3.1. Baseline characteristics of individuals with CKD
Table 1 shows the individual data of the CKD group, which was composed of 25 adults and elderly people (66±10 years) of both genders (12 women and 13 men). CKD was predominantly caused by type II DM (48%) or SAH (32%). The results showed no differences in the proportion between genders related to the main causes of CKD, SAH (female = 3; male = 5) or DM-II (female = 7; male = 4) (Fisher, p = 0.369) (Table 1).
The HD time for the study group was 4.7±4.9 years until conversion to HDF; venous access was predominantly by arteriovenous fistula (60%), followed by long-term catheter (36%).
The results showed no difference in the proportion between genders related to the main causes of CKD, SAH (Female = 3; Male = 5) or DM-II (Female = 7; Male = 4) (Fisher, p = 0.369). In addition, there was no difference in HD time between women and men (t test, p > 0.05); however, there was a negative correlation between HD time and the age of the individuals, that is, elderly individuals remained on HD longer (Spearman = 0.017).
3.2. Evaluation of haematological and biochemical parameters
Table 2 shows the results obtained for haematological and biochemical parameters.
A. Cells and platelets – The results showed that, there is no difference between HD e HDF for leukocytes and platelets (paired t-test, p > 0.05), but when compared to HD, HDF reduced the total EPO level and the EPO resistance index (paired t test, p < 0.05).
B. Metabolic markers – In comparison with HD, HDF caused a reduction in total glucose (Wilcoxon, p = 0.049) but did not affect serum levels of triglycerides and the three types of cholesterol (HDL, LDL and VLDL) (t test paired, p > 0.05).
C. Ionic and nutritional markers – Compared to HD, the serum values of ionic (HCO3-, Na+, K+, Mg2+, PO43-, Ca2+) and nutritional (vitamin D and albumin) markers were not affected by HDF (paired t test or Wilcoxon, p > 0.05).
D. Toxicity markers – The results showed that HDF, compared to HD, reduced the serum level of aspartate aminotransferase (AST) (Wilcoxon, p = 0.049) but did not alter the level of alanine aminotransferase (ALT) (paired t test, p > 0.05).
E. Inflammatory markers – Compared to HD, HDF increased serum levels of alkaline phosphatase (ALP) and C-reactive protein (CRP) (Wilcoxon, p < 0.05) but reduced ꞵ2-microglobulin (ꞵ2M) (paired t test, p = 0.038). However, HDF did not alter serum ferritin and parathyroid hormone levels (p > 0.05).
3.3. Evaluation of phagocytic capacity and production of lipid bodies and cytokines
Table 3 shows the results of phagocytic capacity (3.1) and the production of lipid bodies (3.2) and cytokines (3.3) of individuals with CKD before and 12 weeks after conversion from HD to HDF.
A. Phagocytosis – At a proportion of 5 or 20 yeasts/cell, the phagocytic index (PI) was lower with HD compared to HDF and the control (C > HD < HDF; Kruskal‒Wallis, p < 0.01), when phagocytosis was mediated by receptors for PMP or opsonins. This result was due to the lower recruitment of monocytes for phagocytosis for both receptors (C > HD < HDF; Kruskal‒Wallis, p < 0.001) but also due to the higher number of ingested yeasts in PMP-mediated phagocytosis (C > HD < HDF; Kruskal‒Wallis, p = 0.001). The PI did not differ from the control after conversion to HDF for either receptor (PMP or opsonins).
B. Lipid corpuscles – The basal production of LCs did not differ between the three groups (C ~ HD ~ HDF; ANOVA, p > 0.05); however, when the cells were stimulated, there was an increase in total LCs with HD compared to the control and HDF (C < HD > HDF; ANOVA, p = 0.018). In addition, HDF reduced the stimulated corpuscular index when compared to HD (HD > HDF; ANOVA, p = 0.040) (Table 3B).
C. Cytokines – The production of IL-2, IL-10, IL-17 and INF-γ did not differ between the three groups (C ~ HD ~ HDF; p > 0.05). However, there was higher production of IL-6 in HD and HDF compared to the control (HD > C < HDF; Kruskal‒Wallis, p = 0.001) and lower production of IL-4 in HD compared to the control (C > HD; Kruskal‒Wallis, p = 0.016). In addition, IL-4 and TNF production was higher in HDF than in HD (HD < HDF; Kruskal‒Wallis, p < 0.05).
3.4. Evaluation of superoxide (O2●-) production
Table 4 shows the percentage of cells that reduced the NBT salt (yellow) that, in the presence of O2●- (4.1), forms a blue-coloured pigment in the cytoplasm of the cells (4.2).
A. Basal production of O2●- – The percentage of NBT salt reduction was lower in the HD group than in the control and HDF groups (C > HD < HDF; ANOVA, p = 0.003).
B. Stimulated production of O2●- –
B1. With phagocytosis/with O2●- – The percentage of cells that phagocytized and produced O2●- was lower in HD compared to the control and HDF; HDF was also lower than the control (HDF < C > HD < HDF; ANOVA, p < 0.0001).
B2. Without phagocytosis/with O2●- – The percentage of cells that did not phagocytose but produced O2●- was lower in the HD group than in the control and HDF groups (C > HD < HDF; Kruskal‒Wallis, p = 0.007).
B3. With phagocytosis/without O2●- – The percentage of cells that phagocytized but did not produce O2●- was lower in the HD group than in the control and HDF groups; O2●- was also lower in the HDF group than in the control group (HDF < C > HD < HDF; Kruskal‒Wallis, p < 0.0001).
B4. Without phagocytosis/without O2●- – The percentage of cells that did not phagocytose and did not produce O2●- was lower in the HD group than in the control group (C > HD; Kruskal‒Wallis, p < 0.0001).