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. 2017 Apr-Jun;18(2):1470320317705232.
doi: 10.1177/1470320317705232.

Molecular remodeling of the renin-angiotensin system after kidney transplantation

Marlies Antlanger  1 , Oliver Domenig  1 , Johannes J Kovarik  1 , Christopher C Kaltenecker  1 , Chantal Kopecky  1 , Marko Poglitsch  2 , Marcus D Säemann  1
Affiliations

Molecular remodeling of the renin-angiotensin system after kidney transplantation

Marlies Antlanger et al. J Renin Angiotensin Aldosterone Syst. 2017 Apr-Jun.

Abstract

Objective: We aimed at assessing the molecular adaptation of the renin-angiotensin system (RAS) after successful kidney transplantation (KTX).

Materials and methods: In this prospective, exploratory study we analyzed 12 hemodialysis (HD) patients, who received a KTX and had excellent graft function six to 12 months thereafter. The concentrations of plasma Angiotensin (Ang) peptides (Ang I, Ang II, Ang-(1-7), Ang-(1-5), Ang-(2-8), Ang-(3-8)) were simultaneously quantified with a novel mass spectrometry-based method. Further, renin and aldosterone concentrations were determined by standard immunoassays.

Results: Ang values showed a strong inter-individual variability among HD patients. Yet, despite a continued broad dispersion of Ang values after KTX, a substantial improvement of the renin/Ang II correlation was observed in patients without RAS blockade or on angiotensin receptor blocker (HD: renin/Ang II R2 = 0.660, KTX: renin/Ang II R2 = 0.918). Ang-(1-7) representing the alternative RAS axis was only marginally detectable both on HD and after KTX.

Conclusions: Following KTX, renin-dependent Ang II formation adapts in non-ACE inhibitor-treated patients. Thus, a largely normal RAS regulation is reconstituted after successful KTX. However, individual Ang concentration variations and a lack of potentially beneficial alternative peptides after KTX call for individualized treatment. The long-term post-transplant RAS regulation remains to be determined.

Keywords: Renin-angiotensin system; angiotensin; blood pressure; hemodialysis; kidney transplantation.

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Conflict of interest statement

Declaration of conflicting interests: The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Figures

Figure 1.
Figure 1.
Patient-wise Angiotensin (Ang) I and Angiotensin II course. (a) No RAS blocker before and after KTX; (b) Angiotensin receptor blocker before and after KTX; (c) RAS blocker change after KTX. RASi: renin-angiotensin system inhibitor; KTX: kidney transplantation.
Figure 2.
Figure 2.
Renin/Angiotensin (Ang) correlations. (a) Renin/Ang I correlation on HD; (b) Renin/Ang II correlation on HD; (c) Renin/Ang I correlation after KTX; (d) Renin/Ang II correlation after KTX. Patients on ACEi or on dual RAS blockade were excluded from the analysis. HD: hemodialysis; KTX: kidney transplantation; ACEi: angiotensin-converting enzyme inhibitors; RAS: renin-angiotensin system.
Figure 3.
Figure 3.
Patient-wise Angiotensin concentrations on hemodialysis and after kidney transplantation. Blue spheres represent Ang I, red spheres represent Ang II concentrations. Concentrations are given in pg/ml. RASi: renin-angiotensin system inhibitor; ARB: angiotensin receptor blockers; ACEi: angiotensin-converting enzyme inhibitors; Ang I: Angiotensin I; Ang II: Angiotensin II.
Figure 4.
Figure 4.
Basic model of the RAS, its main enzymes and interfering substances used in the study. RAS: renin-angiotensin system; Ang: Angiotensin; ACE: angiotensin-converting enzyme; ACEi: ACE inhibitor; ARB: angiotensin receptor blocker.
See this image and copyright information in PMC

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