title: Associations between renal function, volume status and endotoxaemia in chronic kidney disease patients.
abstract: Inflammation is an important predictor of increased cardiovascular morbidity and mortality in patients with chronic kidney disease (CKD), but the mechanisms behind the chronic activation of the immune system are not clearly understood. CKD patients develop fluid overload, which has been proposed to be a stimulus for inflammatory activation due to the translocation of macromolecules from the gut. We hypothesize that fluid overload is associated with signs of systemic inflammation and endotoxaemia in stages 1-5 CKD patients. The aim of this prospective study was to evaluate the associations between renal function, fluid status [evaluated by the inferior vena cava diameter (IVCD) and the collapsibility index (CI)], systemic inflammation [plasma levels of C-reactive protein (CRP), fibrinogen and albumin] and endotoxaemia (through the Limulus amebocyte lysate enzymatic assay) in a group of CKD patients in our out-patient clinic. The population consisted of 74 (mean of 57; range 23-83 years of age; 47% males) CKD patients with glomerular filtration rate (based on the mean of urea and creatinine clearances) of 34 ml/min. Both albumin (Rho = 0.25; P = 0.05) and fibrinogen (Rho= - 0.48; P < 0.0001) were significantly correlated to glomerular filtration rate (GFR). According to the IVCD, 84% of the patients were fluid overloaded, while 83% were considered overloaded by the CI. Signs of endotoxaemia were detected in all patients. Endotoxin levels were higher in patients with signs of fluid overload (0.85 +/- 0.11ng/l) when compared with patients with normal values of IVCD (0.61 +/- 0.05 ng/l; P < 0.05). Endotoxin levels correlated to both IVCD (Rho=0.33, P < 0.005) and CI (Rho = -0.25, P < 0.05). There was no correlation between endotoxin levels and GFR, CRP or fibrinogen. In summary, although most CKD patients presented signs of fluid overload that was associated with endotoxaemia, there was no association between endotoxaemia and systemic inflammation, suggesting the endotoxaemia may not be the main determinant of the inflammatory status in this group of patients.
authors.affiliation: Centro de Ciências Biológicas e da Saúde, Pontifícia Universidade Católica do Paraná, Rua Imaculada Conceição, 1155 Curitiba, PR 80215-901, Brazil.
authors.forename: Simone
authors.initials: S
authors.lastname: Gonçalves
authors.forename: Roberto
authors.initials: R
authors.lastname: Pecoits-Filho
authors.forename: Sônia
authors.initials: S
authors.lastname: Perreto
authors.forename: Silvio H
authors.initials: SH
authors.lastname: Barberato
authors.forename: Andréa E M
authors.initials: AE
authors.lastname: Stinghen
authors.forename: Emmanuel G A
authors.initials: EG
authors.lastname: Lima
authors.forename: Roseana
authors.initials: R
authors.lastname: Fuerbringer
authors.forename: Sirlene M
authors.initials: SM
authors.lastname: Sauthier
authors.forename: Miguel C
authors.initials: MC
authors.lastname: Riella
mesh_terms: D000368:Aged; D002097:C-Reactive Protein / Q000378:metabolism; D003404:Creatinine / Q000378:metabolism; D003430:Cross-Sectional Studies; D018450:Disease Progression; D019446:Endotoxemia / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D004731:Endotoxins / Q000378:metabolism; D005260:Female; D005340:Fibrinogen / Q000378:metabolism; D005919:Glomerular Filtration Rate; D006801:Humans; D007249:Inflammation / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D007668:Kidney / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D007676:Kidney Failure, Chronic / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D016014:Linear Models; D008297:Male; D008875:Middle Aged
chemical_list: D004731:Endotoxins; D005340:Fibrinogen; D002097:C-Reactive Protein; D003404:Creatinine