Current Pharmacological Intervention and Medical Management for Diabetic Kidney Transplant Recipients

Abstract

Hyperglycemia after kidney transplantation is common in both diabetic and non-diabetic patients. Both pretransplant and post-transplant diabetes mellitus are associated with increased kidney allograft failure and mortality. Glucose management may be challenging for kidney transplant recipients. The pathophysiology and pattern of hyperglycemia in patients following kidney transplantation is different from those with type 2 diabetes mellitus. In patients with pre-existing and post-transplant diabetes mellitus, there is limited data on the management of hyperglycemia after kidney transplantation. The following article discusses the nomenclature and diagnosis of pre- and post-transplant diabetes mellitus, the impact of transplant-related hyperglycemia on patient and kidney allograft outcomes, risk factors and potential pathogenic mechanisms of hyperglycemia after kidney transplantation, glucose management before and after transplantation, and modalities for prevention of post-transplant diabetes mellitus.

New-Onset Diabetes Mellitus in Post-renal Transplant Patients on Tacrolimus and Mycophenolate: A Systematic Review

“…CMV infection can cause diabetes by the death of pancreatic beta cells or the generation of pro-inflammatory cytokines, and it can independently develop PTDM. The relative risk of PTDM in CMV-positive individuals is 1.94 times higher than in CMV-negative patients, according to a meta-analysis that included data from 1389 renal transplant recipients [ 2 ].CMV infection quadruples the risk of PTDM in the first three months after KT [ 8 ]. The protective role of maximum antiviral drug use in the development of PTDM is still to be investigated, although such research would undoubtedly be beneficial in the future [ 19 ].…”

“…According to a study, it is responsible for increasing insulin resistance by 62%. However, it has no role in beta-cell activity [ 8 ].…”

“…Kidneys usually excrete gliptins except for linagliptin and gemigliptin, which are excreted by bile. The advantages of linagliptin are it lowers the basal-bolus insulin demand in the early KT period, decreases HbA1C compared to other gliptins, and does not need renal dose adjustment [ 8 ]. In an RCT, vidalagliptin decreased the two-hour postprandial glucose compared to placebo.…”

“…This aids in glycemic management promotes natriuresis and energy loss, and so aids in the reduction of obesity, cardiovascular consequences, and renal function, all of which are accomplished without the usage of insulin. Hepatic metabolism is the primary route of drug clearance for SGLT2 inhibitors [ 8 ]. Treatment with SGLT2 inhibitors in type 2 DM patients has been found to slow the course of chronic kidney disease (CKD) and adverse renal events progression, as shown in five clinical trials namely EMPA-REG, CANVAS, DECLARE, CREDENCE, and DAPA-CKD [ 20 ].…”

“…Under the current immunosuppressive regimen of tacrolimus (TAC), mycophenolic acid, and steroids, the incidence of PTDM is estimated to be between 20% and 30% [ 4 ]. According to the United States Renal Data System (USRDS) data from 1996-2000, PTDM occurs in 16% and 24% of cases at one and three years, respectively, following kidney transplantation (KT) [ 8 ]. Historically, the lack of consistent diagnostic criteria is attributed to variations in the prevalence of DM.…”