DIETARY SODIUM INTAKE IS CORRELATED WITH SERUM COPEPTIN IN EARLY-STAGE AUTOSOMAL DOMINANT POLYCYSTIC KIDNEY DISEASE

J ZHANG1,2, C MANNIX2,  A RANGAN1, AT WONG2, G RANGAN2,3
1Discipline of Nutrition and Dietetics, School of Life and Environmental Sciences, University of Sydney, Camperdown, Australia, 2Centre for Transplant and Renal Research, Westmead Institute for Medical Research, University of Sydney, Westmead, Australia, 3Department of Renal Medicine, Westmead Hospital, Westmead, Australia

Aim: To determine the association between dietary sodium and protein intakes with serum copeptin (a marker of arginine vasopressin (AVP)) in patients with autosomal dominant polycystic kidney disease (ADPKD).
Background: Elevated levels of AVP are hypothesised to worsen renal cyst growth in ADPKD. Apart from low fluid intake, the dietary intake of sodium and protein also influence AVP levels, but this has not been specifically investigated in ADPKD.
Methods: Patients with ADPKD (18-65 years, eGFR≥30 mL/min/1.73m²) underwent a structured diet history interview to assess usual intake over the past 3 months, as part of the PREVENT-ADPKD study. Twenty-four-hour urinary sodium and urea excretion were measured to validate the diet history-reported sodium and protein intakes, respectively. Serum copeptin was measured by a sandwich immunoassay (B.R.A.H.M.S).
Results: Twenty-nine participants (age 42±12 yrs; BMI 26±5 kg/m²; mean±SD) were analysed. The diet history was a valid method for estimating dietary protein, as reported intakes demonstrated a strong correlation with 24-h urine-derived estimates (r=0.658; P<0.001), and there was no evidence of systematic bias by the Bland-Altman method. Median±IQR serum copeptin concentration was 4.09±8.55 pmol/L. Multivariate analyses (adjusted for age, gender, 24-h urine volume and serum creatinine) revealed that higher serum copeptin was strongly associated with higher 24-h urine sodium (B=0.695; P=0.017) (the gold-standard for dietary sodium intake), but not with diet history-reported sodium or protein intake, 24-h urine urea, urine osmolality or dietary solute intake.
Conclusions: These cross-sectional, observational data support the hypothesis that dietary sodium intake stimulates AVP release in ADPKD. An ongoing randomised clinical trial will determine the combined long-term effects of adequate hydration and lowering dietary sodium intake on serum copeptin and the renal progression of ADPKD.


Biography:
Jennifer is currently a PhD student in the Polycystic Kidney Disease Group at the Westmead Institute for Medical Research, University of Sydney, under the supervision of Associate Professor Gopi Rangan. She previously completed a Bachelor of Science (Physiology and Nutrition & Metabolism), followed by a Master of Nutrition and Dietetics. Her PhD is focused on preclinical research into what triggers cyst formation in autosomal dominant polycystic kidney disease. She is also currently working as a research dietitian on the PREVENT-ADPKD study.

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