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Abstract: SA-PO475

Acute Tolvaptan Treatment Has No Immediate Effect on Renal Plasma Flow or Glomerular Filtration Rate in Polycystic Kidney Disease

Session Information

  • ADPKD: Clinical Studies
    October 27, 2018 | Location: Exhibit Hall, San Diego Convention Center
    Abstract Time: 10:00 AM - 12:00 PM

Category: Genetic Diseases of the Kidney

  • 1001 Genetic Diseases of the Kidney: Cystic


  • Malmberg, My E.S., Regional Hospital Unit West Jutland, Holstebro, Denmark
  • Sønderbæk, Rikke Lund, Regional Hospital Unit West Jutland, Holstebro, Denmark
  • Mose, Frank H., Regional Hospital Unit West Jutland, Holstebro, Denmark
  • Jensen, Jens jorgen, Regional Hospital Unit West Jutland , Herning, Denmark
  • Ejlersen, June A., Regional Hospital Unit West Jutland , Herning, Denmark
  • Pedersen, Erling B., University Clinic in Nephrology and Hypertension, Hospital Jutland West, Risskov, Denmark
  • Bech, Jesper N., Regional Hospital Unit West Jutland, Holstebro, Denmark

Autosomal dominant polycystic kidney disease ADPKD is a common genetic disorder, characterized by formation of cysts in the kidneys, causing gradual renal failure. Tolvaptan is a vasopressin 2 antagonist that seems to reduce the decline in glomerular filtration rate (GFR) in ADPKD. The mechanisms are not fully understood and could, at least partly, be related to changes in renal plasma flow (RPF). The purpose of this randomized, cross-over, double-blind, placebo-controlled study was to investigate if acute tolvaptan treatment increases RPF and/or GFR in patients with ADPKD.


We studied 18 ADPKD patients (chronic kidney disease stages 1-3) on two separate occasions after a single dose of tolvaptan 60 mg or placebo. Two hours after treatment, RPF and GFR were measured by 99-mTc-DTPA renography. Blood pressure was measured every fifteen minutes throughout the day by Mobil-O-Graph®. Renal vascular resistance (RVR) was estimated by the equation mean arterial pressure/RPF.


99-mTc-DTPA renography showed a similar RPF after tolvaptan treatment and placebo treatment (673 ±262 ml/min vs. 650 ±209 ml/min p = 0.571). GFR estimated by 99-mTc-DTPA renography was also unchanged after tolvaptan (78 ±26 ml/min after tolvaptan vs. 79 ±21 ml/min after placebo p = 0.774). During renography, after tolvaptan intake, the brachial systolic blood pressures dropped significantly (135 ±13 mmHg after tolvaptan vs. 141 ±19 mmHg after placebo p = 0.043). We found no significant change in brachial diastolic, central systolic or central diastolic blood pressure. Estimated RVR during renography was unchanged after tolvaptan treatment (0.20 ±0.12 mmHg/ml/min after tolvaptan vs. 0.20 ±0.08 mmHg/ml/min after placebo p = 0.908).


Our results suggest that acute tolvaptan treatment has no immediate effect on RPF and GFR. Our results do not support the hypothesis that the effect of tolvaptan on ADPKD progression is mediated by changes in renal hemodynamics.


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