COMPARISON OF SPOT AND 24-HOUR URINE OSMOLALITY MEASUREMENTS IN AUTOSOMAL DOMINANT POLYCYSTIC KIDNEY DISEASE

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COMPARISON OF SPOT AND 24-HOUR URINE OSMOLALITY MEASUREMENTS IN AUTOSOMAL DOMINANT POLYCYSTIC KIDNEY DISEASE
Ayub
Akbari
Sriram Sriperumbuduri srisriperumbuduri@gmail.com University of Ottawa Department of Medicine/ Division of Nephrology/Kidney Research Center Ottawa
Shreepryia Mangalgi drshreepriya100@gmail.com University of Ottawa Department of Medicine/ Division of Nephrology/Kidney Research Center Ottawa
Gregory Hundemer ghundemer@toh.ca University of Ottawa Department of Medicine/ Division of Nephrology/Kidney Research Center Ottawa
Manish Sood msood@toh.ca University of Ottawa Department of Medicine/ Division of Nephrology/Kidney Research Center Ottawa
Mohan Biyani mbiyani@toh.ca University of Ottawa Department of Medicine/ Division of Nephrology/Kidney Research Center Ottawa
Pierre Brown pibrown@toh.ca University of Ottawa Department of Medicine/ Division of Nephrology/Kidney Research Center Ottawa
 
 
 
 
 
 
 
 
 

Autosomal dominant polycystic kidney disease (ADPKD), leads to kidney cyst formation, partly due to the role of arginine vasopressin (AVP) in cyst growth. AVP effects can be mitigated through high water intake or pharmacologically via V2 receptor blockers like tolvaptan, with urine osmolality serving as a clinical indicator of AVP suppression. Clinically both spot random urine samples and osmolality from 24 hour urine samples have been utilized to assess AVP suppression. However, correlation between these two measurements is unclear. 

We compared 24 hour urine osmolality with spot urine osmolality in ADPKD patients. Bland-Altman plots were constructed to assess agreement. The percentage of patients with difference in osmolality between 24-hour urine osmolality and spot urine osmolality for cutoff points of > 50, > 100, >150 and > 200 mosm/kg were determined.  

Study sample consisted of 839 samples from 349 patients.  47 (13.5%) of patients were on Tolvaptan at the time of urine collection. The mean (SD) age of the cohort was  46.2 (15.4) years, and 52% of patients were female. Mean (SD) 24-hour urine osmolality was 364 (162) mosm/Kg and mean (SD) random urine osmolality was 424 (202) mosm/kg. Discordance in osmolality between 24 hour-urine and spot  sample at cutoff points of 50, 100, 150 and 200 mosm/kg were present in 452 (53.9%), 300 (35.8%),  202 (24.1%) and 135 (16.1%), of samples respectively. Bland-Altman plots revealed poor agreement between random urine osmolality and 24 hour urine osmolality.  

There is considerable difference between 24-hour urine osmolality and random urine osmolality. They should not be used interchangeably.    Further studies should be performed to determine which urine osmolality is better at predicting clinical outcomes. 

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