there is no study in patients with CKD on peritoneal dialysis (PD). The present study aimed to evaluate the eﬀects of propolis supplementation on inﬂammatory markers in patients with CKD on PD. METHODS: This is a longitudinal, randomized, double-blind, placebo-controlled trial with 19 patients randomized into two groups: propolis (4 capsules of 500 mg/day containing concentrated and standardized dry EPP-AF R  green propolis extract) or placebo (4 capsules of 500 mg/day of magnesium stearate, silicon dioxide and microcrystalline cellulose as placebo) for 2 months. The inﬂammatory cytokines plasma levels such as TNF-α and interleukin-6 (IL-6) were evaluated by ELISA, and quantitative real-time PCR analyses were performed to evaluate the mRNA expression of NF-kB in peripheral blood mononuclear cells (PBMCs). Plasma malondialdehyde (MDA) levels, a peroxidation lipid marker, was measured as thiobarbituric acid reactive substances (TBARS). Routine parameters, including C-reactive protein (CRP), were analyzed using commercial kits. RESULTS: All patients concluded the study: 10 patients in the propolis group [57.2 ± 13.7 years, ﬁve men, 6 (6–36) months on DP] and 9 in the placebo group [56.6 ± 14.7 years, two men, 6 (6–57) months on DP]. The obtained data revealed that the intervention did not aﬀect the mRNA expression of NF-κ B. However, the plasma levels of TNF-α reduced signiﬁcantly after propolis supplementation (Table 1 and Fig. 1). There were no signiﬁcant diﬀerences in the placebo group. CONCLUSION: Short-term EPP-AF R  propolis dry extract supplementation seems to mitigate inﬂammation, reducing the plasma levels of TNF-α in patients with CKD on PD. MO586 LOW-PROTEIN DIET SUPPLEMENTED WITH KETOANALOGUES OF ESSENTIAL AMINO ACIDS IN ADVANCED DIABETIC KIDNEY DISEASE: SAFETY ISSUES IN ELDERLY Carmen-Antonia Mocanu 1,2 , Tudor Petrisor Simionescu 2 , Andreea Elena Mocanu 2 , Gabriel Mircescu 1,2 and Liliana Garneata 1,2 1 Carol Davila University of Medicine and Pharmacy, Internal Medicine and Nephrology, Bucharest, Romania and 2 ‘Dr Carol Davila’ Teaching Hospital of Nephrology, Nephrology, Bucharest, Romania BACKGROUND AND AIMS: Lately, studies support the role of dietary protein restriction in the management of patients with chronic kidney disease (CKD). Beneﬁcial eﬀects were noticed in ameliorating metabolic disturbances in advanced CKD and optimizing the blood pressure control, thus postponing kidney replacement therapy. However, nutritional safety of low-protein diets (LPDs) remains debatable, especially in elderly. This prospective unicenter interventional study aimed to assess the eﬀects of LPD in advanced diabetic kidney disease (DKD). We present a sub-analysis of data focusing on the safety in elderly patients. METHOD: Ninety-two patients with DKD with stable CKD stage 4+, heavy proteinuria (>3 g/g creatininuria), good nutritional status (Subjective Global Assessment—SGA A) and compliant to protein restriction proved during a 3- month run-in phase (21% of the screened population) were enrolled and received conventional LPD (0.6 g mixed protein/kg-day) supplemented with ketoanalogues of essential amino acids (Ketosteril R , Bad Homburg, Germany), 1 tb/10 kg dry ideal body weight per day (sLPD) for 12 months. Eﬃcacy outcomes were the variation of proteinuria (primary outcome) and the variation of estimated glomerular ﬁltration rate, eGFR (secondary outcome). Safety was assessed throughout the study using anthropometric measures (Body Mass Index, BMI), SGA, serum albumin (SAlb). Inﬂammatory parameters (C-reactive protein, CRP) and the occurrence of adverse reactions were also recorded. Compliance was evaluated using urinary urea from 24-h urine collection to estimate the protein intake (ePI) and the 3-day food diary for energy intake (EnI). RESULTS: Ninety-two patients [61% males, median age 61 (58–67) years, eGFR 11.7 (11.2–12.2) mL/min/1.73 m2, proteinuria 4.8 (4.6–5.2) g/g creatininuria] completed the study. For the whole group, proteinuria decreased with 67% from the baseline to the end of study (EOS), and the rate of decline in eGFR was reduced with 80% compared with the period before enrolment. Of the total group, 42% (39 patients) were elderly (≥65 years): median age 75 (71–80) years old, 64% males, median eGFR 12.61 (11.16–13.81) mL/min and median proteinuria 5.14 (4.84–5.25) g/g creatininuria. About 21% (19 patients) were late elderly (≥75 years old). In elderly, proteinuria signiﬁcantly decreased: 1.51 (0.98–1.75) versus 5.14 (4.84– 5.26) g/g creatininuria, i.e. by 70% of the baseline value. eGFR also signiﬁcantly decreased: 10.73 (9.87–11.68) versus 12.61 (11.16–13.81) mL/min. To note, the rate of decline in kidney function was 0.1 versus 0.5 mL/min-month before enrolment, i.e. 5 times slower. The nutritional status was improved: BMI decreased [25.58 (24.68–26.98) versus 27.08 (25.47–28.11) kg/m2 at baseline] and the percentage of overweighted subjects declined (56.4 versus 76.9%), while SGA did not change during the study. SAlb was also stable: 4.19 (4.03–4.30) versus 3.90 (3.86–3.99) mg/dL. The inﬂammatory status was signiﬁcantly ameliorated: CRP decreased, 8 (7–9) versus 14 (12–15) at baseline mg/L. Thus, by the EOS the percentage of patients with inﬂammation (CRP ≥ 10 mg/L) signiﬁcantly decreased: 23.1 versus 92.3% at baseline. The ePI and EnI were very close to recommendations and remained stable during the study: 0.64 (0.63–0.67) versus 0.68 (0.65–0.69) g/kg-day for ePI and 31.30 (28.50–33.00) versus 31.16 (30.16–32.56) kcal/kg-day for EnI at EOS versus baseline, respectively. In a binary regression analysis, lower levels of CRP were associated with sLPD, lower proteinuria and higher SAlb (P < 0.0001, Negelkerke R Square test 58%, Hosmer & Lemeshow test 0.11). No adverse reactions were noted. CONCLUSION: In elderly patients with advanced DKD, low protein diet supplemented with ketoanalogues of essential amino acids seems to be eﬀective in reducing the decline in eGFR and proteinuria, while being also nutritionally safe. MO587 CHRONIC KIDNEY DISEASE INDUCES ENDOTOXIN-RELATED ACTIVATION OF THE INNATE IMMUNE SYSTEM Sander Dejongh 1 , Mara Lauriola 1 , Pieter Evenepoel 1 , Ricard Farré 2 and Björn Meijers 1 1 KU Leuven, Nephrology and Renal Transplantation Research Group, Leuven, Belgium and 2 KU Leuven, Translational Research Center for Gastrointestinal Disorders (TARGID), Leuven, Belgium BACKGROUND AND AIMS: Chronic inﬂammation is common in patients with chronic kidney disease (CKD) and is associated with poor outcomes. Although the etiology is only partly understood, the gut–kidney axis is considered an important contributor [1]. Lipopolysaccharide (LPS), also known as endotoxin, is a well- characterized pyrogen found in the exterior cell membrane of most of the gram- negative bacteria. It plays an important role in promoting intestinal inﬂammatory responses. When absorbed through the intestinal epithelium, LPS induces inﬂammation by activating macrophages and monocytes. Due to short half-life and semi-quantitative assay characteristics of the Limulus Amebocyte Lysate (LAL) assay, direct quantiﬁcation of LPS is not suitable to quantify activation of the innate immune system. Lipoprotein-binding protein (LBP), a more stable biomarker, is an acute phase protein produced mostly by the hepatocytes and intestinal epithelial cells and is an essential component of an eﬀective innate immune response to LPS. Circulating LBP signiﬁcantly enhances the sensitivity of CD14 + cells (mostly monocytes and macrophages) to stimulation by LPS. LBP has been shown to facilitate binding of LPS to CD14 receptor. Levels of LBP peak in serum shortly after endotoxemia and remain increased up to 72 h later. An increased plasma LBP indicates gut epithelial barrier dysfunction [2]. Whether LBP is altered by CKD is not known. METHOD: We analyzed the eﬀects of CKD on LBP plasma concentrations. We used samples from the Leuven mild-to-moderate CKD cohort (NCT00441623). To study causality, we used animal models of experimentally induced CKD. To exclude model- related bias, two diﬀerent rat models of CKD, i.e. 5/6th nephrectomy and adenine supplementation, were used. LBP was measured using commercially available ELISA kits (Hycultbiotech, The Netherlands). RESULTS: In a cohort of 460 patients with CKD, we found a signiﬁcant increase in LBP levels across the diﬀerent stages of CKD (ANOVA, P: 0.001). When analyzed as a continuous variable, LBP is signiﬁcantly inversely correlated with eGFR (P < 0.001; Spearman, r: −0.221), and positively correlated with CRP (P < 0.001; Spearman, r: 0.592). During a median follow-up of 56 (IQR, 53–59) months, 70 patients died, with more deaths observed among patients with LBP in higher tertiles [tertiles 1–3: 11, 22, and 37 events, respectively (Fig. 1)]. In univariate Cox proportional hazard analysis, plasma LBP was signiﬁcantly associated with mortality [hazard ratio (HR) of 1.032; 95% conﬁdence interval (95% CI): 1.014– 1.046; P < 0.001). This association remained signiﬁcant in multivariate models with adjustment for age, sex and BMI. In two diﬀerent rat models, induction of CKD resulted in a signiﬁcant increase in LBP (P < 0.001). In these animals, we observed a signiﬁcant inverse association between eGFR (and measured creatinine clearance) and LBP concentrations (P < 0.001; Spearman, r: −0.460). CONCLUSION: Patients with CKD have higher levels of LBP, with higher levels of plasma LBP present in patients with more advanced CKD. Plasma LBP is an independent predictor of mortality. Experimentally induced CKD equally results in signiﬁcantly increased LBP. Our data suggest that CKD leads to increased passage of LPS across the intestinal barrier. These ﬁndings strengthen the hypothesis of the gut–kidney axis as a source of chronic inﬂammation. REFERENCES 1. Meijers BK and Evenepoel P: The gut-kidney axis: indoxyl sulfate, p-cresyl sulfate and CKD progression. Nephrol Dial Transplant. 2011 2. Seethaler B, Basrai M, Neyrinck AM et al. Biomarkers for assessment of intestinal permeability in clinical practice. Am J Physiol Gastrointest Liver Physiol. 2021 i430 Abstract Downloaded from https://academic.oup.com/ndt/article/37/Supplement_3/gfac074.032/6577531 by guest on 04 March 2023