Basu Rajit K, Wheeler Derek
Division of Critical Care Medicine, Cincinnati Children's Hospital Medical Center, 3333 Burnet Avenue, Cincinnati, OH 45229, USA.
Pulm Med. 2011;2011:414253. doi: 10.1155/2011/414253. Epub 2011 May 24.
Pulmonary edema worsens the morbidity and increases the mortality of critically ill patients. Mechanistically, edema formation in the lung is a result of net flow across the alveolar capillary membrane, dependent on the relationship of hydrostatic and oncotic pressures. Traditionally, the contribution of acute kidney injury (AKI) to the formation of pulmonary edema has been attributed to bulk fluid accumulation, increasing capillary hydrostatic pressure and the gradient favoring net flow into the alveolar spaces. Recent research has revealed more subtle, and distant, effects of AKI. In this review we discuss the concept of nephrogenic pulmonary edema. Pro-inflammatory gene upregulation, chemokine over-expression, altered biochemical channel function, and apoptotic dysregulation manifest in the lung are now understood as "extra-renal" and pulmonary effects of AKI. AKI should be counted as a disease process that alters the endothelial integrity of the alveolar capillary barrier and has the potential to overpower the ability of the lung to regulate fluid balance. Nephrogenic pulmonary edema, therefore, is the net effect of fluid accumulation in the lung as a result of both the macroscopic and microscopic effects of AKI.
肺水肿会加重重症患者的发病率并增加死亡率。从机制上讲，肺内水肿的形成是跨肺泡毛细血管膜净流量的结果，取决于流体静压和胶体渗透压的关系。传统上，急性肾损伤（AKI）对肺水肿形成的作用归因于体液大量积聚，增加毛细血管流体静压以及有利于液体净流入肺泡腔的梯度。最近的研究揭示了AKI更细微、更间接的影响。在本综述中，我们讨论肾源性肺水肿的概念。肺内促炎基因上调、趋化因子过度表达、生化通道功能改变和凋亡失调现在被认为是AKI的“肾外”和肺部效应。AKI应被视为一种改变肺泡毛细血管屏障内皮完整性并有可能破坏肺调节液体平衡能力的疾病过程。因此，肾源性肺水肿是AKI宏观和微观效应导致肺内液体积聚的净效应。
