A. Knoflach et U. Binswanger, SERUM HIPPURIC-ACID CONCENTRATION IN RENAL-ALLOGRAFT REJECTION, URETER OBSTRUCTION, AND TUBULAR-NECROSIS, Transplant international, 7(1), 1994, pp. 17-21
Plasma from 35 renal allograft recipients (21 males and 14 females) wa
s sampled daily and analyzed for hippuric acid (HA) by highperformance
liquid chromatography (HPLC) and serum creatinine. Twelve of these pa
tients experienced an acute renal allograft rejection or a ureter obst
ruction as proven by clinical signs and biopsy, as well as by radiogra
phy or ultrasound, respectively. Two patients suffered from tubular ne
crosis followed by rejection during the postoperative period. Mean ser
um HA increased by 39.9 mu mol/l from baseline (range 20.4-115.5 mu mo
l/l) in patients with acute rejection 3 days after an initial increase
that was observed 24 h before the mean serum creatinine increased by
107.1 mu mol/l (range 21-193 mu mol/l). In cases of ureter obstruction
, HA rose by 1.6 mu mol/l (range 1-8.2 mu mol/l), significantly less t
han elevations due to rejection. The increase in creatinine, however,
amounted to 65.3 mu mol/l (range 22-140 mu mol/l) and was not differen
t from the change in rejecting patients. Successful antirejection trea
tment coincided with a decrease in serum HA starting 24 h earlier than
the decrease in the serum creatinine concentration. Of special intere
st was the observation of a parallel decrease in HA with creatinine co
ncentration in patients with tubular necrosis after allotransplantatio
n; HA increased in cases of an additional rejection. Our data suggest
that HA, which is excreted by tubular secretion and glomerular filtrat
ion, could be a sensitive and early marker of acute allograft rejectio
n. Furthermore, it seems to discriminate between acute renal allograft
rejection and ureter obstruction. It might, therefore, be of value in
the diagnosis of rejection complicating tubular necrosis after transp
lantation.