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Title: Asymmetric Dimethylarginine (ADMA) Levels Are Lower in Hemodialysis Patients Treated With Paricalcitol
Authors: Oliva-Damaso, Elena
Oliva-Damaso, Nestor
Rodriguez-Esparragon, Francisco 
Payan, Juan
Marañes, Alberto
Parodis, Yanet
Baamonde-Laborda, Lopez Eduardo
Diaz, Nicanor Vega
Rodriguez-Perez, Jose Carlos 
UNESCO Clasification: 320506 Nefrología
Keywords: Asymmetric dimethylarginine
Issue Date: 2017
Journal: Kidney International Reports 
Abstract: Introduction:Chronic kidney disease is a major public health problem. In the last decade, it has beenshown that the early stages of chronic kidney disease are associated with an inflammatory conditioninvolving an increased risk of cardiovascular morbidity and long-term mortality. In patients with chronickidney disease and more specifically those on hemodialysis, cardiovascular events are the most commoncause of death. Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide synthaseand 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 ADMAsuch 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 0.19mmol/l) compared with those not treated with paricalcitol (0.42 0.35mmol/l) (P¼0.00027). Dividing ADMAlevels by quartiles, patients treated with paricalcitol were less likely to have very high level ADMA(P¼0.014), whereas there were no significant differences with other medications. Higher dose of paricalcitolwas also related to lower levels of ADMA noting an inverse correlation (r¼–0.36,P¼0.013).Discussion:Hemodialysis patients treated with paricalcitol presented significantly decreased ADMA levelscompared with those who did not receive this treatment. Possible beneficial effects in terms of cardio-vascular morbidity and mortality by paricalcitol and its association with ADMA and nitric oxide synthesisare unknown. Studies to confirm this effect and determine the underlying pathophysiological mechanismare necessary.
ISSN: 2468-0249
DOI: 10.1016/j.ekir.2016.10.002
Source: Kidney International Reports[ISSN 2468-0249],v. 2(2), p. 165-171
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