Organ Crosstalk During Injury: Mechanisms of Lung-Kidney Interaction in Critical Illness.

Summary

This authoritative review synthesizes mechanisms underpinning bidirectional lung–kidney crosstalk in critical illness. It catalogues multiple pathways by which AKI drives lung injury (e.g., leukocyte recruitment, PRR activation, NETs, osteopontin, metabolic dysfunction, impaired alveolar fluid clearance) and how lung injury promotes AKI via inflammation, mechanical ventilation, and fluid strategies.

Key Findings

• Comprehensive synthesis of mechanisms whereby AKI induces lung injury, including leukocyte recruitment, PRR activation, NET formation, osteopontin signaling, metabolic dysfunction, and impaired alveolar fluid clearance.
• Mechanisms by which lung injury precipitates AKI include systemic inflammation, effects of mechanical ventilation, and fluid management consequences.
• Evidence base is richer for lung injury after AKI than for AKI after lung injury, highlighting research gaps.

Clinical Implications

Highlights the need for lung-protective ventilation and judicious fluid management to reduce kidney-lung propagation of injury; suggests potential targets (e.g., NETs, osteopontin) for intervention.

Limitations

• Narrative (non-systematic) review with potential selection bias
• Heavily weighted toward preclinical evidence; limited causal human data

Future Directions

Prospective human studies validating identified pathways; interventional trials targeting NETs, osteopontin, or metabolic pathways; integrated protocols balancing ventilation and fluid strategies to minimize cross-organ injury.