Immunotherapy for acute kidney injury

被引:5
作者
Berry, Miriam [1 ]
Clatworthy, Menna R. [1 ]
机构
[1] Univ Cambridge, Div Renal Med, Dept Med, Cambridge CB2 0XY, England
关键词
acute kidney injury; acute tubular necrosis; damage-associated molecular pattern; delayed graft function; IL-1; beta; inflammasome; neutrophil recruitment; ISCHEMIA-REPERFUSION INJURY; ACUTE-RENAL-FAILURE; DELAYED GRAFT FUNCTION; ACUTE TUBULAR-NECROSIS; STERILE INFLAMMATORY RESPONSE; COLD ISCHEMIA/REPERFUSION INJURY; RABBIT ANTITHYMOCYTE GLOBULIN; RANDOMIZED MULTICENTER TRIAL; CONTRAST-INDUCED NEPHROPATHY; B-CELL DEFICIENCY;
D O I
10.2217/IMT.11.175
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Acute renal failure, now referred to as acute kidney injury, is a common and clinically important problem. Acute kidney injury frequently occurs as a result of acute tubular necrosis (ATN), which is often caused by a reduction in systemic blood pressure or renal blood flow (e.g., as observed in severe sepsis or during renal transplantation). The disease course in ATN is variable, including prolonged dialysis-dependence and chronic renal dysfunction, but there is currently no specific therapy for ATN. There is increasing evidence that the inflammatory response in ATN significantly contributes to disease severity and outcome. In this review, we summarize recent developments in the understanding of how the immune system responds to dying cells, and the relevance of these discoveries to ATN. In particular, NLRP3 inflammasome activation and IL-1 beta-mediated neutrophil recruitment are likely to play a key role and may provide novel therapeutic targets for immunotherapy in ATN.
引用
收藏
页码:323 / 334
页数:12
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