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Sodium normal range at 1461/15/2024 ![]() Serum creatinine was measured by enzymatic assay and serum sodium was determined using indirect potentiometry. Blood samples were processed at a number of laboratories in the local area, all of which are monitored by the United Kingdom National External Quality Assessment Service (NEQAS) to ensure comparable results. Blood test results corresponding to the same date for serum sodium, potassium, creatinine and haematocrit were obtained and an eGFR was calculated for each creatinine value using the CKD-EPI equation. ![]() ![]() Exclusion criteria were as follows: provision of renal replacement therapy during the study period a diagnosis of congestive cardiac failure, diabetes mellitus (type I or II), or decompensated liver disease prior to the study end date.ĭemographic details and laboratory values were extracted from the database and further information was identified manually from clinic letters including cause of CKD, co-morbidity, office blood pressure and medication. Individuals with a mean eGFR of < 60 mL/min/1.73 m 2 at baseline were included in the study. Data collected during the first 2-year period was used to determine baseline values. In order to acutely assess this, the study was separated into three 2-year periods and only included individuals who had had at least three results during each of these periods. The primary outcome was the change in estimated glomerular filtration rate (eGFR) over the 6-year study period. The South West Thames Renal Department database (Clinical Vision 5.3) was used to identify individuals under the follow-up of general nephrology services between January 2009 and December 2014. This was a retrospective cohort study of data collected during a 6-year period. We also considered the possibility that changes in serum sodium may occur secondary to CKD progression and altered sodium handling by the kidney. Therefore, we hypothesised that increased serum sodium is a risk factor for renal function decline and carried out a retrospective analysis to investigate this. However, whether there is a relationship between serum sodium and the progression of established CKD remains unknown. Higher serum sodium concentrations, within the normal range, have recently been reported be a risk factor for the development of incident CKD. Whilst significant abnormalities in serum sodium, especially hyponatraemia, have been consistently associated with mortality in CKD, the influence of small inter-individual differences has largely been ignored. Furthermore, increased sodium concentration has been shown to induce mRNA expression of many hypertrophy-related factors, including transforming growth factor-beta (TGF-β), that are associated with the progression of CKD. In addition, there is in vitro evidence that small increases in sodium concentration have a direct effect on the vascular endothelium: experiments have demonstrated stiffening of endothelial cells, damage to the glycocalyx layer and inhibition of nitric oxide release. Although changes in extracellular volume also occur, a significant positive correlation between serum sodium and blood pressure exists in both animals and humans when volume status is controlled using dialysis. In randomised-controlled trials, acute and large alterations in salt intake (ranging from less than 1 g/day to more than 10 g/day) are associated with parallel changes in serum sodium of up to 3 mmol/L. The mechanisms underlying the adverse effects of salt are incompletely understood, but it has been proposed that small increases in serum sodium concentration are important. Higher dietary salt consumption in those with chronic kidney disease (CKD) is associated with increased blood pressure and proteinuria, independent risk factors for CKD progression.
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