Savazzi G M, Cusmano F, Musini S
Department of Internal Medicine and Nephrology, University of Parma, Via Gramsci 14, I-43100 Parma, Italy.
Nephron. 2001 Sep;89(1):31-6. doi: 10.1159/000046040.
Nonuremic patients with apparently normal memory and behavior, studied by means of cerebral computed tomography and found to have cerebral atrophy (CA), evidenced functional intellectual deficits when they underwent psychometric testing. The finding of CA has been repeatedly reported in limited case groups of uremic patients who also demonstrated functional intellectual deficits on the basis of the same tests. This retrospective study considered all diagnostic cerebral computed tomography scans done in our department between 1981 and 1998. Fifty-five uremic patients in conservative treatment (CT) and 111 patients in hemodialysis treatment (HT) were selected on the basis of the following two criteria: primary nephropathy as the cause of uremia and an age < or =55 years to exclude involutive brain changes occurring with age.
The aims of the study were to determine the percent of uremic patients with CA, the characteristics of their CA (cortical or subcortical), and eventual associated morphological lesions.
CA was detected in 50.9% (cortical atrophy in 47.3% and subcortical atrophy in 3.6%) of the uremic patients in CT and in 77.5% of those in HT (cortical atrophy in 65.7% and subcortical atrophy in 7.7%). The average degree of CA was 0.872 in the patients in CT and 1.765 in the patients in HT. Thirty-four of the patients in the CT group and 46 in the HT group were hypertensive: these patients had a more severe degree of CA than the nonhypertensive subjects. In the CT group, the degree of CA in the hypertensive patients was 1.205 versus 0.428 for the nonhypertensive subjects. In the HT group, the degree of CA was 2.087 for the hypertensive patients versus 1.538 for the nonhypertensive patients. Of the overall population, 7.8% had ischemic lesions, 9.6% had endocranial calcifications, and 5.4% evidenced periventricular white matter hyperintensities.
The high percent of CA found in young uremic patients increased in subjects in HT and, even more so in hypertensive patients. Vascular calcifications, focal ischemia and leukoaraiosis, well-known expressions of a chronic state of cerebrovascular insufficiency, were also found in HT patients; hypertension alone is a recognized accelerator of vascular damage. Thus, early and severe atherosclerosis and related hypoperfusion can be considered as the paramount causes of parenchymal cerebral damage in uremia.
通过脑部计算机断层扫描研究发现，无尿毒症且记忆和行为明显正常的患者存在脑萎缩（CA），在进行心理测量测试时，他们表现出功能性智力缺陷。在有限的尿毒症患者病例组中也反复报告了CA的发现，这些患者基于相同测试也表现出功能性智力缺陷。这项回顾性研究纳入了1981年至1998年间在我们科室进行的所有诊断性脑部计算机断层扫描。根据以下两个标准选择了55例接受保守治疗（CT）的尿毒症患者和111例接受血液透析治疗（HT）的患者：原发性肾病作为尿毒症的病因，年龄≤55岁以排除与年龄相关的脑萎缩变化。
本研究的目的是确定患有CA的尿毒症患者的百分比、其CA的特征（皮质或皮质下）以及最终相关的形态学病变。
CT组中50.9%的尿毒症患者检测到CA（皮质萎缩占47.3%，皮质下萎缩占3.6%），HT组中77.5%的患者检测到CA（皮质萎缩占65.7%，皮质下萎缩占7.7%）。CT组患者的CA平均程度为0.872，HT组患者为1.765。CT组中有34例患者和HT组中有46例患者患有高血压：这些患者的CA程度比非高血压患者更严重。在CT组中，高血压患者的CA程度为1.205，而非高血压患者为0.428。在HT组中，高血压患者的CA程度为2.087，而非高血压患者为1.538。在总体人群中，7.8%有缺血性病变，9.6%有颅内钙化，5.4%有脑室周围白质高信号。
在年轻尿毒症患者中发现的高比例CA在接受HT的患者中增加，在高血压患者中更是如此。血管钙化、局灶性缺血和脑白质疏松症，这些众所周知的慢性脑血管功能不全的表现，在HT患者中也有发现；仅高血压就是公认的血管损伤加速因素。因此，早期和严重的动脉粥样硬化及相关低灌注可被视为尿毒症患者实质性脑损伤的首要原因。
