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Factors of microinflammation in non-diabetic chronic kidney disease: a pilot study

Authors
  • Olivier, Valerie1
  • Dunyach-Remy, Catherine2
  • Corbeau, Pierre3
  • Cristol, Jean-Paul4, 5
  • Sutra, Thibault4, 5
  • Burtey, Stephane6
  • Lavigne, Jean-Philippe2
  • Moranne, Olivier1, 7
  • 1 Caremeau Hospital, University Montpellier-Nîmes, CHU Nîmes, Nimes, France , Nimes (France)
  • 2 U1047, INSERM, University of Montpellier, CHU Nîmes, Nîmes, France , Nîmes (France)
  • 3 CNRS-University of Montpellier, Montpellier, France , Montpellier (France)
  • 4 University of Montpellier, Montpellier, France , Montpellier (France)
  • 5 CHU Montpellier, Montpellier, France , Montpellier (France)
  • 6 C2VN, INSERM 1263, INRA 1260, Aix-Marseille University, Marseille, France , Marseille (France)
  • 7 University of Montpellier, Nîmes, France , Nîmes (France)
Type
Published Article
Journal
BMC Nephrology
Publisher
Springer (Biomed Central Ltd.)
Publication Date
Apr 21, 2020
Volume
21
Issue
1
Identifiers
DOI: 10.1186/s12882-020-01803-y
Source
Springer Nature
Keywords
License
Green

Abstract

BackgroundThe relationships between digestive bacterial translocation, uremic toxins, oxidative stress and microinflammation in a population of chronic kidney disease (CKD) patients without metabolic nor inflammatory disease are unknown.MethodsBacterial translocation, uremic toxins, oxidative stress, and inflammation were assessed by measuring plasma levels of 16S ribosomal DNA (16S rDNA), p-cresyl sulfate (PCS), indoxyl sulfate (IS), indole acetic acid (IAA), F2-isoprostanes, hsCRP and receptor I of TNFα (RITNFα) in patients without metabolic nor inflammatory disease. 44 patients with CKD from stage IIIB to V and 14 controls with normal kidney function were included from the nephrology outpatients. 11 patients under hemodialysis (HD) were also included. Correlations between each factor and microinflammation markers were studied.Results16S rDNA levels were not increased in CKD patients compared to controls but were decreased in HD compared to non-HD stage V patients (4.7 (3.9–5.3) vs 8.6 (5.9–9.7) copies/μl, p = 0.002). IS, PCS and IAA levels increased in HD compared to controls (106.3 (73.3–130.4) vs 3.17 (2.4–5.1) μmol/l, p < 0.0001 for IS; 174.2 (125–227.5) vs 23.7 (13.9–52.6) μmol/l, p = 0.006 for PCS; and 3.7 (2.6–4.6) vs 1.3 (1.0–1.9) μmol/l, p = 0.0002 for IAA). Urea increased in non-HD stage V patients compared to controls (27.6 (22.7–30.9) vs 5.4 (4.8–6.4) mmol/l, p < 0.0001) and was similar in HD and in non-HD stage V (19.3 (14.0–24.0) vs 27.6 (22.7–30.9) mmol/l, p = 0.7). RITNFα levels increased in HD patients compared to controls (12.6 (9.6–13.3) vs 1.1 (1.0–1.4) ng/ml, p < 0.0001); hsCRP levels increased in non-HD stage V patients compared to controls (2.9 (1.4–8.5) vs 0.8 (0.5–1.7) mg/l, p = 0.01) and remained stable in HD patients (2.9 (1.4–8.5) vs 5.1 (0.9–11.5) mg/l, p = 1). F2-isoprostanes did not differ in CKD patients compared to controls. Among uremic toxins, IS and urea were correlated to RITNFα (r = 0.8, p < 0.0001 for both). PCS, IS and urea were higher in patients with hsCRP≧5 mg/l (p = 0.01, 0.04 and 0.001 respectively). 16S rDNA, F2-isoprostanes were not correlated to microinflammation markers in our study.ConclusionsIn CKD patients without any associated metabolic nor inflammatory disease, only PCS, IS, and urea were correlated with microinflammation. Bacterial translocation was decreased in patients under HD and was not correlated to microinflammation.

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