High Levels of Plasma Protein C in Nephrotic Syndrome

1985 ◽  
Vol 53 (01) ◽  
pp. 005-007 ◽  
Author(s):  
I Pabinger-Fasching ◽  
K Lechner ◽  
H Niessner ◽  
P Schmidt ◽  
E Balzar ◽  
...  

SummaryIn patients with severe nephrotic syndrome determinations of plasma protein C : Ag levels (8 patients: 5 adults, 3 children) and protein C activity (3 out of 8 patients) revealed significantly elevated plasma protein C concentrations. Furthermore we observed a significant inverse correlation of protein C : Ag to AT III : Ag levels. No protein C : Ag could be detected in the urine of two patients studied. We conclude from our data, that changes of plasma protein C do not contribute to the high thrombotic tendency in nephrotic syndrome.

1987 ◽  
Author(s):  
T Gadelha-Parente ◽  
M Gouault-Heilmann ◽  
G Rostoker ◽  
M Levent ◽  
S Rafowicz ◽  
...  

25 consecutive patients (15M, 10F ; mean age 30 years) with nephrotic syndrome (NS) of different grade were studied. Control group consisted in 18 healthy adult volunteers. Total protein S antigen (TPS:Ag) and free protein S antigen (FPS:Ag) after precipitation of C4-BP-bound protein S by PEG 3-5 % final concentration were measured by Laurell's technique. PS:Ag was also searched in concentrated urine of 9 patients by ELISA method, more sensitive than the Laurell's technique. In the same plasma samples we measured C4-BP, Protein C Ag and AT III biological activity (all reagents from D.Stago). Serum albumin level, proteinuria, proteinuria selectivity index, triglycerides, cholesterol levels were recorded. TPS:Ag was found elevated in NS (1.30±0.3 U/ml) in comparison with control group (1.09±0.32 U/ml) and the difference was statistically significant (p<0.05). The mean values of FPS:Ag observed in patients and controls were not statistically different, but if we consider 95 % confidence limits (0.99-1-35 U/ml), 16 pts had normal or elevated FPS:Ag level, whereas 9 had decreased FPS:Ag level. A positive correlation was found between TPS:Ag and FPS:Ag in control group (r=0.66 ; p< 0.001) and in patients with NS (r=0.4l, p<0.05). C4-BP was significantly (p<0.01) increased in nephrotic patients ( 1.37 ± 0.36 U/ml) in comparison with control group (1.04±0.27 U/ml). A negative correlation was found between FPS:Ag and C4-BP levels in control group (r = −0.57, P< 0.01) but not in nephrotic patients. A positive correlation was found between FPS:Ag and albumin level and between FPS:Ag and cholesterol level. No correlation was found between TPS:Ag or FPS:Ag and proteinuria, proteinuria selectivity index, AT III and protein C levels. Traces of PS were found in urine (0. to 2.5 U/day) in 9 patients tested. 2/25 pts suffered thromboembolic events : one had a very low level of FPS:Ag in addition to a decreased level of AT III. The other one had normal FPS:Ag and AT III level but a borderline Protein C level. In conclusion. An acquired FPS:Ag deficiency was observed in 9/25 pts with NS despite an increased level of TPS:Ag. In this small series of patients the acquired FPS deficiency does not seem to be related either to an urinary loss of FPS or to an increased binding to C4-BP, as suggested by some authors.


Cardiology ◽  
1992 ◽  
Vol 80 (3-4) ◽  
pp. 252-256 ◽  
Author(s):  
Shinya Goto ◽  
Shunnosuke Handa ◽  
Yohko Kawai ◽  
Kiyoaki Watanabe ◽  
Sumihisa Abe ◽  
...  

Nephron ◽  
1988 ◽  
Vol 49 (1) ◽  
pp. 20-23 ◽  
Author(s):  
N.D. Vaziri ◽  
S. Alikhani ◽  
B. Patel ◽  
Q. Nguyen ◽  
C.H. Barton ◽  
...  

1988 ◽  
Vol 60 (02) ◽  
pp. 137-140 ◽  
Author(s):  
E Grau ◽  
A Oliver ◽  
J Félez ◽  
P Barceló ◽  
C Fernandez ◽  
...  

SummaryHeparin cofactor II (HC II) levels were measured by electroimmunoassay in plasmas and urines from 68 patients with nephrotic syndrome. In addition, antithrombin III (AT III) and protein C (PC) activities and antigens were measured also in the same group of patients. Seven of these patients had histories of thrombosis. Plasma HC II levels (mean ± SD 105 ± 43) were not different from levels in healthy subjects (94 ± 17). Only 5 patients had low plasma levels of HC II. None of the patients with thrombosis had low HC II levels. Even though measurable amounts of HC II were found in 25 urines from 50 patients. There was a relationship in the urinary excretion between HC II and AT III and their urinary clearances were quite similar. However, no correlation was found between plasma HC II and AT III levels, and levels of AT III activity and antigen were significantly lower than in healthy subjects. Three patients with hystories of thrombosis had low AT III levels. Most patients (including those with thrombosis histories) had high plasma PC levels and increased urinary loss.It is suggested that HC II does not play an important role in the pathogenesis of thrombosis in nephrotic syndrome.


2012 ◽  
Vol 107 (05) ◽  
pp. 1000-1002 ◽  
Author(s):  
Daniel P. Potaczek ◽  
Chiharu Nishiyama ◽  
Ko Okumura ◽  
Anetta Undas

2006 ◽  
Vol 229 (11) ◽  
pp. 1761-1771 ◽  
Author(s):  
Olivier Toulza ◽  
Sharon A. Center ◽  
Marjory B. Brooks ◽  
Hollis N. Erb ◽  
Karen L. Warner ◽  
...  

1984 ◽  
Vol 51 (01) ◽  
pp. 001-005 ◽  
Author(s):  
R M Bertina ◽  
A W Broekmans ◽  
C Krommenhoek-van Es ◽  
A van Wijngaarden

SummaryProtein C is a vitamin K dependent protein involved in blood coagulation. A congenital deficiency in protein C antigen - which inherits as an autosomal dominant disorder - has been reported to be associated with a high risk for thrombo-embolic disease at relatively young age. In the present paper we report on the development of a functional assay for plasma protein C. In this assay protein C is adsorbed to Al(OH)3, eluted and activated by thrombin, after which the concentration of the activated protein C is measured with a peptide substrate (S2366). Normal values for protein C activity and protein C antigen were determined in healthy volunteers and patients on stable oral anticoagulant treatment. Protein C activity and antigen levels were compared in 28 patients from 9 different pedigrees with both congenital protein C deficiency and thrombotic disease. Two types of protein C deficiency could be recognized: in type I the deficiency is due to the absence or reduced presence of protein C molecules, while in type II the deficiency is caused by the presence of an abnormal protein C molecule with strongly reduced functional activity.


1987 ◽  
Author(s):  
M Mysliwiec ◽  
D Alderson ◽  
L Poller ◽  
P Ackrill

The occurrence of thrombosis in the nephrotic syn drome has long been known. Thrombotic complications are predominantly associated with membranous glomerulonephritis (MG). The aim of the present work was to study whether the tendency of nephrotic patients with MG to thrombotic episodes could be attributed to a hypercoagulable state. Thirty consecutive patients with the nephrotic syndrome were studied. Of these 17 suffered from MG and 13 had other forms of glomerulonephritis. The control group consisted of 10 healthy volunteers. In addition to standard coagulation assays, we studied: soluble fibrin monomer complexes (FM test, Boehringer), fibrin monomer polymerization, factor VIII:C, factor VIII:vWF, anti thrombin III (AT III) and alpha2 antiplasmin (alpha2AP) using chromogenie substrates; the levels of AT III and alpha2 AP were measured immunologically; beta thromboglobulin (BTG), platelet factor 4 and fibrinopeptide A (FPA) using radioimmunoassay kits; protein C was studied functionally and immunologically. There was a significant shortening of the prothrombin time and activated partial thromboplastin time, increase in alpha9 AP, factor V111:vWF, FPA and BTG in nephrotic patients associated with in or eases in both functional and imminclogical protein C levels and impairment of fibrin polymerization. FM test was negative in all but one of the patients. None of the coagulation tests showed a significant difference in the two nephrotic groups. High protein C and impaired polymerization may be considered as mechanisms counteracting disclosed hypercoagulability in the nephrotic syndrome.


Sign in / Sign up

Export Citation Format

Share Document