Department of Nephrology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands,
Department of Laboratory Medicine, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.
Am J Nephrol. 2020;51(11):861-870. doi: 10.1159/000511000. Epub 2020 Nov 4.
Patients with autosomal dominant polycystic kidney disease (ADPKD) are treated with a vasopressin V2 receptor antagonist (V2RA) to slow disease progression. This drug increases vasopressin considerably in these patients with already elevated baseline levels. Vasopressin is known to stimulate the hypothalamic-pituitary-adrenal (HPA) axis through V1 and V3 receptor activation. It is unknown whether this increase in vasopressin during V2RA treatment affects glucocorticoid production.
Twenty-seven ADPKD patients were studied on and off treatment with a V2RA and compared to age- and sex-matched healthy controls and IgA nephropathy patients, the latter also matched for kidney function. Vasopressin was measured by its surrogate copeptin. Twenty-four-hour urinary excretions of cortisol, cortisone, tetrahydrocortisone, tetrahydrocortisol, allotetrahydrocortisol, and the total glucocorticoid pool were measured.
At baseline, ADPKD patients demonstrated a higher copeptin concentration in comparison with healthy controls, while urinary excretion of cortisol and cortisone was lower (medians of 0.23 vs. 0.34 μmol/24 h, p = 0.007, and 0.29 vs. 0.53 μmol/24 h, p < 0.001, respectively). There were no differences in cortisol and cortisone excretion compared to IgA nephropathy patients. Cortisol, cortisone, and total glucocorticoid excretions correlated with kidney function (R = 0.37, 0.58, and 0.19, respectively; all p < 0.05). Despite that V2RA treatment resulted in a 3-fold increase in copeptin, only cortisone excretion increased (median of 0.44 vs. baseline 0.29 μmol/24 h, p < 0.001), whereas no changes in cortisol or total glucocorticoid excretion were observed.
Increased concentration of vasopressin in ADPKD patients at baseline and during V2RA treatment does not result in activation of the HPA axis. The impaired glucocorticoid production in these patients is related to their degree of kidney function impairment.
常染色体显性多囊肾病(ADPKD)患者使用血管加压素 V2 受体拮抗剂(V2RA)治疗以减缓疾病进展。该药物会使基线水平已经升高的患者的血管加压素显著增加。已知血管加压素通过 V1 和 V3 受体激活来刺激下丘脑-垂体-肾上腺(HPA)轴。尚不清楚 V2RA 治疗期间血管加压素的增加是否会影响糖皮质激素的产生。
研究了 27 例接受 V2RA 治疗的 ADPKD 患者,并与年龄和性别匹配的健康对照组以及 IgA 肾病患者进行了比较,后者也与肾功能相匹配。通过其替代物 copeptin 测量血管加压素。测量了 24 小时尿中皮质醇、皮质酮、四氢皮质醇、四氢皮质素、全异四氢皮质醇和总糖皮质激素库的排泄量。
在基线时,与健康对照组相比,ADPKD 患者的 copeptin 浓度更高,而皮质醇和皮质酮的尿排泄量较低(中位数分别为 0.23 与 0.34 μmol/24 h,p = 0.007 和 0.29 与 0.53 μmol/24 h,p < 0.001)。与 IgA 肾病患者相比,皮质醇和皮质酮的排泄量没有差异。皮质醇、皮质酮和总糖皮质激素排泄量与肾功能相关(R = 0.37、0.58 和 0.19,p < 0.05)。尽管 V2RA 治疗导致 copeptin 增加了 3 倍,但仅观察到皮质酮排泄增加(中位数为 0.44 与基线时的 0.29 μmol/24 h,p < 0.001),而皮质醇或总糖皮质激素排泄量没有变化。
ADPKD 患者在基线时和 V2RA 治疗期间血管加压素浓度增加不会导致 HPA 轴激活。这些患者的糖皮质激素产生受损与他们的肾功能受损程度有关。