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缺血性急性肾衰竭后肾小管周围毛细血管稀疏:进展性肾病的一个潜在易感因素。

Rarefaction of peritubular capillaries following ischemic acute renal failure: a potential factor predisposing to progressive nephropathy.

作者信息

Basile David P

机构信息

Department of Physiology, Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI 53226, USA.

出版信息

Curr Opin Nephrol Hypertens. 2004 Jan;13(1):1-7. doi: 10.1097/00041552-200401000-00001.

DOI:10.1097/00041552-200401000-00001
PMID:15090853
Abstract

PURPOSE OF REVIEW

Long-term renal complications of acute renal failure have generally not been expected in patients that recover from acute renal failure. However, as the incidence of acute renal failure is rising, the incidence of long-term complications is likely to increase. As a corollary to ischemic acute renal failure, ischemic injury in the setting of transplant is a leading cause of delayed graft function. Unlike acute renal failure in native kidneys, delayed graft function is highly predictive of chronic nephropathy and organ failure. It is generally well accepted that acute reversible injuries mediated by ischemia render grafts susceptible toward future demise. The nature of the susceptibility that is conveyed to grafts following ischemic injury is not well understood.

RECENT FINDINGS

Evidence from animal models suggests that acute injury results in microvascular damage and vessel loss in the kidney, which, as opposed to tubular damage, is largely persistent. In addition, various studies of biopsies of renal transplants suggest that ischemia imposes an early and sustained loss in peritubular capillaries in the transplanted graft. The loss of peritubular capillaries has been associated with nephropathies of diverse etiologies and may represent a single, common pathway towards progressive damage.

SUMMARY

It is hypothesized that rarefaction of peritubular capillaries represents a critical event, following ischemic injury, that permanently alters renal function and predisposes patients to the development of chronic renal insufficiency. Factors that affect vascular reactivity or the structural dynamics of the kidney vascular system following injury may represent future treatment modalities following renal injury.

摘要

综述目的

急性肾衰竭患者若康复,一般不会预期出现长期肾脏并发症。然而,随着急性肾衰竭发病率上升,长期并发症的发生率可能也会增加。作为缺血性急性肾衰竭的一个必然结果,移植过程中的缺血损伤是移植肾功能延迟的主要原因。与天然肾脏的急性肾衰竭不同,移植肾功能延迟是慢性肾病和器官衰竭的高度预测指标。普遍认为,由缺血介导的急性可逆性损伤会使移植肾易于出现未来的功能丧失。缺血损伤后移植肾易感性的本质尚未完全明了。

最新发现

动物模型的证据表明,急性损伤会导致肾脏微血管损伤和血管丢失,与肾小管损伤不同,这种损伤在很大程度上是持续性的。此外,多项肾移植活检研究表明,缺血会导致移植肾中肾小管周围毛细血管早期且持续的丢失。肾小管周围毛细血管的丢失与多种病因的肾病有关,可能代表了一条导致进行性损伤的共同途径。

总结

据推测,肾小管周围毛细血管稀疏是缺血损伤后的一个关键事件,它会永久性改变肾功能,并使患者易患慢性肾功能不全。影响损伤后血管反应性或肾脏血管系统结构动力学的因素可能代表肾损伤后的未来治疗方式。

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