A. Jorres et al., URINARY-EXCRETION OF THROMBOXANE AND MARKERS FOR RENAL INJURY IN PATIENTS UNDERGOING CARDIOPULMONARY BYPASS, Artificial organs, 18(8), 1994, pp. 565-569
Urinary excretion of selected markers for renal injury, as well as uri
nary excretion rates of the thromboxane metabolite, 11-keto-thromboxan
e B-2 (11k-TXB(2)), was studied in 36 male patients undergoing coronar
y bypass surgery using cardiopulmonary bypass (CPB). In all patients,
excretion of both tubular (N-acetyl-beta-D-glucosaminidase [beta NAG];
alpha(1)-microglobulin [alpha(1)-MG]) and glomerular markers (albumin
[Alb]; transferrin [Trf]; immunoglobulin G [IgG]) sharply increased o
n Day 1 after CPB, and they remained elevated throughout the observati
on period of 5 days. Urinary excretion rates of 11k-TXB(2) markedly in
creased on Day 1 after surgery, and they rapidly decreased thereafter.
In 12 of the 36 patients, a temporary increase of serum creatinine le
vels (>1.30 mg/dl) was noted following surgery. A positive correlation
was found between serum creatinine levels and excretion of the tubula
r enzyme beta NAG (r = 0.36; p < 0.05), but not between creatinine lev
els and alpha(1)-MG or the glomerular markers. Furthermore, no correla
tion between urinary excretion of 11k-TXB(2) and any of the urinary ma
rkers for renal injury could be detected. Our data do not strengthen t
he hypothesis that acute renal injury observed during CPB is related t
o exaggerated thromboxane biosynthesis in these patients. Monitoring o
f urinary markers for incipient renal damage, particularly excretion o
f beta NAG, might be of additional diagnostic value for detection of o
therwise subclinical renal injury in patients undergoing CPB.