Pulmonary Congestion and Systemic Congestion in Hemodialysis: The Potential Role of Inflammation

 
Pulmonary Congestion and Systemic Congestion in Hemodialysis: The Potential Role of Inflammation
SALEH
KAYSI
BAKHTAR PACHA Bakhtar.Pacha@ulb.be Brugmann University Hospital NEPHROLOGY BRUXELLES
MARIE HELENE ANTOINE marie-helene.antoine@ulb.be Université libre de Bruxelles Laboratory of Experimental Nephrology BRUXELLES
ERIC DE PREZ Eric.De.Prez@ulb.be Université libre de Bruxelles Laboratory of Experimental Nephrology BRUXELLES
FREDERIC COLLART Frederic.COLLART@chu-brugmann.be Brugmann University Hospital NEPHROLOGY BRUXELLES
MAHMOUD BAZ MFBAZ@gmail.com GHEF NEPHROLOGY MEAUX
JOELLE NORTIER Joelle.NORTIER@chu-brugmann.be Brugmann University Hospital NEPHROLOGY BRUXELLES
 
 
 
 
 
 
 
 
 

Systemic congestion and pulmonary congestion PC are common in Haemodialysis HD patients. However, the relation between these two entities is not quite clear. Here we study this relation and try to find out the factors that may affect it, including exploring the role of inflammation. 

A prospective pilot observational study including 18 HD patients. We obtained 1-B-lines scores (BLS) by Lung Ultrasound (LUS) (Reflecting a significant pulmonary congestion if BLS>5), 2-echocardiography, 3-bioelectrical impedance analysis (BIA) (reflecting global volume status), and 4-inferior vena cava (IVC) dynamics (reflecting systemic congestion) before and after the first two consecutive HD sessions of the week, with different inter-dialytic intervals (68 hours, 44 hours). We also measured circulating markers of chronic inflammation; (soluble urokinase Plasminogen Activator Receptor [suPAR] and soluble Suppression of Tumorigenicity 2 [sST2]). Figure 1

We found no correlation between pulmonary congestion represented by BLS and IVC dimensions and dynamics reflecting systemic congestion.

Pulmonary congestion was quit prevalent as mean Pre and post-dialysis BLS were quite elevated (16 ± 5.53), (15.3 ± 6.63) in the first session as in the second one (16.3 ± 5.26), (13.6 ± 5.83). Mean values of BLS were not affected by a longer inter-dialysis interval, as they were not statistically different (68h vs 44h) and were strongly correlated (R²= 0.698, P<0.0001).

Systolic (Left Ventricular Ejection Fraction), diastolic cardiac function (e/è ratio) parameters, from one side and pulmonary congestion (BLS) from the other were not always correlated. BLS was correlated to e/è ratio before HD session 1 (R² =0.476, P=0.002) and after HD session 2 (R²=0.193, P=0.034).

Pulmonary congestion reflected by BLS was correlated to global volume state reflected by BIA only in the second HD session (HD2) (R²= 0.374, P= 0.007).

Systemic congestion was quit prevalent, as mean Pre and post-dialysis IVC dimensions and dynamics were quite elevated in both sessions, with a higher level of systemic congestion in the first HD session; (Diameter, Collapsibility) (2.1 cm, 23%) (2.01cm, 19%) compared to the second session (1.98cm, 17.5%) (1.9cm, 22%) without reaching statistical significance.

IVC dimensions and global volume status measured by BIA were correlated in the second dialysis session (R²=0.260, P=0.031). No correlation was found between IVC dimensions and diastolic cardiac function (e/è ratio) parameters.

Pre-dialysis Mean levels (± SD, ng/ml) of suPAR in the two sessions (7.88 ± 3.07), (7.78 ± 3.02) remained significantly above the normal range (< 4 ng/ml), while sST2 levels reached 2-fold the upper normal value in most patients (27.4 ± 17.8).Figure 2

Pulmonary congestion is common in HD patients even after reaching their dry weight at the end of two consecutive sessions, and it is not correlated to systemic congestion, suggesting a complex multifactorial pathophysiology origin.

Global volume status reflected by BIA and cardiac function are not always related to either systemic congestion represented by IVC dimensions nor to pulmonary congestion represented by BLS.

Chronic inflammation markers were elevated in HD patients, which may be one of the potential factors affecting the alveolar capillary barrier. This structure damage may allow pulmonary congestion accumulation independently from systemic congestion and global volume status (non-cardiogenic pulmonary congestion).

We recommend a personalised approach when managing HD patients integrating systemic and pulmonary congestion parameters.

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