Dipeptidyl peptidase-4 inhibitor-related renal disease.


Journal

Journal of diabetes and its complications
ISSN: 1873-460X
Titre abrégé: J Diabetes Complications
Pays: United States
ID NLM: 9204583

Informations de publication

Date de publication:
10 2023
Historique:
received: 08 05 2023
revised: 29 07 2023
accepted: 19 08 2023
medline: 10 10 2023
pubmed: 8 9 2023
entrez: 7 9 2023
Statut: ppublish

Résumé

Dipeptidyl peptidase-4 (DPP-4) inhibitors are widely used to treat type 2 diabetes (T2D). Lowering blood glucose is expected also to reduce the progression of diabetic nephropathy. We experienced a patient with T2D who achieved good glycemic control with a DPP-4 inhibitor but experienced rapid deterioration of renal function. Therefore, we performed a retrospective study of similar patients treated at our hospital. Out of 56 patients with biopsy-proven diabetic nephropathy who underwent native kidney biopsy at Toranomon Hospital from January 2018 through December 2022, we selected 22 patients who had been receiving DPP-4 inhibitors for at least 9 months at the time of kidney biopsy. Of these patients, we evaluated 16 diagnosed with class IIa diabetic nephropathy according to Tervaert's pathologic classification. The yearly estimated glomerular filtration rate (eGFR) slope in the 16 patients was arranged from the highest to the lowest slope. Ten patients with a large eGFR slope had thrombotic microangiopathy (TMA)-like lesions characterized by glomerular endothelial cell proliferation and GBM duplication on kidney biopsy (group A), whereas the remaining 6 patients did not have TMA-like lesions (group B). Group A had a median (interquartile range [IQR]) eGFR of 18.2 (16.2, 26.2) and a yearly median (IQR) eGFR slope of -11.2 (-17.6, -9.2) mL/min/1.73 m DPP-4 inhibitors promote vascular endothelial regeneration, but when this effect occurs in the glomerulus, glomerular endothelial cell proliferation leads to TMA-like lesions, which may cause an increase in proteinuria and rapid decline in renal function.

Sections du résumé

BACKGROUND
Dipeptidyl peptidase-4 (DPP-4) inhibitors are widely used to treat type 2 diabetes (T2D). Lowering blood glucose is expected also to reduce the progression of diabetic nephropathy. We experienced a patient with T2D who achieved good glycemic control with a DPP-4 inhibitor but experienced rapid deterioration of renal function. Therefore, we performed a retrospective study of similar patients treated at our hospital.
METHODS
Out of 56 patients with biopsy-proven diabetic nephropathy who underwent native kidney biopsy at Toranomon Hospital from January 2018 through December 2022, we selected 22 patients who had been receiving DPP-4 inhibitors for at least 9 months at the time of kidney biopsy. Of these patients, we evaluated 16 diagnosed with class IIa diabetic nephropathy according to Tervaert's pathologic classification. The yearly estimated glomerular filtration rate (eGFR) slope in the 16 patients was arranged from the highest to the lowest slope. Ten patients with a large eGFR slope had thrombotic microangiopathy (TMA)-like lesions characterized by glomerular endothelial cell proliferation and GBM duplication on kidney biopsy (group A), whereas the remaining 6 patients did not have TMA-like lesions (group B).
RESULTS
Group A had a median (interquartile range [IQR]) eGFR of 18.2 (16.2, 26.2) and a yearly median (IQR) eGFR slope of -11.2 (-17.6, -9.2) mL/min/1.73 m
CONCLUSION
DPP-4 inhibitors promote vascular endothelial regeneration, but when this effect occurs in the glomerulus, glomerular endothelial cell proliferation leads to TMA-like lesions, which may cause an increase in proteinuria and rapid decline in renal function.

Identifiants

pubmed: 37678056
pii: S1056-8727(23)00188-5
doi: 10.1016/j.jdiacomp.2023.108590
pii:
doi:

Substances chimiques

Dipeptidyl-Peptidase IV Inhibitors 0
Hypoglycemic Agents 0
Dipeptidyl-Peptidases and Tripeptidyl-Peptidases EC 3.4.14.-
Dipeptidyl Peptidase 4 EC 3.4.14.5

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

108590

Informations de copyright

Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of competing interest The authors declare no competing financial interests and no conflicts of interest.

Auteurs

Atsuhiko Suenaga (A)

Department of Nephrology and Rheumatology, Toranomon Hospital Kajigaya, Kanagawa, Japan; Department of Nephrology, Saga University School of Medicine, Saga, Japan. Electronic address: atsuhiko4822gh@gmail.com.

Naoki Sawa (N)

Department of Nephrology and Rheumatology, Toranomon Hospital Kajigaya, Kanagawa, Japan; Okinaka Memorial Institute for Medical Research, Toranomon Hospital, Tokyo, Japan.

Yuki Oba (Y)

Department of Nephrology and Rheumatology, Toranomon Hospital Kajigaya, Kanagawa, Japan.

Daisuke Ikuma (D)

Department of Nephrology and Rheumatology, Toranomon Hospital Kajigaya, Kanagawa, Japan.

Akinari Sekine (A)

Department of Nephrology and Rheumatology, Toranomon Hospital, Tokyo, Japan.

Eiko Hasegawa (E)

Department of Nephrology and Rheumatology, Toranomon Hospital, Tokyo, Japan; Okinaka Memorial Institute for Medical Research, Toranomon Hospital, Tokyo, Japan.

Hiroki Mizuno (H)

Department of Nephrology and Rheumatology, Toranomon Hospital Kajigaya, Kanagawa, Japan.

Tatsuya Suwabe (T)

Department of Nephrology and Rheumatology, Toranomon Hospital Kajigaya, Kanagawa, Japan.

Sara Ikeda (S)

Department of Diabetes and Endocrinology, Toranomon Hospital Kajigaya, Kanagawa, Japan.

Tetsuro Tsujimoto (T)

Department of Diabetes and Endocrinology, Toranomon Hospital Kajigaya, Kanagawa, Japan.

Kei Kono (K)

Department of Pathology, Toranomon Hospital, Tokyo, Japan.

Yukako Shintani-Domoto (Y)

Department of Pathology, Toranomon Hospital, Tokyo, Japan.

Keiichi Kinowaki (K)

Department of Pathology, Toranomon Hospital, Tokyo, Japan.

Kenichi Ohashi (K)

Department of Pathology, Toranomon Hospital, Tokyo, Japan; Department of Human Pathology, Tokyo Medical Dental University, Tokyo, Japan.

Motoaki Miyazono (M)

Department of Nephrology, Saga University School of Medicine, Saga, Japan.

Yutaka Yamaguchi (Y)

Yamaguchi's Pathology Laboratory, Chiba, Japan.

Yoshifumi Ubara (Y)

Department of Nephrology and Rheumatology, Toranomon Hospital Kajigaya, Kanagawa, Japan; Okinaka Memorial Institute for Medical Research, Toranomon Hospital, Tokyo, Japan.

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