The Association Between Central Venous Pressure and Acute Kidney Injury Development in Patients with Septic Shock

TL;DR

This study finds that higher central venous pressure in septic shock patients is linked to a greater risk of developing acute kidney injury.

Contribution

The study identifies specific time points (12 and 48 hours) where elevated CVP strongly predicts AKI, even after adjusting for blood pressure.

Findings

Elevated CVP levels at 6, 12, 24, and 48 hours are significantly higher in patients who develop AKI.

After adjusting for MAP, elevated CVP at 12 and 48 hours remains significantly associated with AKI.

The odds of AKI increase by 60% for patients with CVP ≥8 mmHg at 12 and 48 hours.

Abstract

Background: Sepsis-associated acute kidney injury (AKI) is linked to increased mortality and prolonged hospital stays. The exact relationship between central venous pressure (CVP) and AKI remains unclear. We explored the correlation between CVP and AKI in septic shock patients. Methods: This retrospective study included adult patients with septic shock admitted to Mayo Clinic Rochester between 2006 and 2018. CVP levels were measured at 6, 12, 24, and 48 h after the diagnosis of sepsis, and patients were stratified into two groups based on CVP levels (CVP < 8 or ≥8 mmHg). Results: Of 5600 patients with septic shock, 3128 patients without AKI on admission are included. One-thousand-and-ninety-eight patients (35.1%) developed AKI within a median of 4.4 days. The median CVP levels and frequency of elevated CVP at 6, 12, 24, and 48 h are significantly higher in the AKI group. Elevated CVP (≥8 mmHg) at 6, 12, 24, and 48 h is associated with AKI incidence, even after adjusting for mean arterial pressure (MAP) levels. This association, after multivariable adjustments, only remains significant at 12 h with an odds ratio (OR) of 1.60 (95% CI, 1.26–2.05), p < 0.001 and 48 h with an OR of 1.60 (95% CI, 1.29–1.99), p < 0.001. Conclusions: Our findings indicate that CVP ≥ 8 mmHg is strongly associated with an increased risk of AKI, even after adjusting for MAP at the 12 and 48 h time points. These findings underscore a critical 12 or 48h window for interventions to lower CVP.

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