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Progressive interstitial fibrosis of kidney allograft early after transplantation from a non‐heart beating donor: possible role of persistent ischemic injury
Author(s) -
Masutani Kohsuke,
Kitada Hidehisa,
Yamada Shunsuke,
Tsuchimoto Akihiro,
Noguchi Hideko,
Tsuruya Kazuhiko,
Katafuchi Ritsuko,
Tanaka Masao,
Iida Mitsuo
Publication year - 2010
Publication title -
clinical transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 76
eISSN - 1399-0012
pISSN - 0902-0063
DOI - 10.1111/j.1399-0012.2010.01273.x
Subject(s) - medicine , transplantation , acute tubular necrosis , hemodialysis , fibrosis , chronic allograft nephropathy , kidney transplantation , urology , nephropathy , surgery , kidney , anemia , creatinine , renal function , gastroenterology , atrophy , endocrinology , diabetes mellitus
Masutani K, Kitada H, Yamada S, Tsuchimoto A, Noguchi H, Tsuruya K, Katafuchi R, Tanaka M, Iida M. Progressive interstitial fibrosis of kidney allograft early after transplantation from a non‐heart beating donor: Possible role of persistent ischemic injury.
Clin Transplant 2010: 24 (Suppl. 22): 70–74. © 2010 John Wiley & Sons A/S. Abstract: The donor was 63‐yr‐old woman with subarachnoid hemorrhage. As she developed severe hypotension for more than four h before cardiac arrest, we biopsied the grafts and decided to transplant those kidneys. Recipient 1 was a 23‐yr‐old man on 13‐yr dialysis program. After 19 d of delayed graft function (DGF), we discontinued hemodialysis (HD). However, the decrease in serum creatinine (sCr) was poor. The minimum sCr was 4.3 mg/dL on post‐operative day (POD) 40, and increased to 6.5 mg/dL. The contralateral graft was transplanted to a 61‐yr‐old man (recipient 2) with 18‐yr HD. After 15 d of DGF period, sCr decreased gradually and has been stable at 1.9 mg/dL. In recipient 1, graft biopsies performed on POD 15, 69, and 110, revealed progressive interstitial fibrosis and tubular atrophy (IF/TA) without evidences of acute rejection, tacrolimus associated injury, reflux nephropathy, or viral nephropathy. The second biopsy on POD 69 showed typical findings of acute tubular necrosis. We compared the clinical courses of the two recipients because certain features of recipient 1, such as age, duration of HD, total ischemic time, and body size were advantageous, whereas graft function was poorer than that in recipient 2. Recipient 1 developed severe anemia following the dissociation of graft function from recipient 2. In this case, posttransplant anemia and lower blood pressure might promote IF/TA through persistent ischemic tubular damage, and positive CMV antigenemia and its treatment could promote anemia. Especially in the kidney allograft from a marginal donor, we should consider various factors to obtain a better graft outcome.