Introduction
Chronic kidney disease (CKD) is defined as the presence as abnormalities
of kidney structure or function, present for more than three months,
with implications for health(1). Currently, stakeholders recognized CKD
as a severe public health problem related to deterioration in the
quality of life and high costs for the health system(2). Patients with
CKD have a lower life expectancy and a higher rate of cardiovascular
complications, as well as anemia, bone disease, infections and
cancer(3). According to Global Burden Disease, Globally, in 2017, 1·2
million people died from CKD, and the global all-age mortality rate from
CKD increased 41·5% between 1990 and 2017(4). In Peru, for the period
2010-2016, the prevalence of CKD increased by 300%, and although rate
the standardized mortality decreased by 10% it is still high for a
country with limited economic resources(5). Due to the high burden of
the disease, it is essential to know the factors associated with higher
mortality.
Although there are different factors associated with mortality in
patients with CKD, there is interest in searching for new markers. The
neutrophil to lymphocyte ratio (NLR) and platelet to lymphocyte ratio
(PLR) are markers of chronic inflammation. These markers are obtained
easily from the quotient between neutrophil and lymphocyte or platelet
and lymphocyte blood counts; respectively(6–8). Neutrophils are
effector cells of the immune system, which rise in inflammation and
generate an increase in oxidative stress(9). Similarly, platelets have
immunomodulatory properties, which lead to inflammation, thrombosis and
cancer(10,11). Indeed, the contribution of interactions between
neutrophils and platelets in infections and inflammatory processes have
begun to be intensively studied(12,13).
Specific lymphocyte subtypes, such as Th2 and regulatory T, decrease
inflammation by different routes, such as GATA3 and FOXP3(14).
Therefore, the elevation of the NLR and PLR reflects a pro-inflammatory
imbalance, as the effector cells are increased, and the regulatory cells
are decreased. In CKD, the oxidative stress, increase in
pro-inflammatory cytokines (PCR, IL-6, TNF-a) and the poor nutritional
status caused by this imbalance contribute to the progression of
disease(15).
The NLR and PLR have proven to be an marker of mortality and
complications in pathologies such as heart failure, peptic ulcer
perforation, chronic obstructive pulmonary disease, rheumatic diseases,
neoplasms, and others(16–18). In patients with CKD, the NLR and PLR
predict disease progression and the presence of albuminuria(19,20).
Although several studies have suggested that both markers also predict
mortality in patients with CKD, there are contradictory results(21),
they are studies done in dialysis patients(22,23), or patients with CKD
in stages 1-5, but in Asian population(24). Because mortality and
associated factors differ according to the stage of the disease and in
Hispanic population(25–27), this study aims to assess the association
between NLR and PLR with all-cause mortality in Peruvian patients with
CKD who was attending tertiary hospital.