Low-Osmolar Diet and Adjusted Water Intake for Vasopressin Reduction in Autosomal Dominant Polycystic Kidney Disease: A Pilot Randomized Controlled Trial

• Published in: American journal of kidney diseases Vol. 68; no. 6; pp. 882 - 891
• Main Authors: Amro, Osama W., MD, MS, Paulus, Jessica K., ScD, Noubary, Farzad, PhD, Perrone, Ronald D., MD
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.12.2016
• Subjects: Adolescent; Adult; Arginine Vasopressin - metabolism; Arginine Vasopressin - urine; Autosomal dominant polycystic kidney disease (ADPKD); clinical trial; copeptin; Drinking; Female; Humans; Male; Middle Aged; Nephrology; nutrition; osmolality; Osmolar Concentration; Pilot Projects; Polycystic Kidney, Autosomal Dominant - diet therapy; Polycystic Kidney, Autosomal Dominant - urine; protein; salt; urea; vasopressin; water; Young Adult; copeptin; clinical trial; nutrition; osmolality; salt; Autosomal dominant polycystic kidney disease (ADPKD); vasopressin; protein; water; urea
• ISSN: 0272-6386; 1523-6838
• DOI: 10.1053/j.ajkd.2016.07.023

Background Autosomal dominant polycystic kidney disease (ADPKD) affects millions of people worldwide. Vasopressin promotes disease progression. Study Design A randomized controlled trial with equal (1:1) allocation. Setting & Participants This trial examined the effect of combining a low-osmolar (low-sodium [1,500 mg/d], low-protein [0.8 g per kilogram of body weight]) diet and adjusted water intake on vasopressin secretion in 34 patients with ADPKD. Intervention Participants were randomly assigned to receive a low-osmolar diet followed by adjusted water intake to achieve urine osmolality ≤ 280 mOsm/kg water versus no intervention for 2 weeks. Outcome The primary outcome of the study was change (delta) in copeptin levels and urine osmolality between the intervention and control groups from baseline to 2 weeks. Measurements Fasting plasma copeptin level, 24-hour urine osmolality, and total solute intake. Results Baseline characteristics of the 2 groups were similar. Mean plasma copeptin levels and urine osmolality declined from 6.2 ± 3.05 (SD) to 5.3 ± 2.5 pmol/L ( P = 0.02) and from 426 ± 193 to 258 ± 117 mOsm/kg water ( P = 0.01), respectively, in the intervention group compared to a nonsignificant change in the control group (from 4.7 ± 3.6 to 5.07 ± 4 pmol/L [ P = 0.2] and 329 ± 159 to 349 ± 139 mOsm/kg water [ P = 0.3], respectively). The change in copeptin levels (primary outcome) and urine osmolality was statistically significant between the intervention and control groups (delta copeptin, −0.86 ± 1.3 vs +0.39 ± 1.2 pmol/L [ P = 0.009]; delta urine osmolality, −167 ± 264 vs +20 ± 80 mOsm/kg water [ P = 0.007], respectively). Total urinary solute decreased in only the intervention group and significantly differed between groups at week 1 ( P = 0.03), reducing mean water prescription from 3.2 to 2.6 L/d. Limitations Small sample size and short follow-up. Conclusions We developed a stepwise dietary intervention that led to a significant reduction in vasopressin secretion in patients with ADPKD. Furthermore, this intervention led to a reduction in water required for vasopressin reduction.