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Kidney-lung cross-talk and acute kidney injury
Rajit K Basu1, Derek S Wheeler
1Division of Critical Care Medicine and the Center for Acute Care Nephrology, Cincinnati, OH, 45229, USA, rajit.basu@cchmc.org.
Insights
Acute kidney injury (AKI) worsens critical illness in children, especially when combined with acute lung injury (ALI). Understanding kidney-lung crosstalk is vital for managing critically ill children.
Area of Science:
- Critical care medicine
- Pediatric nephrology
- Pulmonology
Background:
- Acute kidney injury (AKI) is increasingly recognized as a significant factor in critical illness severity.
- In children, AKI independently predicts morbidity and mortality, with worse outcomes when co-occurring with acute lung injury (ALI).
- Existing research indicates bidirectional, deleterious kidney-lung crosstalk, but molecular mechanisms require further elucidation.
Purpose of the Study:
- To review the pathophysiology of kidney-lung crosstalk in critically ill children.
- To explore the pathways through which AKI impacts kidney-lung homeostasis.
- To highlight unique aspects of these interactions in pediatric critical illness.
Main Methods:
- Literature review focusing on experimental and clinical data.
- Analysis of the impact of ALI on kidney function and AKI on lung physiology.
- Discussion of the endocrine role of the kidney in extra-renal inflammatory responses.
Main Results:
- ALI and its treatments can disrupt kidney function homeostasis.
- AKI adversely affects lung physiology by altering fluid balance, acid-base balance, and vascular tone.
- Experimental models suggest AKI can initiate inflammatory cascades impacting lung health.
Conclusions:
- Kidney-lung crosstalk is a critical factor in pediatric critical illness.
- AKI significantly disrupts the homeostatic communication between kidneys and lungs.
- Understanding these interactions is essential for optimizing care in critically ill children.
Abstract:
There is a growing appreciation for the role that acute kidney injury (AKI) plays in the propagation of critical illness. In children, AKI is not only an independent predictor of morbidity and mortality, but is also associated with especially negative outcomes when concurrent with acute lung injury (ALI). Experimental data provide evidence that kidney-lung crosstalk occurs and can be bidirectionally deleterious, although details of the precise molecular mechanisms involved in the AKI-ALI interaction remain incomplete. Clinically, ALI, and the subsequent clinical interventions used to stabilize gas exchange, carry consequences for the homeostasis of kidney function. Meanwhile, AKI negatively affects lung physiology significantly by altering the homeostasis of fluid balance, acid-base balance, and vascular tone. Experimental AKI research supports an "endocrine" role for the kidney, triggering a cascade of extra-renal inflammatory responses affecting lung homeostasis. In this review, we will discuss the pathophysiology of kidney-lung crosstalk, the multiple pathways by which AKI affects kidney-lung homeostasis, and discuss how these phenomena may be unique in critically ill children. Understanding how AKI may affect a "balance of communication" that exists between the kidneys and the lungs is requisite when managing critically ill children, in whom imbalance is the norm.
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