T. Nagareda et al., CLINICOPATHOLOGY OF KIDNEYS FROM BRAIN-DEAD PATIENTS TREATED WITH VASOPRESSIN AND EPINEPHRINE, Kidney international, 43(6), 1993, pp. 1363-1370
Studies were made on the biochemical and pathological conditions of ki
dneys of 20 brain-dead patients who were maintained for 0 to 48 days a
fter brain death by administration of vasopressin and epinephrine. Twe
nty specimens were obtained by percutaneous biopsy or at autopsy. The
biochemical and pathological degrees were compared with those on the d
ay of brain death (day 0). Biochemical tests on day 0 indicated that t
hey showed the diuretic phase of prerenal failure, and then glomerular
hyperemia was extensive. Renal function recovered on day 1 and remain
ed almost normal during the 14 day period. Their urine retained high l
evels of sodium and osmolarity for days 0 to 14, with mild hyponatremi
a and hypo-osmolarity of the plasma. Tubulointerstitial nephritis grad
ually became extensive. There was no significant change in the degrees
of mesangial widening, mesangial cell proliferation or hyalinosis. Ar
terial intimal proliferation was gradually extensive after day 3 and g
lomerular endothelial proliferation was gradually extensive after a we
ek. Brain-dead patients have been mostly reported to develop diabetes
insipidus, but our brain-dead patients did not show any manifestation
of this disease. We suggest that constant natriurisis and continuing h
igh level of urine osmolarity might have been caused by prerenal renal
failure, brain death followed by neurogenic impairment, high level of
serum vasopressin, or interstitial nephritis.