Abstract: PO1205
Creatine Kinase Elevation in Patients with Autosomal Dominant Polycystic Kidney Disease on Tolvaptan Treatment
Session Information
- Cystic Kidney Disease - I
November 04, 2021 | Location: On-Demand, Virtual Only
Abstract Time: 10:00 AM - 12:00 PM
Category: Genetic Diseases of the Kidneys
- 1001 Genetic Diseases of the Kidneys: Cystic
Authors
- Rodriguez-Espinosa, Diana, Hospital Clinic de Barcelona, Barcelona, Catalunya, Spain
- Payán, Elena Cuadrado, Hospital Clinic de Barcelona, Barcelona, Catalunya, Spain
- Guillen, Elena, Hospital Clinic de Barcelona, Barcelona, Catalunya, Spain
- Blasco pelicano, Josep miquel, Hospital Clinic de Barcelona, Barcelona, Catalunya, Spain
Background
Autosomal dominant polycystic kidney disease (ADPKD) is the most common inherited kidney disease worldwide. Studies such as the TEMPO 3:4 and 4:4 have demonstrated tolvaptan’s (vasopressin V2 receptor antagonist) effectiveness in slowing the progression of this disease. The best described adverse effect seen with this treatment is drug-induced liver injury, however, creatine kinase (CK) elevation has also been described anecdotally in a couple of case reports.
Methods
This is a prospective observational study of adult patients with rapidly progressive ADPKD on tolvaptan treatment under follow-up at Hospital Clínic de Barcelona from October 2018 to March 2021. Quantitative variables are described as mean and standard deviation, while qualitative ones are reported as absolute and relative frequencies.
Results
A total of 37 patients started treatment with tolvaptan during this period. In 34 of them, serum CK levels were measured as part of the monthly biochemical follow-up. A total of 29.11% (10 of 34) of the patients elevated this parameter with a mean of 1368.2 ± 2807.28 U/L. Seven patients had a transient elevation with a mean of 446.43 ± 359.22 U/L, which reversed upon dose decrease or treatment pause. However, treatment had to be interrupted in the remaining three patients (mean 3519 ± 5016.36). In one of them due to concomitant drug-induced liver injury and in the other two due to persistent CK elevation despite dose reduction or temporary treatment interruption. CK elevation was not related to exercise (although one patient did report a weekly intense cycling exercise with increased myalgia afterward) and was not significantly correlated with LDH levels, liver enzymes, calcium, potassium, urinary or plasma osmolarity.
Conclusion
By performing a general screening, we found that CK elevation is more frequent than previously described in the literature, reaching significantly increased levels or producing symptomatology requiring definitive treatment interruption. Based on these results, although the studied sample is small, we suggest adding this parameter as a part of tolvaptan treatment’s follow-up, at the beginning of treatment and when increasing its dose, to promptly detect undesirable adverse effects and gain a better understanding of this phenomenon.