Effects on calcium phosphate homeostasis after sodium-glucose cotransporter 2 inhibitor in patients with advanced chronic kidney disease and type 2 diabetes mellitus.

Chronic kidney disease Phosphate SGLT2i Type 2 diabetes mellitus

Journal

Diabetes research and clinical practice
ISSN: 1872-8227
Titre abrégé: Diabetes Res Clin Pract
Pays: Ireland
ID NLM: 8508335

Informations de publication

Date de publication:
09 Aug 2024
Historique:
received: 01 07 2024
revised: 03 08 2024
accepted: 08 08 2024
medline: 12 8 2024
pubmed: 12 8 2024
entrez: 11 8 2024
Statut: aheadofprint

Résumé

The effects of sodium-glucose cotransporter 2 inhibitors (SGLT2i) on calcium phosphate homeostasis in patients with type 2 diabetes mellitus (T2DM) and chronic kidney disease (CKD) remain uncertain. A retrospective observational cohort study of patients with T2DM at CKD stage G3b-5ND who received SGLT2i as compared to control from 1 January 2015 through 31 December 2021 was recruited. Propensity score assignment at 1:3 ratio by logistic regression was done. All patients were followed for 12 months. Outcomes were changes in phosphate level. We analyzed 1,450 SGLT2i users and 4,350 control subjects. At the 12th month, SGLT2i users had a slower increase in phosphate levels (absolute change: -0.01 ± 0.28 vs + 0.14 ± 0.34 mmol/L; percentage change: -0.74 % ± 25.56 vs + 10.88 ± 28.15 %, P for both < 0.001). The proportion of patients with high phosphate was lower with SGLT2i (8.2 % vs 24.6 % increase). In the generalized estimating equation, SGLT2i was linked to a longitudinal reduction in phosphate (B -0.039, P<0.001). SGLT2i can effectively slow down the progression of phosphate retention in advanced CKD with T2DM.

Sections du résumé

BACKGROUND BACKGROUND
The effects of sodium-glucose cotransporter 2 inhibitors (SGLT2i) on calcium phosphate homeostasis in patients with type 2 diabetes mellitus (T2DM) and chronic kidney disease (CKD) remain uncertain.
METHODS METHODS
A retrospective observational cohort study of patients with T2DM at CKD stage G3b-5ND who received SGLT2i as compared to control from 1 January 2015 through 31 December 2021 was recruited. Propensity score assignment at 1:3 ratio by logistic regression was done. All patients were followed for 12 months. Outcomes were changes in phosphate level.
RESULTS RESULTS
We analyzed 1,450 SGLT2i users and 4,350 control subjects. At the 12th month, SGLT2i users had a slower increase in phosphate levels (absolute change: -0.01 ± 0.28 vs + 0.14 ± 0.34 mmol/L; percentage change: -0.74 % ± 25.56 vs + 10.88 ± 28.15 %, P for both < 0.001). The proportion of patients with high phosphate was lower with SGLT2i (8.2 % vs 24.6 % increase). In the generalized estimating equation, SGLT2i was linked to a longitudinal reduction in phosphate (B -0.039, P<0.001).
CONCLUSIONS CONCLUSIONS
SGLT2i can effectively slow down the progression of phosphate retention in advanced CKD with T2DM.

Identifiants

pubmed: 39128564
pii: S0168-8227(24)00728-9
doi: 10.1016/j.diabres.2024.111818
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

111818

Informations de copyright

Copyright © 2024. Published by Elsevier B.V.

Déclaration de conflit d'intérêts

Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

Gordon Chun Kau Chan (GCK)

Department of Medicine and Therapeutics, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong Special Administrative Regions of China.

Jack Kit Chung Ng (JKC)

Department of Medicine and Therapeutics, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong Special Administrative Regions of China; Li Ka Shing Institute of Health Sciences (LiHS), Faculty of Medicine, The Chinese University of Hong Kong, Shatin, Hong Kong Special Administrative Regions of China.

Cheuk Chun Szeto (CC)

Department of Medicine and Therapeutics, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong Special Administrative Regions of China; Li Ka Shing Institute of Health Sciences (LiHS), Faculty of Medicine, The Chinese University of Hong Kong, Shatin, Hong Kong Special Administrative Regions of China.

Kai Ming Chow (KM)

Department of Medicine and Therapeutics, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong Special Administrative Regions of China. Electronic address: Chow_Kai_Ming@alumni.cuhk.net.

Classifications MeSH