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Abstract: TH-PO409

Altered Lipid Metabolism in Autosomal Dominant Polycystic Kidney Disease Patients Treated With Tolvaptan

Session Information

Category: Genetic Diseases of the Kidneys

  • 1101 Genetic Diseases of the Kidneys: Cystic

Authors

  • Bargagli, Matteo, Department of Nephrology and Hypertension, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland
  • Anderegg, Manuel, Department of Nephrology and Hypertension, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland
  • Ferraro, Pietro Manuel, U.O.C. Nefrologia, Fondazione Policlinico Universitario A. Gemelli IRCCS, Roma, Italy
  • Fuster, Daniel G., Department of Nephrology and Hypertension, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland

Group or Team Name

  • Daniel G. Fuster Research Team
Background

Dyslipidemia is a common finding in patients with autosomal-dominant polycystic kidney disease (ADPKD), and lower HDL is associated with faster disease progression. Vasopressin interacts with both glucose and lipid regulation pathways, hence Tolvaptan treatment might induce changes in lipid and glucose homeostasis in ADPKD patients.

Methods

We conducted an exploratory analysis in the Bern ADPKD registry, a prospective observational cohort study. Glucose and lipid metabolism parameters were measured at baseline and every 12 months thereafter. Patients taking Tolvaptan at baseline were excluded from the analysis. Multivariable mixed-effects regression models adjusted for age, sex, BMI, eGFR, TSH and medications use, including antidiabetic and lipid-lowering drugs, were used to assess changes in plasma glucose and lipid metabolism parameters associated with Tolvaptan treatment.

Results

A total of 189 participants (122 without and 67 with subsequent Tolvaptan treatment) were included in the analysis. At baseline, 58 (31%) patients had high total cholesterol, 26 (14%) low HDL, 61 (32%) high LDL and 41 (22%) high triglycerides. During follow-up, Tolvaptan treatment was associated with reduced HDL (β -0.186; 95% CI −0.260, -0.111; p < 0.001), increased LDL (β 0.216; 95% CI 0.001, 0.430; p = 0.048) and triglycerides (β 0.381; 95% CI 0.130, 0.633; p = 0.003) levels. No significant changes were observed in total cholesterol, plasma glucose or hemoglobin A1c.

Conclusion

Chronic Tolvaptan treatment is associated with a significantly altered plasma lipid profile in ADPKD patients. Our data suggest that patients taking Tolvaptan should undergo regular lipid parameter testing.