Abstract
Acute Kidney Injury (AKI) is an independent risk factor for mortality in hospitalized patients. AKI syndrome leads to fluid overload, electrolyte and acid-base disturbances, immunoparalysis, and propagates multiple organ dysfunction through organ “crosstalk”. Preclinical models suggest AKI causes acute lung injury (ALI), and conversely, mechanical ventilation and ALI cause AKI. In the clinical setting, respiratory complications are a key driver of increased mortality in patients with AKI, highlighting the bidirectional relationship. This article highlights the challenging and complex interactions between the lung and kidney in critically ill patients with AKI and acute respiratory distress syndrome (ARDS) and global implications of AKI. We discuss disease-specific molecular mediators and inflammatory pathways involved in organ crosstalk in the AKI-ARDS construct, and highlight the reciprocal hemodynamic effects of elevated pulmonary vascular resistance and central venous pressure (CVP) leading to renal hypoperfusion and pulmonary edema associated with fluid overload and increased right ventricular afterload. Finally, we discuss the notion of different ARDS “phenotypes” and the response to fluid overload, suggesting differential organ crosstalk in specific pathological states. While the directionality of effect remains challenging to distinguish at the bedside due to lag in diagnosis with conventional renal function markers and lack of tangible damage markers, this review provides a paradigm for understanding kidney-lung interactions in the critically ill patient.
Highlights
Acute respiratory distress syndrome (ARDS) is a life-threatening condition and a leading cause of mortality in critically ill patients causing nearly 200,000 deaths in the United States each year [1]
The angiopoietin/Tie-2 signaling axis plays an important role in vascular development during nephrogenesis, and a study of renal transplant recipients demonstrated that renal ischemia/reperfusion injury leads to rapid release of Ang2, suggesting that Ang-2 could contribute to the development of acute respiratory distress syndrome (ARDS) in patients with acute kidney injury (AKI) [12, 58, 59]
Especially around mechanistic pathways in each syndrome, has enhanced our appreciation of the actual scale of organ crosstalk that extends beyond fluid accumulation and its management in AKI and ARDS
Summary
Acute respiratory distress syndrome (ARDS) is a life-threatening condition and a leading cause of mortality in critically ill patients causing nearly 200,000 deaths in the United States each year [1]. There are many challenging and complex interactions between the lung and kidney in critically ill patients with AKI and ARDS (Figure 1) These include disease specific molecular mediators and inflammatory pathways unique to ARDS and AKI that are involved in organ crosstalk. There are likely reciprocal hemodynamic effects of elevated pulmonary vascular resistance and central venous pressure (CVP) leading to renal hypoperfusion and pulmonary edema associated with fluid overload, which could lead to increased right ventricular afterload. Each of these interactions contribute to the ARDS-AKI construct and highlight how the implications of AKI go beyond just the kidney. This review provides a paradigm for understanding the kidney-lung interactions in critically ill patients
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