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人类免疫缺陷病毒(HIV)相关性肾病的发病机制。

Pathogenesis of human immunodeficiency virus (HIV)-associated nephropathy.

作者信息

Schwartz E J, Klotman P E

机构信息

Division of Nephrology, Mount Sinai School of Medicine, New York, NY 10029, USA.

出版信息

Semin Nephrol. 1998 Jul;18(4):436-45.

PMID:9692355
Abstract

Human immunodeficiency virus-associated nephropathy (HIVAN) is the third leading cause of end-stage renal failure in Blacks between the ages of 20 and 64. Because the incidence of HIV infection has continued to increase in Blacks as survival has improved, the pool of patients alive and at risk for developing HIVAN has vastly expanded. This suggests that HIVAN will continue to increase in importance to the end-stage renal disease program. The racial predilection for the disease in Blacks implies that genetic or environmental cofactors are involved. Evidence in human and animal models has shown that proliferation of renal epithelial cells is the predominant feature of the disease and that apoptosis occurs. The prospect that renal infection is necessary to stimulate cells to proliferate remains a possibility but is not yet proven. Cytokine dysregulation may also be involved in disease progression, but evidence is lacking that altered cytokine production is the proximate cause of HIVAN. Many issues remain to be resolved including the potential for renal infection in vivo, the mechanisms responsible for proliferation and apoptosis, and factors that provide racial susceptibility to HIVAN. Advances in our understanding of pathogenesis will be required to control the growth of HIV-related renal diseases in the ESRD population.

摘要

人类免疫缺陷病毒相关性肾病(HIVAN)是20至64岁黑人终末期肾衰竭的第三大主要病因。由于随着生存率的提高,黑人中HIV感染的发病率持续上升,存活且有发生HIVAN风险的患者群体已大幅扩大。这表明HIVAN对终末期肾病项目的重要性将持续增加。该病在黑人中的种族偏好意味着存在遗传或环境协同因素。人和动物模型的证据表明,肾上皮细胞增殖是该病的主要特征,且发生了细胞凋亡。肾脏感染是刺激细胞增殖所必需的这一可能性仍然存在,但尚未得到证实。细胞因子失调也可能参与疾病进展,但缺乏证据表明细胞因子产生改变是HIVAN的直接病因。许多问题仍有待解决,包括体内肾脏感染的可能性、增殖和凋亡的机制,以及导致对HIVAN种族易感性的因素。需要在发病机制的理解上取得进展,以控制ESRD人群中HIV相关肾脏疾病的发展。

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