Sex differences in soluble prorenin receptor in patients with type 2 diabetes.


Journal

Biology of sex differences
ISSN: 2042-6410
Titre abrégé: Biol Sex Differ
Pays: England
ID NLM: 101548963

Informations de publication

Date de publication:
01 05 2021
Historique:
received: 06 10 2020
accepted: 07 04 2021
entrez: 2 5 2021
pubmed: 3 5 2021
medline: 15 12 2021
Statut: epublish

Résumé

The soluble prorenin receptor (sPRR), a member of the renin-angiotensin system (RAS), is elevated in plasma of patients with preeclampsia, hypertension, chronic kidney disease (CKD), and type 2 diabetes. Our goal was to examine the relationship between sPRR and RAS activation to define whether sexual dimorphisms in sPRR might explain sex disparities in renal outcomes in patients with type 2 diabetes. Two hundred sixty-nine participants were included in the study (mean age, 48 ± 16 years; 42% men, 58% women), including 173 controls and 96 subjects with type 2 diabetes. In plasma and urine, we measured sPRR, plasma renin activity (PRA), and prorenin. In the urine, we also measured angiotensinogen along with other biomarkers of renal dysfunction. Plasma sPRR and PRA were significantly higher in women with type 2 diabetes compared to men. In these women, plasma sPRR was positively correlated with PRA, age, and body mass index (BMI). In contrast, in men the sPRR in urine but not in plasma positively correlated with eGFR in urine, but negatively correlated with urine renin activity, plasma glucose, age, and BMI. In patients with type 2 diabetes, sPRR contributes to RAS stimulation in a sex-dependent fashion. In diabetic women, increased plasma sPRR parallels the activation of systemic RAS; while in diabetic men, decreased sPRR in urine matches intrarenal RAS stimulation. sPRR might be a potential indicator of intrarenal RAS activation and renal dysfunction in men and women with type 2 diabetes.

Sections du résumé

BACKGROUND
The soluble prorenin receptor (sPRR), a member of the renin-angiotensin system (RAS), is elevated in plasma of patients with preeclampsia, hypertension, chronic kidney disease (CKD), and type 2 diabetes. Our goal was to examine the relationship between sPRR and RAS activation to define whether sexual dimorphisms in sPRR might explain sex disparities in renal outcomes in patients with type 2 diabetes.
METHODS
Two hundred sixty-nine participants were included in the study (mean age, 48 ± 16 years; 42% men, 58% women), including 173 controls and 96 subjects with type 2 diabetes. In plasma and urine, we measured sPRR, plasma renin activity (PRA), and prorenin. In the urine, we also measured angiotensinogen along with other biomarkers of renal dysfunction.
RESULTS
Plasma sPRR and PRA were significantly higher in women with type 2 diabetes compared to men. In these women, plasma sPRR was positively correlated with PRA, age, and body mass index (BMI). In contrast, in men the sPRR in urine but not in plasma positively correlated with eGFR in urine, but negatively correlated with urine renin activity, plasma glucose, age, and BMI.
CONCLUSIONS
In patients with type 2 diabetes, sPRR contributes to RAS stimulation in a sex-dependent fashion. In diabetic women, increased plasma sPRR parallels the activation of systemic RAS; while in diabetic men, decreased sPRR in urine matches intrarenal RAS stimulation. sPRR might be a potential indicator of intrarenal RAS activation and renal dysfunction in men and women with type 2 diabetes.

Identifiants

pubmed: 33933156
doi: 10.1186/s13293-021-00374-3
pii: 10.1186/s13293-021-00374-3
pmc: PMC8088668
doi:

Substances chimiques

Receptors, Cell Surface 0
Renin EC 3.4.23.15
Prorenin Receptor 0

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

33

Subventions

Organisme : NIDDK NIH HHS
ID : RO1-DK114321
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK107444
Pays : United States
Organisme : NICHD NIH HHS
ID : K12 HD043451
Pays : United States
Organisme : NIGMS NIH HHS
ID : U54 GM104940
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA008748
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR003096
Pays : United States
Organisme : U.S. Department of Veterans Affairs
ID : #BX003725
Organisme : NIDDK NIH HHS
ID : R01 DK074970
Pays : United States
Organisme : NIGMS NIH HHS
ID : P30 GM103337
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK104375
Pays : United States

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Auteurs

Bruna Visniauskas (B)

Department of Physiology, Tulane University School of Medicine, 1430 Tulane Avenue, SL39, New Orleans, LA, 70112, USA.

Danielle Y Arita (DY)

Department of Physiology, Tulane University School of Medicine, 1430 Tulane Avenue, SL39, New Orleans, LA, 70112, USA.

Carla B Rosales (CB)

Department of Physiology, Tulane University School of Medicine, 1430 Tulane Avenue, SL39, New Orleans, LA, 70112, USA.

Mohammed A Feroz (MA)

Department of Physiology, Tulane University School of Medicine, 1430 Tulane Avenue, SL39, New Orleans, LA, 70112, USA.

Christina Luffman (C)

Department of Physiology, Tulane University School of Medicine, 1430 Tulane Avenue, SL39, New Orleans, LA, 70112, USA.

Michael J Accavitti (MJ)

Department of Physiology, Tulane University School of Medicine, 1430 Tulane Avenue, SL39, New Orleans, LA, 70112, USA.

Gabrielle Dawkins (G)

Department of Physiology, Tulane University School of Medicine, 1430 Tulane Avenue, SL39, New Orleans, LA, 70112, USA.

Jennifer Hong (J)

Department of Physiology, Tulane University School of Medicine, 1430 Tulane Avenue, SL39, New Orleans, LA, 70112, USA.

Andrew C Curnow (AC)

Department of Physiology, Tulane University School of Medicine, 1430 Tulane Avenue, SL39, New Orleans, LA, 70112, USA.

Tina K Thethi (TK)

Department of Medicine, Endocrinology Division, Tulane University School of Medicine, New Orleans, LA, USA.
AdventHealth, Translational Research Institute, Orlando, FL, USA.

John J Lefante (JJ)

Department of Biostatistics and Data Science, School of Public Health and Tropical Medicine, New Orleans, LA, USA.

Edgar A Jaimes (EA)

Renal Service, Memorial Sloan Kettering Cancer Center, New York, NY, USA.

Franck Mauvais-Jarvis (F)

Department of Medicine, Endocrinology Division, Tulane University School of Medicine, New Orleans, LA, USA.
Southeast Louisiana Veterans Healthcare System, New Orleans, LA, USA.
Tulane Center of Excellence in Sex-Based Biology and Medicine, New Orleans, LA, USA.

Vivian A Fonseca (VA)

Department of Medicine, Endocrinology Division, Tulane University School of Medicine, New Orleans, LA, USA.
Southeast Louisiana Veterans Healthcare System, New Orleans, LA, USA.

Minolfa C Prieto (MC)

Department of Physiology, Tulane University School of Medicine, 1430 Tulane Avenue, SL39, New Orleans, LA, 70112, USA. mprieto@tulane.edu.
Tulane Hypertension and Renal Center of Excellence, Tulane University School of Medicine, New Orleans, LA, USA. mprieto@tulane.edu.

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