Microvascular remodeling and altered angiogenic signaling in human kidneys distal to occlusive atherosclerotic renal artery stenosis.


Journal

Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association
ISSN: 1460-2385
Titre abrégé: Nephrol Dial Transplant
Pays: England
ID NLM: 8706402

Informations de publication

Date de publication:
22 09 2022
Historique:
received: 08 11 2021
pubmed: 23 4 2022
medline: 24 9 2022
entrez: 22 4 2022
Statut: ppublish

Résumé

Renal artery stenosis (RAS) is an important cause of chronic kidney disease and secondary hypertension. In animal models, renal ischemia leads to downregulation of growth factor expression and loss of intrarenal microcirculation. However, little is known about the sequelae of large-vessel occlusive disease on the microcirculation within human kidneys. This study included five patients who underwent nephrectomy due to renovascular occlusion and seven nonstenotic discarded donor kidneys (four deceased donors). Micro-computed tomography was performed to assess microvascular spatial densities and tortuosity, an index of microvascular immaturity. Renal protein expression, gene expression and histology were studied in vitro using immunoblotting, polymerase chain reaction and staining. RAS demonstrated a loss of medium-sized vessels (0.2-0.3 mm) compared with donor kidneys (P = 0.037) and increased microvascular tortuosity. RAS kidneys had greater protein expression of angiopoietin-1, hypoxia-inducible factor-1α and thrombospondin-1 but lower protein expression of vascular endothelial growth factor (VEGF) than donor kidneys. Renal fibrosis, loss of peritubular capillaries (PTCs) and pericyte detachment were greater in RAS, yet they had more newly formed PTCs than donor kidneys. Therefore, our study quantified significant microvascular remodeling in the poststenotic human kidney. RAS induced renal microvascular loss, vascular remodeling and fibrosis. Despite downregulated VEGF, stenotic kidneys upregulated compensatory angiogenic pathways related to angiopoietin-1. These observations underscore the nature of human RAS as a microvascular disease distal to main vessel stenosis and support therapeutic strategies directly targeting the poststenotic kidney microcirculation in patients with RAS.

Sections du résumé

BACKGROUND
Renal artery stenosis (RAS) is an important cause of chronic kidney disease and secondary hypertension. In animal models, renal ischemia leads to downregulation of growth factor expression and loss of intrarenal microcirculation. However, little is known about the sequelae of large-vessel occlusive disease on the microcirculation within human kidneys.
METHOD
This study included five patients who underwent nephrectomy due to renovascular occlusion and seven nonstenotic discarded donor kidneys (four deceased donors). Micro-computed tomography was performed to assess microvascular spatial densities and tortuosity, an index of microvascular immaturity. Renal protein expression, gene expression and histology were studied in vitro using immunoblotting, polymerase chain reaction and staining.
RESULTS
RAS demonstrated a loss of medium-sized vessels (0.2-0.3 mm) compared with donor kidneys (P = 0.037) and increased microvascular tortuosity. RAS kidneys had greater protein expression of angiopoietin-1, hypoxia-inducible factor-1α and thrombospondin-1 but lower protein expression of vascular endothelial growth factor (VEGF) than donor kidneys. Renal fibrosis, loss of peritubular capillaries (PTCs) and pericyte detachment were greater in RAS, yet they had more newly formed PTCs than donor kidneys. Therefore, our study quantified significant microvascular remodeling in the poststenotic human kidney. RAS induced renal microvascular loss, vascular remodeling and fibrosis. Despite downregulated VEGF, stenotic kidneys upregulated compensatory angiogenic pathways related to angiopoietin-1.
CONCLUSIONS
These observations underscore the nature of human RAS as a microvascular disease distal to main vessel stenosis and support therapeutic strategies directly targeting the poststenotic kidney microcirculation in patients with RAS.

Identifiants

pubmed: 35451482
pii: 6572378
doi: 10.1093/ndt/gfac156
pmc: PMC9494086
doi:

Substances chimiques

Angiopoietin-1 0
Hypoxia-Inducible Factor 1, alpha Subunit 0
Thrombospondins 0
Vascular Endothelial Growth Factor A 0

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

1844-1856

Subventions

Organisme : NIDDK NIH HHS
ID : R01 DK120292
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK122734
Pays : United States
Organisme : NIA NIH HHS
ID : R21 AG062104
Pays : United States

Informations de copyright

© The Author(s) 2022. Published by Oxford University Press on behalf of the ERA.

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Auteurs

Nattawat Klomjit (N)

Division of Nephrology and Hypertension, Mayo Clinic, Rochester, MN, USA.
Division of Nephrology and Hypertension, University of Minnesota, Minneapolis, MN, USA.

Xiang-Yang Zhu (XY)

Division of Nephrology and Hypertension, Mayo Clinic, Rochester, MN, USA.

Alfonso Eirin (A)

Division of Nephrology and Hypertension, Mayo Clinic, Rochester, MN, USA.

Aditya S Pawar (AS)

Division of Nephrology and Hypertension, Mayo Clinic, Rochester, MN, USA.

Sabena M Conley (SM)

Division of Nephrology and Hypertension, Mayo Clinic, Rochester, MN, USA.

Amrutesh S Puranik (AS)

Division of Nephrology and Hypertension, Mayo Clinic, Rochester, MN, USA.

Christopher M Ferguson (CM)

Division of Nephrology and Hypertension, Mayo Clinic, Rochester, MN, USA.

Seo Rin Kim (SR)

Division of Nephrology and Hypertension, Mayo Clinic, Rochester, MN, USA.

Hui Tang (H)

Division of Nephrology and Hypertension, Mayo Clinic, Rochester, MN, USA.

Kyra L Jordan (KL)

Division of Nephrology and Hypertension, Mayo Clinic, Rochester, MN, USA.

Ishran M Saadiq (IM)

Division of Nephrology and Hypertension, Mayo Clinic, Rochester, MN, USA.

Amir Lerman (A)

Department of Cardiovascular Medicine, Mayo Clinic, Rochester, MN, USA.

Joseph P Grande (JP)

Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, USA.

Stephen C Textor (SC)

Division of Nephrology and Hypertension, Mayo Clinic, Rochester, MN, USA.

Lilach O Lerman (LO)

Division of Nephrology and Hypertension, Mayo Clinic, Rochester, MN, USA.

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