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Rangan G. et al. 2021

Prescribed Water Intake in Autosomal Dominant Polycystic Kidney Disease

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Arginine vasopressin promotes kidney cyst growth in autosomal dominant polycystic kidney disease (ADPKD). Increased water intake reduces arginine vasopressin and urine osmolality and may slow kidney cyst growth.


In this randomized controlled 3-year clinical trial, we randomly assigned adults with ADPKD who had a height-corrected total kidney volume in Mayo imaging subclass categories 1B to 1E and an estimated glomerular filtration rate of 30 ml/min/1.73 m2 or greater to (1) water intake prescribed to reduce 24-hour urine osmolality to 270 mOsmol/kg or less or (2) ad libitum water intake irrespective of 24-hour urine osmolality. The primary end point was the percentage annualized rate of change in height-corrected total kidney volume.


A total of 184 patients participated in either the ad libitum water intake group (n592) or the prescribed water intake group (n592). Over 3 years, there was no difference in the annualized rate of change in height-corrected total kidney volume between the ad libitum (7.8% per year; 95% confidence interval [CI], 6.6 to 9.0) and prescribed (6.8% per year; 95% CI, 5.8 to 7.7) water intake groups (mean difference, 20.97% per year; 95% CI, 22.37 to 0.44; P50.18). The difference in mean 24-hour urine osmolality between the ad libitum and prescribed water intake groups was 291 mOsmol/kg (95% CI, 2127 to 254 mOsmol/kg), with 52.3% of patients achieving adherence to the target 24-hour urine osmolality and no reduction in serum copeptin over 3 years. The frequency of adverse events was similar between groups.


For patients with ADPKD, prescribed water intake was not associated with excess adverse events and achieved the target 24-hour urine osmolality for half of the patients but did not reduce copeptin or slow the growth of total kidney volume over 3 years compared with ad libitum water intake.

A word from our expert Dr. Juliane Zemdegs, France

This is the largest and longest study investigating the effects of personalized prescribed water intake on ADPKD progression. The intervention led to a sustained increase in urine volume, but the targeted urine concentration was achieved in only half of the patients, possibly explaining no changes in disease progression. It remains to be seen whether water induced AVP suppression would slow down ADPKD progression.

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