In animal studies of ADPKD, giving the animal large amounts of water suppresses vasopressin levels in the blood and cyclic AMP levels in the kidneys, slowing cyst enlargement. This study tested whether water ingestion is a potential therapeutic strategy in people with ADPKD.
This study was designed so that water intake for each individual was calculated so that urine solute concentration reached a specific target level of 285 mOsm. Five of the eight individuals enrolled in the study were able to achieve a urine osmolality of 285 mOsm. (Osmolality is a measure of solutes in the urine.) The success of this study shows that a quantitative method to determine the amount of water intake needed for a given individual to achieve a target osmolality can be calculated.
Several limitations of the study were acknowledged by the researchers. First, the sample size was much smaller than required for a clinical trial because a methodology was being developed and validated. The effect of water intake on the course of the disease was not tested. Secondly, the small sample size included almost all Caucasian women. Daily solute intake, urine solute concentration and blood levels of vasopressin vary by race and gender, so these findings cannot be generalized to a more diverse population. Thirdly, study participants had normal blood pressure with GFRs in chronic kidney disease stages 1 and 2. NOTE: For those with advanced kidney disease (stages 3, 4 & 5) it is important to not increase fluid intake above normal.
Whether or not water intake can affect the course of ADPKD by lowering vasopressin levels in the kidney is a critical factor that must be studied further.