**3. Results**

#### *3.1. Data Obtained during Recruitment*

The study population's demographic and descriptive data are shown in Tables 1 and 2 (divided as control and CKD stage-based subgroups) and Table 3 (divided as control and whole CKD group).

**Table 1.** Descriptive data of the subgroups together with statistical evaluation (Kruskal-Wallis ANOVA). Data are shown as mean ± SD and median (lower quartile–upper quartile).


Abbreviations: BP—blood pressure; eGFR—estimated glomerular filtration rate; LDL—low-density cholesterol; HDL—high-density cholesterol; TC—total cholesterol; TG—triglycerides; CV—Cardiovascular. 1,2,3,4—the result of the post-hoc analysis showing differences between the indicated groups.

**Table 2.** Qualitative risk factors occurrence in analyzed subgroups (*p*-values derived from Kruskal–Wallis ANOVA analysis).


Arterial hypertension was significantly more common in all CKD subgroups than in control. There was no statistical difference between diagnosed diabetes and active smoking in all groups. 1,2,3—the result of the post-hoc analysis showing differences between the indicated groups.

**Table 3.** Demographic and descriptive data and statistical evaluation between control and the whole CKD group (Mann– Whitney U test).


Abbreviations: BP—blood pressure; eGFR—estimated glomerular filtration rate; LDL—low-density cholesterol; HDL—high-density cholesterol; TC—total cholesterol; TG—triglycerides; CV—Cardiovascular.

> When analyzing the control group and CKD-based subgroups, renalase levels were significantly higher in HD than in any other group and the CKD IV group compared to the CKD III group. There was no significant difference in renalase levels between the control group and CKD III and IV groups.

Renalase levels in subgroups are shown graphically below in Figure 1.

**Figure 1.** Renalase levels in the studied groups.

In the control group, renalase correlated negatively with body weight (Rs = −0.39, *p* < 0.05). There was also a borderline correlation with systolic (Rs = −0.31, *p* = 0.08) and diastolic (Rs = −0.32, *p* = 0.09) blood pressure.

In the CKD III group, renalase did not correlate with any of the analyzed parameters, but in the stage IV CKD group, it correlated again with eGFR (Rs = −0.48, *p* < 0.01) and body weight (Rs = −0.44, *p* < 0.05).

In the HD group, renalase correlated negatively with eGFR (Rs = −0.55, *p* < 0.05) and positively with residual diuresis (Rs = −0.36, *p* < 0.05).

Comparing adults with no kidney disease and the whole CKD group, there was no significant difference in renalase levels, but this difference was at the borderline significance level (*p* = 0.07).

In the whole CKD group, we found a strong negative correlation between renalase levels and eGFR (Rs = −0.83, *p* < 0.001), as shown in Figure 2.

**Figure 2.** The negative, strong correlation between renalase and eGFR in the CKD group.

When analyzing data from all participants together (control and CKD patients), renalase correlates with diastolic blood pressure (Rs = −0.18, *p* < 0.05), eGFR (Rs = −0.59, *p* < 0.001) and body weight (Rs = −0.32, *p* < 0.001).

#### *3.2. Follow-Up Data*

During the follow-up period, we recorded 22 MACEs—2 in control, 2 in CKD III, 5 in CKD IV, and 13 in the HD group. There were 11 deaths; none in control and CKD III, four in CKD IV and seven in HD. We observed five HD initiations. There was no RRT other than hemodialysis initiated. Data are shown in Tables 4 and 5.

**Table 4.** Qualitative data on recorded endpoints; data are shown as number of individuals (*p*-values derived from Kruskal– Wallis ANOVA analysis).


Abbreviations: MACE—major adverse cardiovascular events, CKD—chronic kidney disease.


**Table 5.** Quantitative data on recorded endpoints with statistical evaluation (Kruskal-Wallis ANOVA). Data are shown as mean ± SD and median (lower quartile—upper quartile).

Abbreviations: MACE—major adverse cardiovascular events; CKD—chronic kidney disease; HD—hemodialysis. 1—the result of the post-hoc analysis showing differences between the indicated groups.

> Even though statistical analysis showed significant differences in both MACE occurrence and all-cause mortality in all subgroups, the post-hoc analysis did not show specific significance between particular groups. All RRT initiations were observed in the CKD IV group.

> Observed time to first MACE was significantly shorter in the HD group than in the CKD IV group. There was no statistical difference between time to all-cause death between groups in which deaths were observed. The median time to RRT initiation was 12 months.

> In CKD subgroups, RNLS correlated with all-cause death occurrence in the HD group (Rs = 0.49, *p <* 0.01), but no other significant correlation was found.

> When analyzing the whole CKD patient population, we found a positive correlation of RNLS concentration and MACE occurrence (Rs = 0.38, *p* < 0.001) and a negative correlation with time to first MACE occurrence (Rs = −0.52, *p* < 0.05). The correlation of RNLS and MACE occurrence was stronger than that of the algorithm derived, calculated risk (Rs = 0.25, *p* < 0.05). All-cause death also correlated positively with renalase concertation (Rs = 0.34, *p* < 0.005).

> Data pooled from all participants (both with and without CKD) concerning endpoints have shown a correlation between RNLS and MACE occurrence (Rs = 0.33, *p* < 0.001), time to MACE (Rs = −0.50, *p* < 0.05) and all-cause death (Rs = 0.31, *p* < 0.001). This conclusion takes into account that a small number of endpoints were observed in the control group.
