Literature DB >> 25926129

Urine and plasma osmolality in patients with autosomal dominant polycystic kidney disease: reliable indicators of vasopressin activity and disease prognosis?

Niek F Casteleijn1, Debbie Zittema, Stephan J L Bakker, Wendy E Boertien, Carlo A Gaillard, Esther Meijer, Edwin M Spithoven, Joachim Struck, Ron T Gansevoort.   

Abstract

BACKGROUND: Vasopressin plays an essential role in osmoregulation, but has deleterious effects in patients with ADPKD. Increased water intake to suppress vasopressin activity has been suggested as a potential renoprotective strategy. This study investigated whether urine and plasma osmolality can be used as reflection of vasopressin activity in ADPKD patients.
METHODS: We measured urine and plasma osmolality, plasma copeptin concentration, total kidney volume (TKV, by MRI) and GFR ((125)I-iothalamate). In addition, change in estimated GFR (eGFR) during follow-up was assessed.
RESULTS: Ninety-four patients with ADPKD were included (56 males, age 40 ± 10, mGFR 77 ± 32 ml/min/1.73 m(2), TKV 1.55 (0.99-2.40) l. Urine osmolality, plasma osmolality and copeptin concentration were 420 ± 195, 289 ± 7 mOsmol/l and 7.3 (3.2-14.6) pmol/l, respectively. Plasma osmolality was associated with copeptin concentration (R = 0.54, p < 0.001), whereas urine osmolality was not (p = 0.4). In addition, urine osmolality was not associated with TKV (p = 0.3), in contrast to plasma osmolality (R = 0.52, p < 0.001) and copeptin concentration (R = 0.61, p < 0.001). Fifty-five patients were followed for 2.8 ± 0.8 years. Baseline plasma and urine osmolality were not associated with change in eGFR (p = 0.6 and p = 0.3, respectively), whereas baseline copeptin concentration did show an association with change in eGFR, in a crude analysis (St. β = -0.41, p = 0.003) and also after adjustment for age, sex and TKV (St. β = -0.23, p = 0.05).
CONCLUSIONS: These data suggest that neither urine nor plasma osmolality are valid measures to identify ADPKD patients that may benefit from increasing water intake. Copeptin appears a better alternative for this purpose.
© 2015 S. Karger AG, Basel.

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Year:  2015        PMID: 25926129     DOI: 10.1159/000382081

Source DB:  PubMed          Journal:  Am J Nephrol        ISSN: 0250-8095            Impact factor:   3.754


  5 in total

1.  Plasma copeptin levels predict disease progression and tolvaptan efficacy in autosomal dominant polycystic kidney disease.

Authors:  Ron T Gansevoort; Maatje D A van Gastel; Arlene B Chapman; Jaime D Blais; Frank S Czerwiec; Eiji Higashihara; Jennifer Lee; John Ouyang; Ronald D Perrone; Katrin Stade; Vicente E Torres; Olivier Devuyst
Journal:  Kidney Int       Date:  2019-03-09       Impact factor: 10.612

Review 2.  New treatment paradigms for ADPKD: moving towards precision medicine.

Authors:  Matthew B Lanktree; Arlene B Chapman
Journal:  Nat Rev Nephrol       Date:  2017-10-09       Impact factor: 28.314

Review 3.  Recent advances in managing and understanding enuresis.

Authors:  Charlotte Van Herzeele; Johan Vande Walle; Karlien Dhondt; Kristian Vinter Juul
Journal:  F1000Res       Date:  2017-10-24

4.  Study on the Mechanism of circRNA Regulating the miRNA Level in Nephrotic Syndrome.

Authors:  Qianyu Li; Min Yin; Zhiping Zhang; Yuanzhi Yu; Feng Liu
Journal:  Evid Based Complement Alternat Med       Date:  2022-07-11       Impact factor: 2.650

5.  Increased water intake reduces long-term renal and cardiovascular disease progression in experimental polycystic kidney disease.

Authors:  Priyanka S Sagar; Jennifer Zhang; Magda Luciuk; Carly Mannix; Annette T Y Wong; Gopala K Rangan
Journal:  PLoS One       Date:  2019-01-02       Impact factor: 3.240

  5 in total

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