Montada-Atin T, Prasad GVR. Recent advances in new-onset diabetes mellitus after kidney transplantation. World J Diabetes 2021; 12(5): 541-555 [PMID: 33995843 DOI: 10.4239/wjd.v12.i5.541]
Corresponding Author of This Article
G V Ramesh Prasad, MBBS, PhD, Professor, Kidney Transplant Program, St. Michael's Hospital, 61 Queen Street East, 9th Floor, Toronto M5C 2T2, Ontario, Canada. ramesh.prasad@unityhealth.to
Research Domain of This Article
Endocrinology & Metabolism
Article-Type of This Article
Review
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Diabetes. May 15, 2021; 12(5): 541-555 Published online May 15, 2021. doi: 10.4239/wjd.v12.i5.541
Recent advances in new-onset diabetes mellitus after kidney transplantation
Tess Montada-Atin, G V Ramesh Prasad
Tess Montada-Atin, G V Ramesh Prasad, Kidney Transplant Program, St. Michael's Hospital, Toronto M5C 2T2, Ontario, Canada
G V Ramesh Prasad, Department of Medicine, University of Toronto, Toronto M5C 2T2, Canada
Author contributions: Montada-Atin T critically reviewed and appraised the literature, and wrote the paper; Prasad GVR designed the study, critically reviewed and appraised the literature and wrote the paper; all authors read and approved the final manuscript.
Conflict-of-interest statement: Authors declare no conflict of interests for this article.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: G V Ramesh Prasad, MBBS, PhD, Professor, Kidney Transplant Program, St. Michael's Hospital, 61 Queen Street East, 9th Floor, Toronto M5C 2T2, Ontario, Canada. ramesh.prasad@unityhealth.to
Received: January 27, 2021 Peer-review started: January 27, 2021 First decision: February 25, 2021 Revised: March 5, 2021 Accepted: April 14, 2021 Article in press: April 14, 2021 Published online: May 15, 2021
Abstract
A common challenge in managing kidney transplant recipients (KTR) is post-transplant diabetes mellitus (PTDM) or diabetes mellitus (DM) newly diagnosed after transplantation, in addition to known pre-existing DM. PTDM is an important risk factor for post-transplant cardiovascular (CV) disease, which adversely affects patient survival and quality of life. CV disease in KTR may manifest as ischemic heart disease, heart failure, and/or left ventricular hypertrophy. Available therapies for PTDM include most agents currently used to treat type 2 diabetes. More recently, the use of sodium glucose co-transporter 2 inhibitors (SGLT2i), glucagon-like peptide-1 receptor agonists (GLP-1 RA), and dipeptidyl peptidase 4 inhibitors (DPP4i) has cautiously extended to KTR with PTDM, even though KTR are typically excluded from large general population clinical trials. Initial evidence from observational studies seems to indicate that SGLT2i, GLP-1 RA, and DPP4i may be safe and effective for glycemic control in KTR, but their benefit in reducing CV events in this otherwise high-risk population remains unproven. These newer drugs must still be used with care due to the increased propensity of KTR for intravascular volume depletion and acute kidney injury due to diarrhea and their single-kidney status, pre-existing burden of peripheral vascular disease, urinary tract infections due to immunosuppression and a surgically altered urinary tract, erythrocytosis from calcineurin inhibitors, and reduced kidney function from acute or chronic rejection.
Core Tip: Kidney transplant recipients commonly develop post-transplant diabetes mellitus. Sodium glucose co-transporter 2 inhibitors, glucagon-like peptide-1 receptor agonists, and dipeptidyl peptidase 4 inhibitors are now available for treating type 2 diabetes mellitus. There is increasing evidence that these classes of drugs are effective in kidney transplant recipients, but caution is still advised due to their increased propensity otherwise for intravascular volume depletion, infections, and reduced kidney function.
