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.