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Effects of anti‐hypertensive treatment on graft function and proteinuria in a kidney transplant from an elderly hypertensive donor
Author(s) -
Kobayashi Akimitsu,
Yamamoto Hiroyasu,
Matsuoka Kentaro,
Ito Hideyuki,
Yamamoto Izumi,
Kawamura Yoshimi,
Tanno Yudo,
Yaginuma Tatsuhiro,
Mitome Jun,
Hayakawa Hiroshi,
Miyazaki Yoichi,
Utsunomiya Yasunori,
Yamaguchi Yutaka,
Hosoya Tatsuo
Publication year - 2008
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.1399-0012.2008.00853.x
Subject(s) - arteriolosclerosis , medicine , transplantation , blood pressure , urology , renal function , kidney transplantation , proteinuria , kidney , glomerulosclerosis , nephrosclerosis , endocrinology , surgery , disease
Hypertension is a common complication after kidney transplantation and adversely affects graft and patient survival. Strategies for anti‐hypertensive therapy in an allograft from a hypertensive donor with arteriolosclerosis and the target blood pressure have not been clearly defined. Here, we report the case of deteriorating transplanted kidney function after anti‐hypertensive treatment. A 40‐yr‐old man had received a kidney transplant from a living relative donor (his 69‐yr‐old father), who was hypertensive and had severe arteriolosclerosis. The recipient showed good allograft function immediately (s‐Cr 1.8 mg/dL); however, blood pressure and proteinuria increased markedly two wk after transplantation (blood pressure 180/90, urinary protein 3.4 g/d). We then started anti‐hypertensive agents (a calcium channel blocker and an angiotensin II receptor blocker). Blood pressure and proteinuria were corrected to the normal range within two wk of starting the treatment (blood pressure 130/80, urinary protein 0.3 g/d). However, his kidney function continued to deteriorate (s‐Cr 2.7 mg/dL). A biopsy, performed at that time, revealed glomerular collapse, advanced interstitial fibrosis and severe arteriolosclerosis, with no evidence of rejection. These findings could have been the result of renal allograft hypoperfusion. We then reduced the anti‐hypertensive agents on day 45 after transplantation and observed improved allograft function within a week (s‐Cr 1.6 mg/dL). This case suggests that renal hemodynamic responses may be impaired and renal perfusion may not be appropriately maintained in an allograft with severe arteriolosclerosis at a blood pressure level suitable for the recipient. Anti‐hypertensive treatment should be performed carefully when the allograft is from an elderly hypertensive donor.