Burdese M, Consiglio V, Mezza E, Savio D, Guarena C, Rossetti M, Messina M, Soragna G, Suriani C, Rabbia C, Segoloni G P, Piccoli G B
Department of Internal Medicine, University of Turin, Bramante 88, 10126 Turin, Italy.
Transplant Proc. 2005 Jun;37(5):2063-5. doi: 10.1016/j.transproceed.2005.03.032.
Vascular lesions are an increasing challenge after renal transplantation due to the wider indications for recipients and acceptance criteria for donors. Diagnostic approach and prognostic interpretation are still matter of controversy. The case reported herein may summarize some of the issues in this regard. A 54-year-old woman, on renal replacement therapy since 1974, and a kidney graft recipient from 1975 to 1999, received a second graft in 2001. The donor age was 65 years (cold ischemia 22 hours; two mismatches). The early posttransplant follow-up was characterized by delayed graft function, hypertension, and diabetes. During the initial hypertension workup, renal graft ultrasound (US) Doppler demonstrated increased vascular resistances, stable over time (resistance index 0.74 to 0.77); renal scintiscan displayed homogeneously parenchymoa and angio-magnetic resonance imaging (MRI), an homogeneous parenchymal vascularization. Initial immunosuppression with tacrolimus and steroids was modulated by adding mycophenolate mofetil to taper tacrolimus (to reduce nephrotoxicity and hypertension). Despite this, kidney function slowly deteriorated; serum creatinine reached 3 to 3.5 mg/dL by the second year. After a severe hypertensive crisis with unchanged scintiscan and US doppler examinations, angio-MRI revealed the almost complete disappearance of parenchymal enhancement beyond the lobar arteries. A renal biopsy confirmed the severe vascular damage. The patient was switched to rapamycine and a low-dose of an angiotension converting enzyme (ACE) inhibitor. She did relatively well (serum creatinine 2.2 to 3 mg/dL) for 6 months, when rapid functional impairment forced her to restart hemodialysis. This case, almost paradigmatic of the problems occurring when the rigid vasculature of long-term dialysis patients is matched with "marginal kidneys," suggests that MRI may be a sensible good to define vascular damage in the grafted kidney.
由于肾移植受者的适应证范围扩大以及供体接受标准的变化,血管病变在肾移植后成为日益严峻的挑战。诊断方法和预后解读仍存在争议。本文报道的病例可总结这方面的一些问题。一名54岁女性,自1974年起接受肾脏替代治疗,1975年至1999年为肾移植受者,2001年接受了第二次移植。供体年龄65岁(冷缺血时间22小时;两个错配)。移植后早期随访的特点是移植肾功能延迟恢复、高血压和糖尿病。在最初的高血压检查过程中,肾移植超声(US)多普勒显示血管阻力增加,随时间稳定(阻力指数0.74至0.77);肾闪烁扫描显示实质均匀,血管造影磁共振成像(MRI)显示实质血管化均匀。最初使用他克莫司和类固醇进行免疫抑制,通过添加霉酚酸酯来调整他克莫司剂量(以降低肾毒性和高血压)。尽管如此,肾功能仍缓慢恶化;到第二年血清肌酐达到3至3.5mg/dL。在一次严重高血压危象后,闪烁扫描和US多普勒检查结果未变,血管造影MRI显示叶间动脉以外的实质强化几乎完全消失。肾活检证实了严重的血管损伤。患者改用雷帕霉素和低剂量血管紧张素转换酶(ACE)抑制剂。她在6个月内情况相对较好(血清肌酐2.2至3mg/dL),之后快速的功能损害迫使她重新开始血液透析。这个病例几乎是长期透析患者僵硬血管系统与“边缘肾脏”匹配时出现问题的典型例子,表明MRI可能是确定移植肾血管损伤的一种明智方法。