient in a kidney brush-border metallo-endopeptidase activity

1983 ◽  
Vol 209 (1) ◽  
pp. 251-255 ◽  
Author(s):  
J S Bond ◽  
J D Shannon ◽  
R J Beynon
Keyword(s):  
Brush Border ◽  
Inbred Mice ◽  
Neutral Endopeptidase ◽  
Renal Tissue ◽  
Mouse Strains ◽  
Ph Optimum ◽  
Brush Border Enzymes ◽  
Endogenous Inhibitors ◽  
Endopeptidase Activity ◽  
Proteinase A

Preparations of microvilli from kidneys of BALB/c mice contain an alkaline metallo-endopeptidase, meprin (metallo-endopeptidase from renal tissue). Certain genealogically related inbred mice are markedly deficient in meprin activity. The meprin-deficient strains (CBA/J and C3H/HeJ) exhibit normal levels of other brush-border enzymes: alkaline phosphatase, aminopeptidase M and another proteinase, a phosphoramidon-sensitive neutral endopeptidase. Meprin deficiency cannot be attributed to a shift in pH optimum and is unlikely to be due to the presence of endogenous inhibitors.

Pi transport, phosphorylation, and dephosphorylation in renal membranes from HYP/Y mice

1983 ◽  
Vol 245 (6) ◽  
pp. F701-F706
Author(s):  
M. R. Hammerman ◽  
L. R. Chase
Keyword(s):  
Brush Border ◽  
Brush Border Membrane ◽  
Sodium Dodecyl ◽  
Membrane Vesicles ◽  
Hypophosphatemic Rickets ◽  
Dependent Protein Kinase ◽  
Phosphoprotein Phosphatase ◽  
Pi Transport ◽  
Dependent Protein ◽  
Renal Tubular

To ascertain whether cAMP-dependent phosphorylation could be demonstrated in brush border membrane vesicles (BBMV) isolated from kidneys of mice with X-linked hypophosphatemic rickets (HYP/Y) and normal littermates (+/Y) and, if so, to determine whether the absence of dephosphorylation might underlie differences in Na+-dependent 32Pi transport in BBMV, we measured 1) 32Pi transport, 2) cAMP-dependent phosphorylation, and 3) dephosphorylation in BBMV from +/Y and HYP/Y mice. Na+ gradient-dependent 32Pi transport was decreased in BBMV from HYP/Y mice as reflected in a decreased apparent Vmax. cAMP-dependent phosphorylation of a 62,000 Mr protein was demonstrated in sodium dodecyl sulfate polyacrylamide gels of BBMV from +/Y and HYP/Y mice and was associated with decreased Na+-dependent 32Pi transport. Dephosphorylation of the 62,000 Mr band was demonstrable in both types of membranes. Thus, both cAMP-dependent protein kinase and phosphoprotein phosphatase activities were demonstrable in BBMV isolated from +/Y and HYP/Y mice. These results are consistent with the renal tubular defect in the HYP/Y mouse reflecting an intrinsic abnormality of Pi transport in the brush border membrane independent from mediation of the phosphaturic effect of parathyroid hormone.

Effects of vitamin D-induced chronic hypercalcemia on rat renal cortical plasma membranes and mitochondria

1987 ◽  
Vol 252 (2) ◽  
pp. F267-F275 ◽  
Author(s):  
M. Levi ◽  
B. A. Molitoris ◽  
T. J. Burke ◽  
R. W. Schrier ◽  
F. R. Simon
Keyword(s):  
Brush Border ◽  
Cell Injury ◽  
Specific Activity ◽  
Total Phospholipid ◽  
Basolateral Membrane ◽  
Calcium Content ◽  
Molar Ratio ◽  
Renal Tubular Cell ◽  
Molar Composition ◽  
Renal Tubular

Increases in intracellular and mitochondrial calcium content that accompany ischemic and toxic acute renal failure have been suggested to mediate renal tubular cell injury and dysfunction, but the mechanism(s) are unknown. We studied the effects of in vivo vitamin D-induced chronic hypercalcemia on rat renal cortical brush-border and basolateral membranes and mitochondria. In the brush-border membrane, hypercalcemia caused significant decreases in alkaline phosphatase-specific activity, total phospholipid molar content, and phosphatidylserine percent molar composition and increases in the cholesterol-to-total phospholipid molar ratio and phosphatidylinositol percent molar composition. In the basolateral membrane, hypercalcemia caused significant decreases in Na+-K+-ATPase-specific activity and total phospholipid molar content and increases in the cholesterol-to-total phospholipid molar ratio and phosphatidylinositol 4,5-bisphosphate percent molar composition. In the mitochondria, hypercalcemia caused a mild increase in the mitochondrial calcium content, but no alterations in succinic dehydrogenase-specific activity, succinate-, ADP-, or uncoupler-induced respiration. Thus hypercalcemia caused alterations in brush-border and basolateral membrane enzyme activity and lipid composition, but no functional changes were detected in mitochondria. These hypercalcemia-induced plasma membrane biochemical alterations may be markers of early cell injury and suggest a role for calcium in causing or predisposing to renal tubular cell injury.

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