The CRISP study of
polycystic kidney disease (PKD) found that urinary
sodium excretion associated with the rate of total kidney volume increase. Whether
sodium restriction slows the progression of Autosomal Dominant PKD (
ADPKD) is not known. To evaluate this we conducted a post hoc analysis of the HALT-PKD clinical trials of
renin-
angiotensin blockade in patients with
ADPKD. Linear mixed models examined whether
dietary sodium affected rates of total kidney volume or change in estimated glomerular filtration rate (eGFR) in patients with an eGFR over 60 ml/min/1.73 m2 (Study A) or the risk for a composite endpoint of 50% reduction in eGFR,
end-stage renal disease or death, or the rate of eGFR decline in patients with an eGFR 25-60 ml/min/1.73 m2 (Study B) all in patients initiated on an under100 mEq
sodium diet. During the trial urinary
sodium excretion significantly declined by an average of 0.25 and 0.41 mEq/24 hour per month in studies A and B, respectively. In Study A, averaged and time varying urinary
sodium excretions were significantly associated with kidney growth (0.43%/year and 0.09%/year, respectively, for each 18 mEq urinary
sodium excretion). Averaged urinary
sodium excretion was not significantly associated with faster eGFR decline (-0.07 ml/min/1.73m2/year for each 18 mEq urinary
sodium excretion). In Study B, the averaged but not time-varying urinary
sodium excretion significantly associated with increased risk for the composite endpoint (hazard ratio 1.08 for each 18 mEq urinary
sodium excretion) and a significantly faster eGFR decline (-0.09 ml/min/1.73m2/year for each mEq 18 mEq urinary
sodium excretion). Thus,
sodium restriction is beneficial in the management of
ADPKD.