Kidney360 · 2026
The Relationship of Osmolality and Kidney Outcomes in Patients with Autosomal Dominant Polycystic Kidney Disease.
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Fung Winston Wing-Shing, Szeto Cheuk-Chun, Chow Kai-Ming, Chao Amelia Chien-Wei, Kwong Vickie Wai-Ki, Lau Sam Lik-Fung, Pang Wing-Fai, Sin Ho-Kwan, Ho Elaine, Kwan Lorraine Pui-Yuen, Chan Koon-Ming, Shum Gary Tung-Sen, Hau Anthony Kai-Ching, Chan Ka-Lok, Lin Ronald Chi-Chun, Kwok Lap-Ming, Yuen Sze-Kit, Lui Sing-Leung, Fung Samuel Ka-Shun, Wong Sunny, Chu Winnie Chiu-Wing, Ong Albert Chee Meng, Devuyst Olivier, Li Philip Kam-Tao, On behalf of the CysticHK cohort collaborators
Аннотация
KEY POINTS: The causal relationship between serum osmolality and kidney outcome remained unclear in patients with autosomal dominant polycystic kidney disease. Serum osmolality may be a possible surrogate marker for the clinical monitoring of autosomal dominant polycystic kidney disease patients, especially when access to copeptin level is limited. High serum osmolality conveys possible detrimental effect on the kidney outcomes.
BACKGROUND: Current treatment of autosomal dominant polycystic kidney disease (ADPKD) is mainly focused on inhibiting cystogenesis through arginine vasopressin suppression, and there has been interest in achieving similar vasopressin suppression by reduction of osmolality with increased water intake. However, the causal relationship between serum osmolality (sOSM) and kidney outcome remained unclear in patients with ADPKD. We aim to evaluate the relationship of sOSM and its effect on kidney outcome in patients with ADPKD.
METHODS: Three hundred and eleven tolvaptan treatment-naïve patients with ADPKD were recruited prospectively from the CysticHK cohort, a territory-wide ADPKD registry across 12 tertiary hospitals in Hong Kong. Beside clinical data, serial measurement of serum, and urinary osmolality were obtained every 6 months over 5 years. All participants were treated according to the standard of clinical care. The primary outcome was the 40% decline from baseline eGFR.
RESULTS: Patients with a high sOSM have a worse kidney outcome, as shown by the Kaplan-Meier plots (log-rank P ≤ 0.001) and the Cox regression model that showed a 5.91 times higher risk of reaching 40% eGFR decline compared with the top with bottom quartiles of osmolality ( P = 0.018). By contrast, there is an inverse relationship for urine osmolality. A receiver-operating characteristic analysis to assess the predictive efficacy of osmolality for identifying those at high risk of kidney decline also showed a good performance for sOSM (area under the curve, 0.81; 95% confidence interval, 0.73 to 0.89; P < 0.001). The urinary osmolality did not show a clinical meaningful predictive efficacy (area under the curve, 0.35; 95% confidence interval, 0.28 to 0.43; P = 0.003).
CONCLUSIONS: sOSM may be a possible surrogate marker for the clinical monitoring of patients with ADPKD, especially when access to copeptin level is limited; and high sOSM conveys possible detrimental effect on the kidney outcomes.
BACKGROUND: Current treatment of autosomal dominant polycystic kidney disease (ADPKD) is mainly focused on inhibiting cystogenesis through arginine vasopressin suppression, and there has been interest in achieving similar vasopressin suppression by reduction of osmolality with increased water intake. However, the causal relationship between serum osmolality (sOSM) and kidney outcome remained unclear in patients with ADPKD. We aim to evaluate the relationship of sOSM and its effect on kidney outcome in patients with ADPKD.
METHODS: Three hundred and eleven tolvaptan treatment-naïve patients with ADPKD were recruited prospectively from the CysticHK cohort, a territory-wide ADPKD registry across 12 tertiary hospitals in Hong Kong. Beside clinical data, serial measurement of serum, and urinary osmolality were obtained every 6 months over 5 years. All participants were treated according to the standard of clinical care. The primary outcome was the 40% decline from baseline eGFR.
RESULTS: Patients with a high sOSM have a worse kidney outcome, as shown by the Kaplan-Meier plots (log-rank P ≤ 0.001) and the Cox regression model that showed a 5.91 times higher risk of reaching 40% eGFR decline compared with the top with bottom quartiles of osmolality ( P = 0.018). By contrast, there is an inverse relationship for urine osmolality. A receiver-operating characteristic analysis to assess the predictive efficacy of osmolality for identifying those at high risk of kidney decline also showed a good performance for sOSM (area under the curve, 0.81; 95% confidence interval, 0.73 to 0.89; P < 0.001). The urinary osmolality did not show a clinical meaningful predictive efficacy (area under the curve, 0.35; 95% confidence interval, 0.28 to 0.43; P = 0.003).
CONCLUSIONS: sOSM may be a possible surrogate marker for the clinical monitoring of patients with ADPKD, especially when access to copeptin level is limited; and high sOSM conveys possible detrimental effect on the kidney outcomes.