CLINICOPATHOLOGY OF KIDNEYS FROM BRAIN-DEAD PATIENTS TREATED WITH VASOPRESSIN AND EPINEPHRINE

Citation
T. Nagareda et al., CLINICOPATHOLOGY OF KIDNEYS FROM BRAIN-DEAD PATIENTS TREATED WITH VASOPRESSIN AND EPINEPHRINE, Kidney international, 43(6), 1993, pp. 1363-1370
Citations number
44
Categorie Soggetti
Urology & Nephrology
Journal title
ISSN journal
00852538
Volume
43
Issue
6
Year of publication
1993
Pages
1363 - 1370
Database
ISI
SICI code
0085-2538(1993)43:6<1363:COKFBP>2.0.ZU;2-P
Abstract
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.