Open AccessLipopolysaccharide‐binding‐protein as a new and reliable infection marker after kidney transplantation
Author(s) -
Kaden J.,
Zwerenz P.,
Lambrecht H.G.,
Dostatni R.
Publication year - 2002
Publication title -
transplant international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.998
H-Index - 82
eISSN - 1432-2277
pISSN - 0934-0874
DOI - 10.1111/j.1432-2277.2002.tb00147.x
Subject(s) - lipopolysaccharide binding protein , medicine , kidney transplantation , sepsis , transplantation , cytomegalovirus , gastroenterology , renal function , immunology , lipopolysaccharide , urology , human immunodeficiency virus (hiv) , herpesviridae , inflammation , viral disease , acute phase protein
The early and reliable differentiation of rejections, viral infections and bacterial infections is one of the main problems after organ transplantation. One promising solution to this problem is the lipopolysaccharide‐binding protein (LBP), which is regulated upwards in gram‐negative sepsis and related conditions. Therefore, the aim of our study was to explore the diagnostic potential of LBP serum levels in well‐defined, non‐infectious and infectious events after kidney transplantation (KTx). In a retrospective study the LBP serum levels were measured in a total of 686 serum samples from 52 kidney graft recipients. In all pre‐KTx sera tested, the mean LBP level was 8.8±3.5 μg/ml (reference range: 2.0–15.2 μg/ml). In 7 of 52 recipients without intraoperative T‐cell depletion, the mean LBP level was significantly ( P <0.01) increased (13.0±1.5 μg/ml) at post‐KTx day 1, but was within the reference range. In contrast, the intraoperative T‐cell depletion by antilymphocyte antibodies resulted in a significant ( P <0.01) increase to 25.8±11.4 μg/ml (range: 13.3–47.2 μg/ml). In recipients with immediate ( n =14) or delayed ( n =9) graft function without any other complications, all post‐KTx values (except the post‐KTx peak) were within the reference range. In 10 recipients with steroid‐sensitive rejections and in 11 recipients with steroid‐resistant rejections, no rejection‐associated changes of the LBP levels could be shown. In six recipients with cytomegalovirus infection, the detection of an antigenemia (pp65) also was not associated with alterations of the LBP levels. In addition, there was no correlation between LBP levels and the number of pp65‐positive leukocytes in peripheral blood. In contrast, a strong elevation of LBP levels was seen in five recipients with gram‐positive bacteremia as well as in other severe bacterial infections (e.g., purulent extravasate, heavily infected grafts, bacterial pneumonia and contaminated hematoma). In two recipients with superinfected (bacterial and mycotic or viral) Pneumocystis carinii pneumonias requiring assisted ventilation, LBP levels were elevated, too. Thus, in our study only systemic non‐viral infections and massive lymphocytolysis were associated with elevated LBP serum levels.