title: Correlation between volume overload, chronic inflammation, and left ventricular dysfunction in chronic kidney disease patients.
abstract: BACKGROUND
  Fluid overload is common in chronic kidney disease (CKD) patients, potentially driving chronic inflammation and left ventricular dysfunction. We investigated the association between volume overload, chronic inflammation, and left ventricular dysfunction across subgroups of CKD patients.
  
  
  METHODS
  The study included 160 participants, comprising peritoneal dialysis (PD), hemodialysis (HD), stage-3 CKD patients, and age- and sex-matched controls (40 in each group). Fluid status was assessed using a body composition monitor (BCM); serum endotoxin, lipopolysaccharide binding protein (LBP), C-reactive protein (CRP). and interleukin-6 (IL-6) levels were measured as markers of inflammation. Echocardiography was done to assess left ventricular dimension and function.
  
  
  RESULTS
  Endotoxemia and volume overload were common across the spectrum of CKD patients and were aggravated by worsening kidney function. Among HD cohorts, postdialysis endotoxemia was increased among patients with dialysis-induced hemodynamic instability and was also closely related to ultrafiltration volume. Endotoxin, IL-6, CRP, and LBP levels were elevated in patients with volume overload compared to euvolemic patients (p < 0.05). Patients with elevated circulating endotoxemia had higher left ventricular mass index (LVMI) compared to patients with lower endotoxin levels. Fluid overload correlated with endotoxin levels, IL-6, and LVMI; while LVMI correlated weakly with LBP and CRP.
  
  
  CONCLUSIONS
  CKD patients typically presented with significant endotoxemia and overt volume overload, which may contribute significantly to chronic low-grade inflammation and left ventricular dysfunction. An additive contribution from hemodialysis treatment may strongly enhance the severity of endotoxemia in HD patients.
authors: Muzamil Olamide
authors: MO
authors: Hassan
authors: Raquel
authors: R
authors: Duarte
authors: Therese
authors: T
authors: Dix-Peek
authors: Ahmed
authors: A
authors: Vachiat
authors: Sagren
authors: S
authors: Naidoo
authors: Caroline
authors: C
authors: Dickens
authors: Sacha
authors: S
authors: Grinter
authors: Pravin
authors: P
authors: Manga
authors: Saraladevi
authors: S
authors: Naicker
mesh_terms: D000209:Acute-Phase Proteins; D000328:Adult; D015415:Biomarkers / Q000097:blood; D001823:Body Composition / Q000502:physiology; D002097:C-Reactive Protein / Q000032:analysis; D002306:Cardiac Volume / Q000502:physiology*; D002352:Carrier Proteins / Q000097:blood; D016022:Case-Control Studies; D015331:Cohort Studies; D003430:Cross-Sectional Studies; D004452:Echocardiography / Q000379:methods; D004487:Edema / Q000503:physiopathology; D004731:Endotoxins / Q000097:blood; D045604:Extracellular Fluid / Q000378:metabolism; D006801:Humans; D007249:Inflammation; D015850:Interleukin-6 / Q000097:blood; D007676:Kidney Failure, Chronic / Q000503:physiopathology; D008562:Membrane Glycoproteins / Q000097:blood; D008875:Middle Aged; D010530:Peritoneal Dialysis / Q000379:methods; D006435:Renal Dialysis / Q000379:methods; D051436:Renal Insufficiency, Chronic / Q000000981:diagnostic imaging / Q000503:physiopathology* / Q000628:therapy; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging / Q000503:physiopathology*; D000099231:Lipopolysaccharide-Binding Protein
chemical_list: D000209:Acute-Phase Proteins; D015415:Biomarkers; D002097:C-Reactive Protein; D002352:Carrier Proteins; D004731:Endotoxins; D015850:Interleukin-6; D008562:Membrane Glycoproteins; D000099231:Lipopolysaccharide-Binding Protein; C508600:IL6 protein, human