Low-Osmolar Diet and Adjusted Water Intake for Vasopressin Reduction in Autosomal Dominant Polycystic Kidney Disease: A Pilot Randomized Controlled Trial.
BACKGROUND
Autosomal dominant polycystic kidney disease (ADPKD) affects millions of people worldwide. Vasopressin promotes disease progression.


METHODS
A randomized controlled trial with equal (1:1) allocation.


METHODS
This trial examined the effect of combining a low-osmolar (low-sodium [1,500mg/d], low-protein [0.8g per kilogram of body weight]) diet and adjusted water intake on vasopressin secretion in 34 patients with ADPKD.


METHODS
Participants were randomly assigned to receive a low-osmolar diet followed by adjusted water intake to achieve urine osmolality ≤ 280mOsm/kg water versus no intervention for 2 weeks.


RESULTS
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.


METHODS
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±2.5pmol/L (P=0.02) and from 426±193 to 258±117mOsm/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±4pmol/L [P=0.2] and 329±159 to 349±139mOsm/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±1.2pmol/L [P=0.009]; delta urine osmolality, -167±264 vs +20±80mOsm/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 2.6L/d.


CONCLUSIONS
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.
Division of Nephrology, Department of Medicine, Tufts Medical Center, Boston, MA; Tufts University School of Medicine, Boston, MA.
Osama W
OW
Amro
Tufts University School of Medicine, Boston, MA; The Institute for Clinical Research and Health Policy Studies, Tufts Medical Center, Boston, MA; Tufts Clinical and Translational Science Institute, Tufts University, Boston, MA.
Jessica K
JK
Paulus
Tufts University School of Medicine, Boston, MA; The Institute for Clinical Research and Health Policy Studies, Tufts Medical Center, Boston, MA; Tufts Clinical and Translational Science Institute, Tufts University, Boston, MA.
Farzad
F
Noubary
Division of Nephrology, Department of Medicine, Tufts Medical Center, Boston, MA; Tufts University School of Medicine, Boston, MA. Electronic address: rperrone@tuftsmedicalcenter.org.
Ronald D
RD
Perrone
D000293:Adolescent; D000328:Adult; D001127:Arginine Vasopressin / Q000378:metabolism* / Q000652:urine; D004326:Drinking; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009994:Osmolar Concentration; D010865:Pilot Projects; D016891:Polycystic Kidney, Autosomal Dominant / Q000178:diet therapy* / Q000652:urine; D055815:Young Adult
D001127:Arginine Vasopressin
Autosomal dominant polycystic kidney disease (ADPKD); clinical trial; copeptin; nutrition; osmolality; protein; salt; urea; vasopressin; water
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