Evidence map›Paper›PMID 41678280›Full record

ArticleKidney3602026

The Relationship of Osmolality and Kidney Outcomes in Patients with Autosomal Dominant Polycystic Kidney Disease.

Winston Wing-Shing Fung, Cheuk-Chun Szeto, Kai-Ming Chow, Amelia Chien-Wei Chao, Vickie Wai-Ki Kwong, Sam Lik-Fung Lau, Wing-Fai Pang, Ho-Kwan Sin, Elaine Ho, Lorraine Pui-Yuen Kwan and 15 more

Abstract read
In one paragraph

Article in Kidney360, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

25 authors.

Winston Wing-Shing FungDepartment of Medicine and Therapeutics, Prince of Wales Hospital, Hong Kong, Hong Kong SAR.ORCID 0000-0001-7676-7628
Cheuk-Chun SzetoDepartment of Medicine and Therapeutics, Prince of Wales Hospital, Hong Kong, Hong Kong SAR.ORCID 0000-0002-8898-8505
Kai-Ming ChowDepartment of Medicine and Therapeutics, Prince of Wales Hospital, Hong Kong, Hong Kong SAR.ORCID 0000-0001-5310-5197
Amelia Chien-Wei ChaoDepartment of Medicine and Therapeutics, Prince of Wales Hospital, Hong Kong, Hong Kong SAR.ORCID 0000-0002-2276-9043
Vickie Wai-Ki KwongDepartment of Medicine and Therapeutics, Prince of Wales Hospital, Hong Kong, Hong Kong SAR.ORCID 0009-0003-0880-9998
Sam Lik-Fung LauDepartment of Medicine and Therapeutics, Prince of Wales Hospital, Hong Kong, Hong Kong SAR.ORCID 0000-0002-0005-6878
Wing-Fai PangDepartment of Medicine and Therapeutics, Prince of Wales Hospital, Hong Kong, Hong Kong SAR.ORCID 0009-0001-2963-511
Ho-Kwan SinDepartment of Medicine and Geriatrics, Kwong Wah Hospital, Hong Kong, Hong Kong SAR.ORCID 0000-0002-6625-8536
Elaine HoDepartment of Medicine, Tseung Kwan O Hospital, Hong Kong, Hong Kong SAR.ORCID 0009-0006-2476-1033
Lorraine Pui-Yuen KwanDepartment of Medicine, Tung Wah Hospital, Hong Kong, Hong Kong SAR.
Koon-Ming ChanDepartment of Medicine, Queen Elizabeth Hospital, Hong Kong, Hong Kong SAR.
Gary Tung-Sen ShumDepartment of Medicine and Geriatrics, Princess Margaret Hospital, Hong Kong, Hong Kong SAR.ORCID 0000-0002-4581-4724
Anthony Kai-Ching HauDepartment of Medicine and Geriatrics, Tuen Mun Hospital, Hong Kong, Hong Kong SAR.ORCID 0000-0001-6391-7172
Ka-Lok ChanDepartment of Medicine and Geriatrics, United Christian Hospital, Hong Kong, Hong Kong SAR.
Ronald Chi-Chun LinDepartment of Medicine and Geriatrics, Caritas Medical Centre, Hong Kong, Hong Kong SAR.
Lap-Ming KwokDepartment of Medicine, Yan Chai Hospital, Hong Kong, Hong Kong SAR.ORCID 0009-0007-7395-7435
Sze-Kit YuenDepartment of Medicine and Geriatrics, Caritas Medical Centre, Hong Kong, Hong Kong SAR.ORCID 0009-0002-8025-3595
Sing-Leung LuiDepartment of Medicine, Tung Wah Hospital, Hong Kong, Hong Kong SAR.ORCID 0000-0002-1816-4754
Samuel Ka-Shun FungDepartment of Medicine and Geriatrics, Princess Margaret Hospital, Hong Kong, Hong Kong SAR.ORCID 0000-0003-2955-638
Sunny WongDepartment of Medicine and Geriatrics, United Christian Hospital, Hong Kong, Hong Kong SAR.ORCID 0000-0003-3136-0941
Winnie Chiu-Wing ChuDepartment of Imaging and Interventional Radiology, The Chinese University of Hong Kong, Hong Kong, Hong Kong SAR.ORCID 0000-0003-4962-4132
Albert Chee Meng OngKidney Genetics Group, Division of Clinical Medicine, School of Medicine and Population Health, University of Sheffield, Sheffield, United Kingdom.ORCID 0000-0002-7211-5400
Olivier DevuystInstitute of Physiology, University of Zurich, Zürich, Switzerland.ORCID 0000-0003-3744-4767
Philip Kam-Tao LiDepartment of Medicine and Therapeutics, Prince of Wales Hospital, Hong Kong, Hong Kong SAR.ORCID 0000-0001-9879-8388
On behalf of the CysticHK cohort collaborators

Funding

Chinese University of Hong Kong 6905134Chinese University of Hong Kong 7101215Hong Kong Society of Nephrology 35th Anniversary Research Grant
6 · The paper itself

Abstract

key pointsThe 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.

backgroundCurrent 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.

methodsThree 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.

resultsPatients 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).

conclusionssOSM 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.

Indexed as

KidneyPolycystic Kidney, Autosomal DominantAdultAntidiuretic Hormone Receptor AntagonistsBiomarkersDisease ProgressionFemaleGlomerular Filtration RateGlycopeptidesHumansMaleMiddle AgedOsmolar ConcentrationProspective StudiesTolvaptanAntidiuretic Hormone Receptor AntagonistsBiomarkerscopeptinsGlycopeptidesTolvaptanADPKDosmolalityoutcomespolycystic kidney disease

Identifiers

PMID41678280
PMCPMC13229416

What Socratic holds

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LicenceCC BY-NC-ND
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.