Dramatic worsening of vascular calcifications after kidney transplantation in spite of early parathyroidectomy.
Dramatic worsening of vascular calcifications after kidney transplantation in spite of early parathyroidectomy.
复制标题
尽管早期进行了甲状旁腺切除术，但肾移植后血管钙化仍急剧恶化。
作者：
C. Canavese;F. Cesarani;C. Stratta;E. Maddalena;M. Messina;D. Hamido;D. Bianchi;G. Segoloni
血管钙化是慢性透析患者的常见特征，但其临床意义存在争议，肾移植（TP）在其发展的自然史中的作用很少受到关注。我们将描述一个年轻患者在TP期间血管钙化急剧恶化的病例，尽管早期和成功的甲状旁腺切除术（PTX），并将讨论其他可能与TP期间血管损伤有关的原因。一名37岁的男子定期透析治疗（RDT）11年，接受了他的第一次尸体移植在1993年1月。尽管移植物功能正常，但由于甲状旁腺激素值没有下降，他在TP后6个月接受了PTX。尽管PTX是有效的，但在随后三年的TP期间，大动脉以及中小动脉的急剧恶化是明显的。1997年2月，在因原发性膜增生性肾小球肾炎（MPGN）复发而再次开始透析几个月后，患者发生心肌梗死，随后行冠状动脉搭桥术（右冠状动脉和前降支冠状动脉）和腿部“跛行”。虽然甲状旁腺激素在血管疾病中的作用已被普遍接受，但本文报告的病例清楚地表明，在TP期间，钝化甲状旁腺活性可能无法避免血管疾病过程的恶化。许多其他因素-与TP的时间-可能涉及血管疾病，如肾病综合征，血脂异常，高血压和药物。在我们的病例中，进行性动脉粥样硬化的一个明确的危险因素可以被指定为高血压性水肿和继发于MPGN复发引起的肾病综合征的其他紊乱，以及持续性高血压。这是英文文献中的第一个病例报告，它清楚地表明TP可能会在年轻人中甚至在没有甲状旁腺功能亢进的情况下助长血管疾病的火焰，这可能是基于有利的遗传背景。此外，我们的病人的历史表明，血管钙化预示着主要的心血管疾病。
Vascular calcification is a common feature in chronic dialysis patients, but their clinical significance is debated and the role of kidney transplantation (TP) in the natural history of their development has received scanty attention. We will describe a case of dramatic worsening of vascular calcifications during TP in a young patient in spite of early and successful parathyroidectomy (PTX), and will discuss other causes which might be putatively linked to vascular damage during the time of TP. A 37-year-old man on regular dialytic treatment (RDT) for 11 years, received his first cadaveric transplantation in January 1993. He underwent PTX 6 months after TP because of the lack of decreasing in parathyroid hormone values despite normal graft function. Although PTX was effective, a dramatic worsening was evident in large as well as in medium and small-sized arteries during the following three years of TP. In February 1997, few months after starting dialysis again because of the recurrence of his primary membranoproliferative glomerulonephritis (MPGN), the patient experienced myocardial infarction followed by aorto-coronary bypass (right coronary artery and anterior descending coronary artery) and leg "claudicatio". Though a role for parathyroid hormone in vascular disease has been commonly accepted, the case here reported clearly shows that blunting parathyroid gland activity may be unable to avoid the worsening of a process of vascular disease during the time of TP. Many other factors--linked to the time of TP--may be involved in vascular diseases, such as nephrotic syndrome, dyslipidemia, hypertension and drugs. In the case of our patient, a clear cut risk factor for his progressive atherosclerosis can be designated hyperlipidema and other disturbancies secondary to a nephrotic syndrome due to relapse of MPGN, together with persistent hypertension. This is the first case report in the English literature which clearly demonstrates that TP may add fuel to the fire of vascular disease also in young people and even in the absence of parathyroid hyperactivity, perhaps on the basis of a favorable genetic background. Furthermore, the history of our patient demonstrates that vascular calcifcation heralds major cardiovascular diseases.