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Graft, Vol. 5, No. 3, 153-155 (2002)
DOI: 10.1177/1522162802005003008
© 2002 SAGE Publications

Acceleration of Chronic Rejection of Kidney Allografts from Non-Heartbeating Donors

Igor A. Laskowski

Martin Gasser

Johann Pratschke

Wayne W. Hancock

Nicholas L. Tilney

The authors have previously shown that dysfunction of isografts correlates with the intervalof cardiac arrest of the non-heartbeating donor (NHBD). In this study, the authorsinvestigated the nonspecific effects of donor asystole on rat allografts over time. F344kidney donors were killed, and after 45 min the left kidney was transplanted orthotopicallyinto Lewis (LEW) recipients (group 1, n= 14). Organs from living donors (LD) actedas controls (group 2, n= 10). All host animals received low-dose cyclosporine (1.5mg/day x 10). LEW recipients of kidney isografts from NHBD (group 3, n= 15) and LDcontrols (group 4, n = 6) were examined in parallel. All animals were followed for 12weeks. Proteinuria was assessed every 4 weeks, and tissue samples examined at 2 and12 weeks ( n= 3/time point). All animals survived. Proteinuria increased progressively inall group-1 NHBD allograft and group-3 isograft recipients. From control LD groups 2and 4, proteinuria remained at baseline. Morphologically, group-3 kidney isograftsshowed early acute tubular necrosis followed later by moderate interstitial fibrosis andglomerular injury. In contrast, group-1 allografts developed massive cortical atrophy,with rapidly progressive focal and segmental glomerular proliferation and sclerosis. Isoandallograft LD kidneys remained unaffected. The immunologically independent earlyand late structural changes occurring in NHBD kidney isografts are dramatically acceleratedin allografted organs.

Key Words: non-heartbeating donors (NHBDs) • "marginal" or "extended" cadaver donors

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