A rapid laser immunonephelometric assay for serum amyloid A (SAA) and its application to the diagnosis of kidney allograft rejection

1989 ◽  
Vol 67 (8) ◽  
pp. 447-451 ◽  
Author(s):  
G. Hocke ◽  
H. Ebel ◽  
K. Bittner ◽  
T. Müller ◽  
H. Kaffarnik ◽  
...  
2004 ◽  
Vol 132 (7-8) ◽  
pp. 267-271 ◽  
Author(s):  
Dijana Jovanovic

Serum amyloid A (SAA) is an acute phase first class protein discovered a quarter of the century ago. Its concentration depends on clinical findings of the patient, illness activity and the therapy applied. SAA increases moderately to markedly (100-1000 mg/l) in bacterial and fungal infections, invasive malignant diseases, tissue injuries in the acute myocardial infarction and autoimmune diseases such as rheumatoid arthritis and vasculitis. Mild elevation (10-100 mg/l) is often seen in viral infections, systemic lupus erythematosus and localized inflammation or tissue injuries in cystitis and cerebral infarction. SAA as sensitive, non-invasive parameter is used in organ transplantation where early and correct diagnosis is needed as well as where prompt therapy is required. Besides acute kidney allograft rejection, SAA is used in the diagnosis of rejection after liver transplantation, simultaneous pancreas and kidney transplantation and also in bone marrow transplantation (acute ?graft vs. host disease"). Simultaneous determination of C-reactive protein (CRP) and SAA may point to acute kidney allograft rejection. Standard immunosuppressive therapy with cyclosporine A and prednisolone significantly suppresses the acute phase CRP reaction both in operation itself and acute rejection, but not in infection. On the other hand, SAA rejection in operation, acute allograft rejection and infection is present in spite of cyclosporine A and steroids therapy. Different reaction of SAA and CRP in transplant patients to cyclosporine A therapy helps in differentiation between the infection and rejection. Although CRP and SAA are sensitive and acute phase reactants, their serum concentrations cannot be valued as prognostic and diagnostic criteria without creatinine serum concentration and clinical findings. In addition, they offer important information for clinical diagnosis as well as the kind of therapy.


Nephron ◽  
1995 ◽  
Vol 70 (1) ◽  
pp. 112-113 ◽  
Author(s):  
Martin T. Časl ◽  
Goran Bulatović ◽  
Petar Orlić ◽  
Mirjana Sabljar-Matovinović

2004 ◽  
Vol 78 (6) ◽  
pp. 950-951 ◽  
Author(s):  
Emmanuelle Vermes ◽  
Matthias Kirsch ◽  
Titi Farrokhi ◽  
Daniel Loisance ◽  
Pascale Fanen ◽  
...  

1983 ◽  
Vol 65 (5) ◽  
pp. 547-550 ◽  
Author(s):  
C. P. J. Maury ◽  
A. M. Teppo ◽  
B. Eklund ◽  
P. Häyry ◽  
J. Ahonen

1. Serum amyloid A (SAA) levels were studied in 35 recipients of cadaveric renal transplants. Marked SAA elevations were seen during all acute allograft rejection episodes. The mean peak SAA level in well-documented rejections was 446 mg/l (median 415 mg/l, range 132–1040 mg/l; controls < 1 mg/l). 2. Rejections in patients receiving cyclosporin-A alone as post-transplantation immunosuppressive medication were characterized by a significantly higher peak SAA level than rejections in patients receiving cyclosporin-A in combination with methylprednisolone (539 ± 53 mg/l, mean ± sem, vs 226 ± 9 mg/l, P < 0.01). 3. Excluding surgery-induced SAA elevations in the immediate postoperative period, seven significant SAA peaks not related to allograft rejection were observed. These were associated with surgical complications and infections, and in one case probably with the underlying rheumatic disease, which was complicated by amyloidosis. 4. The results show that acute renal allograft rejection induces a dramatic acute phase SAA response. Since SAA is an easily measured serum component and the rejection-induced elevation is an early event, monitoring of SAA in kidney transplant patients-5-have considerable clinical significance.


1997 ◽  
Vol 12 (1) ◽  
pp. 161-166 ◽  
Author(s):  
A. Hartmann ◽  
T. Eide ◽  
P. Fauchald ◽  
O. Bentdal ◽  
J. Harbert ◽  
...  

1994 ◽  
Vol 72 (12) ◽  
pp. 1007-1011 ◽  
Author(s):  
G. Feussner ◽  
C. Stech ◽  
J. Dobmeyer ◽  
H. Schaefer ◽  
G. Otto ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document