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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
The clinical feasibility and efficacy of tolvaptan in autosomal dominant polycystic kidney disease (ADPKD) patients remains uncertain. In ADPKD, increased adenosine-3', 5'-cyclic monophosphate (cAMP) in the renal tubules causes growth of kidney cysts and progression of renal dysfunction. Tolvaptan, a vasopressin type-2 receptor antagonist, inhibits cAMP synthesis by blocking arginine vasopressin (AVP) stimulation in the renal collecting ducts. The level of urine cAMP relative to plasma AVP, which indicates the residual function of the renal collecting ducts in response to AVP stimulation, might be a key to predicting the therapeutic magnitude of tolvaptan in ADPKD patients.
Consecutive patients with ADPKD receiving tolvaptan between April 2016 and December 2024 were included in this single-center prospective study. The patients had a total kidney volume of 750 mL or more, and its annual increase rate was approximately 5% or more. The impact of baseline urine cAMP/plasma AVP ratio on the response to tolvaptan, which was defined as an improvement in estimated glomerular filtration rate (GFR) slope, was investigated.
A total of 24 patients (median age 48 years; 14 men; median estimated GFR 54.5 mL/min/1.73 m2; median height-adjusted total kidney volume 835 mL/m) were included. Comparing before and after tolvaptan therapy, the estimated GFR slope changed from −3.4 (−5.7, −2.1) to −2.9 (−4.4, −1.9) mL/min/1.73 m2 per year (p = 0.069), and the annual increase rate of total kidney volume changed from 7.6 (5.9, 12.2) to 2.1 (−1.1, 7.3) % (p <0.01). During a median follow-up period of 3.3 years after the initiation of tolvaptan, the estimated GFR slope improved, as compared to before tolvaptan therapy, in 16 responders. Baseline urine cAMP level was 2.6 (2.2, 3.1) nmol/mg of creatinine, plasma AVP level was 1.6 (1.0, 1.8) pg/mL, and urine cAMP/plasma AVP ratio ranged from 0.95 and 5.55 with a median of 1.81. The baseline urine cAMP/plasma AVP ratio was a significant predictor of tolvaptan responder, with an adjusted odds ratio of 59.7 (95% confidence interval 1.2–2940, p = 0.040). The optimal cutoff value for predicting tolvaptan response was identified as 1.66 (sensitivity 0.81, specificity 0.88), yielding an area under the receiver operating characteristic curve of 0.91 (95% confidence interval 0.78–1.0). Although improvement in the growth of total kidney volume after tolvaptan therapy was observed in 19 patients, the urine cAMP/plasma AVP ratio was not a significant predictor of suppression of kidney volume growth, with an adjusted odds ratio of 1.7 (95% confidence interval 0.37–8.1, p = 0.49).
Baseline urine cAMP/plasma AVP ratio is an independent predictor of response to tolvaptan, as defined by improvement in estimated GFR slope, in patients with ADPKD.
