Barbey F, Matthieu C, Nseir G, Burnier M, Teta D
Department of Nephrology, University Hospital, Lausanne, Switzerland.
J Intern Med. 2003 Dec;254(6):605-8. doi: 10.1111/j.1365-2796.2003.01214.x.
We report the case of a 35-year-old man with no cardiovascular morbidity, presenting with acute flank pain, microscopic haematuria and normal blood pressure. Initially diagnosed as a ureteral colic, the patient was recovered 6 weeks later with severe hypertensive crisis. Further investigations revealed a massive renal infarction secondary to medial fibromuscular dysplasia (FMD). Several aspects of this presentation are intriguing. Renal infarcts are usually seen in older patients having cardiac problems and/or major atheromatous plaques. In addition, FMD is mainly observed in young females and rarely progresses to renal artery occlusion. Furthermore, in this case, FMD remained silent until the acute renal infarction occurred, despite a significant kidney size reduction at the time of diagnosis. Finally, the observation of a delayed hypertensive response to a major renovascular insult provides incentives to discuss possible pathophysiological mechanisms involved in renovascular hypertension.
我们报告了一例35岁男性患者，无心血管疾病史，表现为急性胁腹痛、镜下血尿且血压正常。最初诊断为输尿管绞痛，患者6周后出现严重高血压危象。进一步检查发现，这是一例继发于内侧纤维肌发育不良（FMD）的大面积肾梗死。该病例的几个方面颇具吸引力。肾梗死通常见于患有心脏问题和/或主要动脉粥样硬化斑块的老年患者。此外，FMD主要见于年轻女性，很少进展为肾动脉闭塞。而且，在该病例中，尽管诊断时肾脏体积显著缩小，但FMD在急性肾梗死发生前一直未被发现。最后，对严重肾血管损伤出现延迟性高血压反应的观察，促使我们讨论肾血管性高血压可能涉及的病理生理机制。
