Department of Cardiovascular Surgery, Methodist DeBakey Heart and Vascular Center, The Methodist Hospital, Houston, Tex, USA.
J Vasc Surg. 2010 May;51(5):1222-9; discussion 1229. doi: 10.1016/j.jvs.2009.09.050. Epub 2010 Feb 9.
The intent of endovascular therapy for symptomatic atherosclerotic renal artery stenosis (ARAS) is to preserve parenchyma and avoid renal-related morbidity. The aim of this study is to examine the impact of renal artery intervention on parenchymal preservation.
We performed a retrospective analysis of records from patients who underwent endovascular intervention for ARAS and were followed by duplex ultrasound between 1990 and 2008. Renal volume (in cm(3)) was estimated in all patients as renal length (cm) x renal width (cm) x renal depth (cm) x 0.5. The normal renal volume was calculated as 2 x body weight (kg) in cm(3). Failure of preservation was considered to be a persistent 10% decrease in volume. Clinical benefit defined as freedom from renal-related morbidity (increase in persistent creatinine >20% of baseline, progression to hemodialysis, death from renal-related causes) was calculated.
Five hundred ninety-two renal artery interventions were performed. One hundred eighty-six kidneys suffered parenchymal loss (>5%) with an actuarial parenchymal loss rate of 29% +/- 1% at five years respectively. There were no significant differences in age, gender, starting renal volume, or kidney size. However, patients with parenchymal loss had lower eGFR (45 +/- 24 vs 53 +/- 24 mL/min/1.73 m(2); Loss vs noLoss, P = .0002, Mean +/- SD) higher resistive index (0.75 +/- 0.9 vs 0.73 +/- 0.10; P = .0001) and worse nephrosclerosis grade (1.43 +/- 0.55 vs 1.30 +/- 0.49; P = .006) then those not suffering parenchymal loss. Parenchymal loss was associated with significantly worse five-year survival (26% +/- 4% vs 48% +/- 2%; Loss vs noLoss; P < .001) and freedom from renal-related morbidity (70% +/- 5% vs 82% +/- 2%; P < .05) with increased numbers progressing to dialysis (17% vs 7%; P < .006).
While parenchymal preservation occurs in most patients, parenchymal loss occurs in 31% of patients and is associated with markers of impaired parenchymal perfusion (resistive index and nephrosclerosis grade) at the time of intervention. Pre-existing renal size or volumes were not predictive of parenchymal loss. Parenchymal loss is associated with a significant decrease in survival and a marked increased renal related morbidity and progression to hemodialysis.
有症状的动脉粥样硬化性肾动脉狭窄（ARAS）的血管内治疗目的是保存实质并避免与肾脏相关的发病率。本研究的目的是检查肾动脉干预对实质保存的影响。
我们对 1990 年至 2008 年间接受 ARAS 血管内治疗并通过双功超声随访的患者的记录进行了回顾性分析。所有患者均按肾长度（cm）x 肾宽度（cm）x 肾深度（cm）x 0.5 估算肾体积（cm3）。正常肾体积按 2x 体重（kg）计算为 cm3。体积持续下降 10%被认为是保存失败。计算免于肾脏相关发病率的临床益处（持续肌酐升高>基线的 20%，进展为血液透析，肾脏相关原因死亡）。
共进行了 592 例肾动脉介入治疗。186 个肾脏发生实质损失（>5%），五年时的实际实质损失率分别为 29% +/- 1%。年龄、性别、起始肾体积或肾脏大小无显著差异。然而，发生实质损失的患者的 eGFR（45 +/- 24 比 53 +/- 24 mL/min/1.73 m2；损失比无损失，P =.0002，Mean +/- SD）更高，阻力指数（0.75 +/- 0.9 比 0.73 +/- 0.10；P =.0001）和更严重的肾硬化程度（1.43 +/- 0.55 比 1.30 +/- 0.49；P =.006）高于未发生实质损失的患者。实质损失与五年生存率明显下降（26% +/- 4%比 48% +/- 2%；损失比无损失；P <.001）和免于肾脏相关发病率（70% +/- 5%比 82% +/- 2%；P <.05）相关，并导致更多患者进展为透析（17%比 7%；P <.006）。
虽然大多数患者的实质都得到了保存，但仍有 31%的患者发生了实质损失，且与介入时的实质灌注受损标志物（阻力指数和肾硬化程度）相关。预先存在的肾大小或体积不能预测实质损失。实质损失与生存率显著下降、明显增加的肾脏相关发病率和进展为血液透析相关。
