Plasma levels of myeloperoxidase and resistin independently predict mortality in dialysis patients.

Background: In patients with kidney failure (KF) undergoing dialysis, neutrophils are dysfunctionally activated. Such chronic activation does not correspond to increased protection against infections and is thought to cause direct vascular damage accounting for the higher incidence of cardiovascular (CV) events. We hypothesized that circulating levels of neutrophil degranulation products (i.e. myeloperoxidase (MPO) and resistin) can predict overall and CV-specific mortality in dialysis patients.
Methods: MPO and resistin levels were assessed in plasma samples from n = 1182 dialysis patients who were followed-up for median 2.9 years (IQR: 1.7-4.2).
Results: Patients were 65 ± 14 (SD) years old and 36 % women. Median value of MPO and resistin were 78 ng/mL (IQR: 54 - 123) and 72 ng/mL (IQR: 46 - 110), respectively. MPO and resistin levels correlated with biomarkers of organ damage, nutritional status and inflammation. Both MPO and resistin levels predicted all-cause mortality even after adjustment for traditional risk factors and inflammation, nutritional and KF-related indexes (MPO, HR _{for 1 ln unit increase} : 1.26, 95 %CI 1.11 - 1.42, P < 0.001; Resistin, HR _{for 1 ln unit increase} : 1.25, 95 %CI 1.09 - 1.44, P = 0.001). Similarly, their predictive ability held true also for CV death (MPO, HR _{for 1 ln unit increase} : 1.19, 95 %CI 1.01 - 1.41, P = 0.04; Resistin, HR _{for 1 ln unit increase} : 1.29, 95 %CI 1.07 - 1.56, P = 0.007).
Conclusion: Plasma levels of MPO and resistin correlate with prospective overall and CV-specific mortality risk in KF patients undergoing dialysis and might be useful prognostic tools. Mediators of inflammation may be potential target to improve survival of those patients.
Competing Interests: Declaration of competing interests LL is co-inventor on the International Patent WO/2020/226,993 filed in April 2020; the patent relates to the use of antibodies which specifically bind interleukin-1a to reduce various sequelae of ischemia-reperfusion injury to the central nervous system. The other authors have nothing to disclose.
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