scholarly journals Effects of Ischemic Acute Kidney Injury on Lung Water Balance: Nephrogenic Pulmonary Edema?

2011 ◽  
Vol 2011 ◽  
pp. 1-6 ◽  
Author(s):  
Rajit K. Basu ◽  
Derek Wheeler
Keyword(s):  
Acute Kidney Injury ◽  
Pulmonary Edema ◽  
Disease Process ◽  
Kidney Injury ◽  
Fluid Accumulation ◽  
Lung Water ◽  
Edema Formation ◽  
Bulk Fluid ◽  
Capillary Membrane ◽  
Alveolar Capillary

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.

scholarly journals Acute kidney injury in patients with acute lung injury: Impact of fluid accumulation on classification of acute kidney injury and associated outcomes*

2011 ◽  
Vol 39 (12) ◽  
pp. 2665-2671 ◽  
Author(s):  
Kathleen D. Liu ◽  
B. Taylor Thompson ◽  
Marek Ancukiewicz ◽  
Jay S. Steingrub ◽  
Ivor S. Douglas ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Kidney Injury ◽  
Fluid Accumulation

Effect of eicosanoid inhibition on the development of pulmonary edema after acute lung injury

1996 ◽  
Vol 80 (3) ◽  
pp. 915-923 ◽  
Author(s):  
D. P. Schuster ◽  
A. H. Stephenson ◽  
S. Holmberg ◽  
P. Sandiford
Keyword(s):  
Acute Lung Injury ◽  
Oleic Acid ◽  
Lung Injury ◽  
Pulmonary Edema ◽  
Experimental Models ◽  
Nuclear Medicine Imaging ◽  
Lung Water ◽  
Edema Formation ◽  
Cyclooxygenase Inhibition ◽  
Positron Emission

In experimental models of acute lung injury, cyclooxygenase inhibition improves oxygenation, presumably by causing a redistribution of blood flow away from edematous lung regions. This effect on perfusion pattern could also reduce alveolar edema formation. On the other hand, pulmonary pressures usually increase after cyclooxygenase inhibition, an effect that could exacerbate edema accumulation. Therefore we tested the following hypothesis: the total accumulation of pulmonary edema in dogs during a 24- to 28-h period of observation after acute lung injury caused by oleic acid will be less in a group of animals treated with meclofenamate (n = 6) or with the thromboxane-receptor blocker ONO-3708 (n = 5) than in a group of animals treated with oleic acid alone (placebo, n = 6). Lung water concentrations (LWC), the regional pattern of pulmonary perfusion, and protein permeability were measured with the nuclear medicine imaging technique of positron emission tomography. After 24-28 h, LWC was significantly less (P < 0.05) in the ONO-3708 group than in the meclofenamate group (a similar trend was seen compared with the placebo group, P = 0.12). After 24-28 h, pulmonary arterial pressures were highest in the meclofenamate group. Regardless of group, the only significant correlation with the change in LWC was with the integral of pulmonary pressures over the 24- to 28-h period. The data suggest that thromboxane inhibition will reduce edema accumulation in acute lung injury but that this effect depends on reducing as much as possible the simultaneous development of pulmonary hypertension from other causes.

scholarly journals Rhodiola crenulataExtract Alleviates Hypoxic Pulmonary Edema in Rats

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Shih-Yu Lee ◽  
Min-Hui Li ◽  
Li-Shian Shi ◽  
Hsin Chu ◽  
Cheng-Wen Ho ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Pulmonary Edema ◽  
High Altitude ◽  
Hypobaric Hypoxia ◽  
Capillary Barrier ◽  
Lung Water ◽  
Stress Markers ◽  
Rhodiola Crenulata ◽  
High Altitude Illness ◽  
Alveolar Capillary

Sudden exposure of nonacclimatized individuals to high altitude can easily lead to high altitude illnesses. High altitude pulmonary edema (HAPE) is the most lethal form of high altitude illness. The present study was designed to investigate the ability ofRhodiola crenulataextract (RCE), an herbal medicine traditionally used as an antiacute mountain sickness remedy, to attenuate hypoxia-induced pulmonary injury. Exposure of animals to hypobaric hypoxia led to a significant increase in pathological indicators for pulmonary edema, including the lung water content, disruption of the alveolar-capillary barrier, and protein-rich fluid in the lungs. In addition, hypobaric hypoxia also increased oxidative stress markers, including (ROS) production, (MDA) level, and (MPO) activity. Furthermore, overexpression of plasma (ET-1), (VEGF) in (BALF), and (HIF-1α) in lung tissue was also found. However, pretreatment with RCE relieved the HAPE findings by curtailing all of the hypoxia-induced lung injury parameters. These findings suggest that RCE confers effective protection for maintaining the integrity of the alveolar-capillary barrier by alleviating the elevated ET-1 and VEGF levels; it does so by reducing hypoxia-induced oxidative stress. Our results offer substantial evidence to support arguments in favor of traditional applications ofRhodiola crenulatafor antihigh altitude illness.

scholarly journals Aggressive fluid accumulation is associated with acute kidney injury and mortality in a cohort of patients with severe pneumonia caused by influenza A H1N1 virus

PLoS ONE ◽  
2018 ◽  
Vol 13 (2) ◽  
pp. e0192592 ◽  
Author(s):  
Gustavo Alejandro Casas-Aparicio ◽  
Isabel León-Rodríguez ◽  
Rafael de Jesús Hernández-Zenteno ◽  
Manuel Castillejos-López ◽  
Claudia Alvarado-de la Barrera ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Influenza A ◽  
H1n1 Virus ◽  
Kidney Injury ◽  
Severe Pneumonia ◽  
Fluid Accumulation ◽  
Influenza A H1n1
Sign in / Sign up

Export Citation Format

Share Document