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Abstract: PO0854

Systemic Parameters of the Renin-Angiotensin-Aldosterone System Remain Unaffected by Changes in Fibroblast Growth Factor 23 Levels in Hemodialysis Patients

Session Information

Category: Dialysis

  • 701 Dialysis: Hemodialysis and Frequent Dialysis


  • Dörr, Katharina, Medizinische Universitat Wien, Wien, Wien, Austria
  • Kammer, Michael, Medizinische Universitat Wien, Wien, Wien, Austria
  • Reindl-Schwaighofer, Roman, Medizinische Universitat Wien, Wien, Wien, Austria
  • Lorenz, Matthias, Medizinische Universitat Wien, Wien, Wien, Austria
  • Marculescu, Rodrig, Medizinische Universitat Wien, Wien, Wien, Austria
  • Poglitsch, Marko, Attoquant, Vienna, Austria
  • Oberbauer, Rainer, Medizinische Universitat Wien, Wien, Wien, Austria

Fibroblast growth factor 23 (FGF23) is elevated in patients with chronic kidney disease and promotes the development of left ventricular hypertrophy (LVH). Decreasing the levels of FGF23 with the calcimimetic drug etelcalcetide can abate that effect in hemodialysis patients. It is unknown if the prohypertrophic effect of FGF23 is modified by the renin-angiotensin-aldosterone system (RAAS). The aim of the analysis was to determine whether changes in FGF23 levels are associated with differences in RAAS-parameters in hemodialysis patients, possibly explaining its influence on LVH.


Serum samples were obtained at baseline and one year from participants in the randomized EtECAR-HD trial. In this study 62 hemodialysis patients were treated with either calcimimetic or vitamin D treatment, which have opposite effects on FGF23. We analyzed PRA-S as the angiotensin-based marker for renin activity, angiotensin II (AngII), angiotensin-converting enzyme-2 (ACE2) and aldosterone using a high throughput mass spectrometry assay.


The median levels of FGF23 were 2386 pg/ml (1st to 3rd quartile 819–5166) and 1386 pg/ml (288–4068) at baseline and end of study, respectively. The association of changes between baseline and end of study in FGF23 with the levels of the RAAS-components (i.e. PRA-S, AngII, ACE2, aldosterone) estimated by linear regression models was weak, with effect sizes for log2-fold-change in FGF23 close to zero. The amount of explained variation by FGF23 fold-change was generally small (drop-in-R2 values all below 0.03). The median overall levels of PRA-S were 130 pg/ml (1st to 3rd quartile 46-269), of AngII 70 pg/ml (28-157), of aldosterone 130 pg/ml (54-278) and of ACE2 1.4 ng/ml (1.1-1.8), as compared with healthy controls (PRA-S 196 pg/ml [98-238], AngII 137 pg/ml [76-201], aldosterone 335 pg/ml [139-454], ACE2 1.38 ng/ml [1.17-1.65]).


In the present study we were able to show that systemic RAAS activity was grossly unaffected by the treatment induced changes in FGF23 levels in this cohort. Overall, the levels of PRA-S, AngII and aldosterone were well below the ranges measured in healthy controls suggesting that the RAAS is not systemically activated in hemodialysis patients.


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