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1.
Clin Nephrol ; 90(6): 396-403, 2018 Dec.
Artículo en Inglés | MEDLINE | ID: mdl-30232952

RESUMEN

INTRODUCTION: Low pre-hemodialysis (pre-HD) serum sodium or hyponatremia is associated with higher mortality. Pre-HD serum sodium can be more stable over time with low fluctuation compared to other serum parameters. MATERIALS AND METHODS: We examined variation of pre-HD serum sodium in 24 months and after this point examined all-cause mortality in a cohort of 261 patients followed-up for 48.8 (standard deviation (SD) = 19.1) months. 6,221 determinations of pre-HD serum sodium were made and corrected for glucose concentrations. Serum sodium was measured pre-HD monthly, and the variability was calculated using the coefficient of variation (CV). RESULTS: The mean age was of 60 ± 14.1 years, 60.9% were men, 48% had diabetes mellitus, and diabetic nephropathy was the most frequent cause of end-stage renal disease. Median CV of sodium in 24 months was 1.7% with a mean of 1.78% (95% CI 1.73 - 1.83). Patients with CV > 1.7% had a higher mortality (53 patients a 36.8%) compared to CV < 1.7% (22 patients a 18.8%) (p = 0.002). In Kaplan-Meier analysis, patients with CV > 1.7% had significantly worse overall survival (log rank = 6.395, p = 0.011). We also stratified the sample in serum sodium tertiles (< 138 mEq/L; 138 - 140 mEq/L; > 140 mEq/L) and made a Kaplan-Meier analysis which showed persistent worse survival outcomes in patients with CV > 1.7% (log rank Mantel-Cox 7.64; p = 0.006). Cox regression multivariate model showed that CV of sodium was significantly associated with overall mortality after adjusting for confounder variables (hazard ratio 2.16, 95% CI 1.37 - 3.41; p = 0.001). CONCLUSION: Variation of pre-HD serum sodium in 2 years is less than a 2%. With the limitations of our study, a higher variability of pre-HD serum sodium in 2 years of treatment (CV > 1.7%) is associated with increased mortality.
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Asunto(s)
Hiponatremia/sangre , Hiponatremia/complicaciones , Fallo Renal Crónico/sangre , Fallo Renal Crónico/complicaciones , Sodio/sangre , Anciano , Femenino , Estudios de Seguimiento , Humanos , Estimación de Kaplan-Meier , Fallo Renal Crónico/terapia , Masculino , Persona de Mediana Edad , Modelos de Riesgos Proporcionales , Diálisis Renal , Estudios Retrospectivos , Tasa de Supervivencia
2.
Kidney Int Rep ; 2(2): 165-171, 2017 Mar.
Artículo en Inglés | MEDLINE | ID: mdl-29142954

RESUMEN

INTRODUCTION: Chronic kidney disease is a major public health problem. In the last decade, it has been shown that the early stages of chronic kidney disease are associated with an inflammatory condition involving an increased risk of cardiovascular morbidity and long-term mortality. In patients with chronic kidney disease and more specifically those on hemodialysis, cardiovascular events are the most common cause of death. Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide synthase and may be an independent risk factor for endothelial dysfunction and cardiovascular disease. METHODS: We performed a cross-sectional analysis to identify factors that were associated with ADMA such as certain medications related to cardiovascular disease in dialysis patients. RESULTS: Patients who were treated with paricalcitol had significantly lower levels of ADMA (0.21 ± 0.19 µmol/l) compared with those not treated with paricalcitol (0.42 ± 0.35 µmol/l) (P = 0.00027). Dividing ADMA levels by quartiles, patients treated with paricalcitol were less likely to have very high level ADMA (P = 0.014), whereas there were no significant differences with other medications. Higher dose of paricalcitol was also related to lower levels of ADMA noting an inverse correlation (r = -0.36, P = 0.013). DISCUSSION: Hemodialysis patients treated with paricalcitol presented significantly decreased ADMA levels compared with those who did not receive this treatment. Possible beneficial effects in terms of cardiovascular morbidity and mortality by paricalcitol and its association with ADMA and nitric oxide synthesis are unknown. Studies to confirm this effect and determine the underlying pathophysiological mechanism are necessary.

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