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Kidney Week

Abstract: PO1535

Tolvaptan and Renal Function in Autosomal Dominant Polycystic Disease: A Two-Center Experience of 186 Cases

Session Information

Category: Genetic Diseases of the Kidneys

  • 1001 Genetic Diseases of the Kidneys: Cystic

Authors

  • Oda, Yasuhiro, Toranomon Hospital Kajigaya, Kawasaki, Kanagawa, Japan
  • Ikuma, Daisuke, Toranomon Hospital Kajigaya, Kawasaki, Kanagawa, Japan
  • Mizuno, Hiroki, Toranomon Hospital Kajigaya, Kawasaki, Kanagawa, Japan
  • Sekine, Akinari, Toranomon Hospital Kajigaya, Kawasaki, Kanagawa, Japan
  • Yamanouchi, Masayuki, Toranomon Hospital Kajigaya, Kawasaki, Kanagawa, Japan
  • Suwabe, Tatsuya, Toranomon Hospital Kajigaya, Kawasaki, Kanagawa, Japan
  • Hoshino, Junichi, Toranomon Hospital Kajigaya, Kawasaki, Kanagawa, Japan
  • Ubara, Yoshifumi, Toranomon Hospital Kajigaya, Kawasaki, Kanagawa, Japan
Background

TEMPO and REPRISE trials demonstrated that tolvaptan slows the decline in the estimated glomerular filtration rate (eGFR) in patients with autosomal dominant polycystic kidney disease (ADPKD). However, the real-world data of the change in eGFR in patients with ADPKD taking tolvaptan is lacking. Also, comparison of the slopes of the change in eGFR before and after starting taking tolvaptan in a same patient has not been reported.

Methods

Patients who started taking tolvaptan for ADPKD between June 2014 and June 2019 at Toranomon Hospital and Toranomon Hospital Kajigaya were retrospectively analysed for the change in eGFR before and after starting taking tolvaptan. Note that approved indication of tolvaptan for ADPKD patients in Japan includes total kidney volume larger than 750 mL and eGFR greater than 15 mL/min/1.73 m2. The eGFR at 1, 2, 3, 4, 5 years before and after starting tolvaptan were collected from the medical record. Patients with none of these values were excluded from the study.

Results

186 patients were included in the study. 43% were men. Average age was 50.2 ± 10.2 (mean ± standard deviation). Total kidney volume was as follows when stratified by chronic kidney disease (CKD) stages: stage 1, 1119 ± 266; stage 2, 1521 ± 600; stage 3a, 1659 ± 787; stage 3b, 2106 ± 1330; stage 4, 2847 ± 1976 mL. 139 patients had eGFR data before and after starting tolvaptan, whereas 24 patients only had data before and 23 patients only had data after starting tolvaptan. The eGFR slope after starting taking tolvaptan was -3.7 ± 2.3 mL/min/1.73 m2 (n=162), and was as follows when stratified by CKD stages: stage 1, -5.9 ± 4.3 (n=4); stage 2, -4.5 ± 2.8 (n=47); stage 3a, -3.1 ± 2.1 (n=38); stage 3b, -3.5 ± 1.8 (n=40); stage 4, -3.3 ± 1.8 mL/min/1.73 m2/year (n=33). The change in eGFR slope after starting tolvaptan was -1.2 ± 5.4 in stage 1-3a patients (n=76) and +0.8 ± 2.3 mL/min/1.73 m2/year in stage 3b-4 patients (n=63), which showed statistically significant difference (p=0.003).

Conclusion

Real-world data from our institution observed the eGFR slope of -3.7 ± 2.3 mL/min/1.73 m2 after starting taking tolvaptan. The eGFR slope in patients with CKD stage 3b-4 improved on average after taking tolvaptan. The same was not observed in patients with CKD stage 1-3a.