For ages physicians have appreciated the diagnostic value of examining
the urinary sediment to detect renal disease because urine is a direc
t product of the kidney, Because kidney transplant failure is usually
caused by rejection processes, there is an urgent need to find a clini
cally relevant marker that can provide an early warning that distingui
shes allograft rejection from other forms of allograft insult and/or p
roffers a reliable index to monitor antirejection therapy. The occurre
nce of allograft rejection correlates inconsistently with the content
of urinary electrolytes or cellular elements, such as lymphocytes, tub
ular epithelial cells, or eosinophils, Although non-selective proteinu
ria appears to be a useful indicator of allograft rejection, the measu
rement of microproteins or urinary enzymes tends to be limited in its
clinical application because it fails to distinguish alloimmune proces
ses from ischemic injury or systemic infection, Improved accuracy and
specificity has been obtained by the recent development of monoclonal
antibodies that quantitatively detect distinctive epitopes on the surf
ace of exfoliated cells in the sediment or cytokines released into the
supernate of urine during the process of immune activation, Among the
se non-invasive tests, urinary interleukin-2 receptor, intercellular a
dhesion molecules, adenosine binding protein, or eosinophilic cationic
protein are the most promising ne tv markers, Ongoing efforts to clar
ify the events during cytokine signalling, induction, and interaction
seek to discover even better markers to detect key steps in the reject
ion cascade, including tumor necrosis factor-alpha and interferon-gamm
a, These studies of urinary markers forecast the future discovery of a
panel of immunoreactive antibodies to identify specific urine markers
of acute allogaft rejection.