CAPILLARY LEAK SYNDROME: THE PULMONARY COST OF RESUSCITATING ACUTE KIDNEY INJURY.

Acute kidney injury is often accompanied by hypoperfusion and oliguria. The standard approach, which includes aggressive fluid resuscitation to restore urine output, can lead to iatrogenic complications, the most critical being capillary leak syndrome with subsequent development of pulmonary edema. We present a clinical case that clearly illustrates this pathophysiological phenomenon.

Patient M, 70 years old, was admitted with AKI (Acute Kidney Injury) due to obstruction of the right kidney and ureter. Initial Findings: Chest CT: No pathology detected. Echocardiography: LVEF 50%. IVC 1.3 cm with >50% collapsibility, E/e' = 8. CRP 236 mg/L, WBC 14 K/μL. A percutaneous nephrostomy was performed. Due to persistent hypotension, aggressive fluid resuscitation was initiated, resulting in a positive daily fluid balance of +4200 mL with a urine output of 950 mL. The patient's condition worsened over 24 hours, with progressive respiratory failure and hypotension, necessitating transfer to the Intensive Care Unit (ICU). The patient rapidly developed severe ARDS (Chest CT: bilateral pleural effusions and interstitial edema), requiring respiratory and vasopressor support. Lung Ultrasound: Revealed multiple B-lines bilaterally. Echocardiography Dynamics: Showed a significant decrease in LVEF to 38-40%, an increase in IVC diameter to 1.7 cm, LVOT VTI 12 cm, E/e' = 10. These findings are consistent with combined systolic and diastolic dysfunction induced by fluid overload ("fluid overload cardiomyopathy") and sepsis. Treatment: Continuous Veno-Venous Hemodiafiltration (CVVHDF) with active ultrafiltration was initiated. This led to hemodynamic stabilization and regression of respiratory failure, allowing for de-escalation of respiratory support.

The development of life-threatening complications in our patient is a classic example of capillary leak syndrome. The pathophysiological basis can be represented as a 3-phase process: Ischemic Phase: Urinary tract obstruction leads to endothelial dysfunction and activation of the inflammatory cascade. Reperfusion Phase: Following decompressive nephrostomy, blood flow is restored, but the endothelium remains damaged and hyperpermeable. Leak Phase: Aggressive fluid resuscitation causes a sharp increase in hydrostatic pressure within the systemic capillaries. Combined with the underlying endothelial permeability, this results in massive fluid extravasation into the interstitium. The clinical manifestations include non-cardiogenic pulmonary edema, pleural effusions, and refractory vasodilatory hypotension. Given their extensive capillary network, the lungs become the primary target for fluid sequestration in systemic endothelial injury. Mechanism of Respiratory Failure Development: Interstitial edema→Impaired gas diffusion →Hypoxemia→ARDS.

We advocate for the rational use of infusion therapy, adhering to the principles of Fluid Stewardship: Rapid, aggressive fluid resuscitation should be limited to the initial resuscitation phase in septic shock to restore perfusion. Early initiation of vasopressors (e.g., norepinephrine) to minimize volume overload and stabilize hemodynamics. Continuous re-assessment of volume status, evaluating the response to fluid boluses based on dynamic changes in HR, BP, and urine output. Timely de-escalation: After stabilization, aim for a negative fluid balance using diuretics or renal replacement therapy. Mandatory monitoring of volume status using ultrasound (IVC, BLUE protocol) and dynamic assessment of daily fluid balance is essential in managing these patients. Evidence Base: The FACTT Trial demonstrated that a positive fluid balance was associated with increased duration of mechanical ventilation and mortality in patients with ARDS. The PICARD Study showed that cumulative fluid overload (>10%) at the initiation of RRT was an independent predictor of mortality (58% vs. 32% in the group with <10% overload). Every 1% increase in fluid overload was associated with a 6% increase in the risk of death. The RENAL Trial, along with a systematic review and meta-analysis "Fluid overload and mortality in critically ill patients with acute kidney injury," have conclusively and independently confirmed that fluid overload is an independent risk factor for mortality in patients with AKI.