Casteleijn Niek F, Zittema Debbie, Bakker Stephan J L, Boertien Wendy E, Gaillard Carlo A, Meijer Esther, Spithoven Edwin M, Struck Joachim, Gansevoort Ron T
Department of Nephrology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.
Am J Nephrol. 2015;41(3):248-56. doi: 10.1159/000382081. Epub 2015 Apr 25.
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.
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.
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).
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.
血管加压素在渗透压调节中起重要作用，但对常染色体显性多囊肾病（ADPKD）患者有不良影响。增加水摄入量以抑制血管加压素活性已被认为是一种潜在的肾脏保护策略。本研究调查了尿渗透压和血浆渗透压是否可用于反映ADPKD患者的血管加压素活性。
我们测量了尿渗透压、血浆渗透压、血浆 copeptin 浓度、总肾体积（通过 MRI 测量）和肾小球滤过率（(125)I-碘肽酸盐法）。此外，评估了随访期间估计肾小球滤过率（eGFR）的变化。
纳入了 94 例 ADPKD 患者（56 例男性，年龄 40±10 岁，平均肾小球滤过率 77±32 ml/min/1.73 m²，总肾体积 1.55（0.99 - 2.40）l）。尿渗透压、血浆渗透压和 copeptin 浓度分别为 420±195、289±7 mOsmol/l 和 7.3（3.2 - 14.6）pmol/l。血浆渗透压与 copeptin 浓度相关（R = 0.54，p < 0.001），而尿渗透压与之无关（p = 0.4）。此外，尿渗透压与总肾体积无关（p = 0.3），与血浆渗透压（R = 0.52，p < 0.001）和 copeptin 浓度（R = 0.61，p < 0.001）相反。55 例患者随访了 2.8±0.8 年。基线血浆和尿渗透压与 eGFR 的变化无关（分别为 p = 0.6 和 p = 0.3），而基线 copeptin 浓度在粗分析中（标准化β = -0.41，p = 0.003）以及在调整年龄、性别和总肾体积后（标准化β = -0.23，p = 0.05）确实与 eGFR 的变化相关。
这些数据表明，尿渗透压和血浆渗透压都不是识别可能从增加水摄入量中获益的 ADPKD 患者的有效指标。copeptin 似乎是用于此目的的更好选择。
