Abstract

BackgroundHigher serum sodium concentration has been reported to be a risk factor for the development of incident chronic kidney disease (CKD), but its relationship with the progression of established CKD has not been investigated. We hypothesised that increased serum sodium concentration is a risk factor for estimated glomerular filtration rate (eGFR) decline in CKD.MethodsThis was a retrospective cohort study using data collected over a 6-year period, with baseline data obtained during the first 2 years. We included patients known to our renal service who had had a minimum of three blood tests every 2 years and an eGFR of < 60 mL/min/1.73 m2 at baseline. Exclusion criteria were renal replacement therapy, diabetes mellitus, heart failure and decompensated liver disease. A multiple linear regression model investigated the relationship between baseline serum sodium and eGFR decline after adjustment for confounding factors.Results7418 blood results from 326 patients were included. There was no relationship between serum sodium concentration and estimated glomerular filtration rate at baseline. After multivariable adjustment, a 1 mmol/L increase in baseline serum sodium was associated with a 1.5 mL/min/1.73 m2 decline in eGFR during the study period (95% CI 0.9, 2.0). A reduction in eGFR was not associated with significant changes in serum sodium concentration over 6 years.ConclusionHigher serum sodium concentration is associated with the progression of CKD, independently of other established risk factors. Conversely, significant alterations in serum sodium concentration do not occur with declining kidney function.

Highlights

  • 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 [1]

  • 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 [2, 3]

  • 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 [6, 7]

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Summary

Introduction

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 [1]. Higher serum sodium concentration has been reported to be a risk factor for the development of incident chronic kidney disease (CKD), but its relationship with the progression of established CKD has not been investigated. We hypothesised that increased serum sodium concentration is a risk factor for estimated glomerular filtration rate (eGFR) decline in CKD. A 1 mmol/L increase in baseline serum sodium was associated with a 1.5 mL/min/1.73 m2 decline in eGFR during the study period (95% CI 0.9, 2.0). Conclusion Higher serum sodium concentration is associated with the progression of CKD, independently of other established risk factors. Significant alterations in serum sodium concentration do not occur with declining kidney function

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