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Plasma Lipopolysaccharide Concentrations in Cardiorenal Syndrome Type 1

Grazia Maria Virzì^1,2, Andrea Breglia^3,4, Ghada Ankawi^3,5

¹IRRIV-International Renal Research Institute Vicenza, Vicenza, Italy, graziamaria.virzi@gmail.com.

Cardiorenal Medicine

|June 26, 2019

Insights

Lipopolysaccharide (LPS) levels are elevated in cardiorenal syndrome (CRS) type 1, correlating with kidney injury markers. This suggests LPS may be a key factor in CRS type 1 pathophysiology.

Area of Science:

Nephrology
Cardiology
Immunology

Background:

Cardiorenal syndrome (CRS) type 1 involves acute heart failure (AHF) leading to acute kidney injury (AKI).
The role of lipopolysaccharide (LPS) in CRS type 1 pathophysiology remains unclear.

Purpose of the Study:

To investigate the association between plasma LPS levels and renal parameters in AHF patients with CRS type 1.
To explore LPS as a potential pathophysiological factor in CRS type 1.

Main Methods:

32 AHF patients were studied, with 15 diagnosed with CRS type 1.
Plasma LPS concentrations were measured alongside renal markers like serum creatinine, urea, NGAL, and cystatin C.

Main Results:

LPS levels were significantly higher in CRS type 1 patients compared to controls.
A positive correlation was observed between LPS levels and markers of kidney injury (NGAL, serum creatinine, urea).

Conclusions:

Elevated LPS levels are present in CRS type 1.
LPS may play a significant role in the development of AKI in AHF patients, warranting further investigation.

Read full analysis

Abstract

Background:

Cardiorenal syndrome (CRS) type 1 is characterized by a rapid worsening of cardiac function that leads to acute kidney injury (AKI). This study evaluated the role of lipopolysaccharide (LPS) in the development of AKI in patients with acute heart failure (AHF) and its relationship with renal parameters, to enable a better comprehension of the pathophysiology of CRS type 1.

Methods:

We enrolled 32 AHF patients, 15 of whom were classified as having CRS type 1. Eight of these 15 exhibited AKI at the time of admission (caused by AHF) and the other 7 developed AKI during their stay in hospital (in the first 48 h). We evaluated the plasmatic LPS concentrations as well as conventional (serum creatinine [sCr] and urea) and unconventional (neutrophil gelatinase-associated lipocalin [NGAL] and cystatin C) renal markers.

Results:

LPS levels were significantly higher in the CRS type 1 patients. No significant difference in LPS level was found in patients who were admitted with AKI and those developed AKI in hospital, but there was a tendency towards a higher level of LPS in CRS type 1 patients admitted with AKI. The LPS concentrations at admission were similar in CRS type 1 survivors (n = 12) and nonsurvivors (n = 3) (p = 0.22). We observed a positive correlation between LPS level and NGAL, Scr at admission and peak Scr during hospitalization and urea at admission.

Conclusion:

CRS type 1 patients present with an increased level of LPS and there is a direct correlation between LPS and renal parameters. This pilot research is the first study to explore the premise of LPS as novel pathophysiological factor in CRS type 1.

Keywords:

Acute kidney injury Cardiorenal syndrome Heart failure Lipopolysaccharide

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