Post-transplant erythrocytosis refractory to ACE inhibitors and angiotensin receptor blockers

Prakash Vishnu, Yenny Moreno Vanegas, Hani M. Wadei, Candido E Rivera

Research output: Contribution to journalArticle

Abstract

Post-transplant erythrocytosis (PTE) is a condition with elevated haematocrit (hct) in renal allograft recipients. The mainstay of treatment is ACE inhibitors (ACEi) or angiotensin II receptor blockers (ARB), but seldom phlebotomy. PTE must be recognised early to prevent major thromboembolic events. We present a case of PTE that was refractory to blockade of renin-angiotensin system (RAS) by ACEi and ARB and required phlebotomy for control of hct. Our review of medical literature about prevalence and pathophysiology of PTE suggests that approximately 22% of patients with PTE are refractory to ACEi/ARB treatment. There are four plausible pathways that appear to play a role in causing PTE: disruption of erythropoietin regulation, mitogenic effect of the RAS on erythroid lineage, insulin-like growth factor 1 and androgenic stimulation. Presently, there is no unifying hypothesis involving these factors, but refractoriness to ACEi/ARB may represent a distinct subcategory of PTE.

Original languageEnglish (US)
Article numberbcr-2018-224622
JournalBMJ Case Reports
Volume2018
DOIs
StatePublished - Jan 1 2018

Fingerprint

Polycythemia
Angiotensin Receptor Antagonists
Angiotensin-Converting Enzyme Inhibitors
Transplants
Phlebotomy
Renin-Angiotensin System
Hematocrit
Somatomedins
Erythropoietin
Allografts
Kidney
Therapeutics

Keywords

  • haematology (drugs and medicines)
  • renal transplantation

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Post-transplant erythrocytosis refractory to ACE inhibitors and angiotensin receptor blockers. / Vishnu, Prakash; Vanegas, Yenny Moreno; Wadei, Hani M.; Rivera, Candido E.

In: BMJ Case Reports, Vol. 2018, bcr-2018-224622, 01.01.2018.

Research output: Contribution to journalArticle

@article{4b371c5df4ad4b6c8c0034cb033c0395,
title = "Post-transplant erythrocytosis refractory to ACE inhibitors and angiotensin receptor blockers",
abstract = "Post-transplant erythrocytosis (PTE) is a condition with elevated haematocrit (hct) in renal allograft recipients. The mainstay of treatment is ACE inhibitors (ACEi) or angiotensin II receptor blockers (ARB), but seldom phlebotomy. PTE must be recognised early to prevent major thromboembolic events. We present a case of PTE that was refractory to blockade of renin-angiotensin system (RAS) by ACEi and ARB and required phlebotomy for control of hct. Our review of medical literature about prevalence and pathophysiology of PTE suggests that approximately 22{\%} of patients with PTE are refractory to ACEi/ARB treatment. There are four plausible pathways that appear to play a role in causing PTE: disruption of erythropoietin regulation, mitogenic effect of the RAS on erythroid lineage, insulin-like growth factor 1 and androgenic stimulation. Presently, there is no unifying hypothesis involving these factors, but refractoriness to ACEi/ARB may represent a distinct subcategory of PTE.",
keywords = "haematology (drugs and medicines), renal transplantation",
author = "Prakash Vishnu and Vanegas, {Yenny Moreno} and Wadei, {Hani M.} and Rivera, {Candido E}",
year = "2018",
month = "1",
day = "1",
doi = "10.1136/bcr-2018-224622",
language = "English (US)",
volume = "2018",
journal = "BMJ Case Reports",
issn = "1757-790X",
publisher = "BMJ Publishing Group",

}

TY - JOUR

T1 - Post-transplant erythrocytosis refractory to ACE inhibitors and angiotensin receptor blockers

AU - Vishnu, Prakash

AU - Vanegas, Yenny Moreno

AU - Wadei, Hani M.

AU - Rivera, Candido E

PY - 2018/1/1

Y1 - 2018/1/1

N2 - Post-transplant erythrocytosis (PTE) is a condition with elevated haematocrit (hct) in renal allograft recipients. The mainstay of treatment is ACE inhibitors (ACEi) or angiotensin II receptor blockers (ARB), but seldom phlebotomy. PTE must be recognised early to prevent major thromboembolic events. We present a case of PTE that was refractory to blockade of renin-angiotensin system (RAS) by ACEi and ARB and required phlebotomy for control of hct. Our review of medical literature about prevalence and pathophysiology of PTE suggests that approximately 22% of patients with PTE are refractory to ACEi/ARB treatment. There are four plausible pathways that appear to play a role in causing PTE: disruption of erythropoietin regulation, mitogenic effect of the RAS on erythroid lineage, insulin-like growth factor 1 and androgenic stimulation. Presently, there is no unifying hypothesis involving these factors, but refractoriness to ACEi/ARB may represent a distinct subcategory of PTE.

AB - Post-transplant erythrocytosis (PTE) is a condition with elevated haematocrit (hct) in renal allograft recipients. The mainstay of treatment is ACE inhibitors (ACEi) or angiotensin II receptor blockers (ARB), but seldom phlebotomy. PTE must be recognised early to prevent major thromboembolic events. We present a case of PTE that was refractory to blockade of renin-angiotensin system (RAS) by ACEi and ARB and required phlebotomy for control of hct. Our review of medical literature about prevalence and pathophysiology of PTE suggests that approximately 22% of patients with PTE are refractory to ACEi/ARB treatment. There are four plausible pathways that appear to play a role in causing PTE: disruption of erythropoietin regulation, mitogenic effect of the RAS on erythroid lineage, insulin-like growth factor 1 and androgenic stimulation. Presently, there is no unifying hypothesis involving these factors, but refractoriness to ACEi/ARB may represent a distinct subcategory of PTE.

KW - haematology (drugs and medicines)

KW - renal transplantation

UR - http://www.scopus.com/inward/record.url?scp=85049419803&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85049419803&partnerID=8YFLogxK

U2 - 10.1136/bcr-2018-224622

DO - 10.1136/bcr-2018-224622

M3 - Article

C2 - 29954763

AN - SCOPUS:85049419803

VL - 2018

JO - BMJ Case Reports

JF - BMJ Case Reports

SN - 1757-790X

M1 - bcr-2018-224622

ER -