Sodium-glucose cotransporter 2 inhibitors for diabetes mellitus control after kidney transplantation: Review of the current evidence

Publikation: Bidrag til tidsskriftReviewForskningfagfællebedømt

Sodium-glucose cotransporter type 2 inhibitors (SGLT2i) are promising drugs to treat chronic kidney disease patients with or without diabetes mellitus (DM). Besides improving glycemic control, SGLT2i are cardioprotective and kidney protective and decrease bodyweight, serum uric acid, blood pressure, albuminuria and glomerular hyperfiltration. These effects may benefit graft function and survival in kidney transplant (KT) patients. In this review, we evaluate data on the efficacy and safety of SGLT2i for KT patients with DM. Eleven studies with 214 diabetic KT patients treated with SGLT2i have been reported. SGLT2i lowered haemoglobin A1c and bodyweight. While glomerular filtration rate may be reduced in the short-term, it remained similar to baseline after 3–12 months. In two studies, blood pressure decreased and remained unchanged in the others. There were no significant changes in urine protein to creatinine ratio. Regarding safety, 23 patients had urinary tract infections, 2 patients had a genital yeast infection, one had acute kidney injury, and one had mild hypoglycaemia. No cases of ketoacidosis or acute rejection were reported. In conclusion, the limited experience so far suggests that SGLT2i are safe in KT patients with DM, decrease bodyweight and improve glycemic control. However, some of the benefits observed in larger studies in the non-KT population have yet to be demonstrated in KT recipients, including preservation of kidney function, reduction in blood pressure and decreased proteinuria.

OriginalsprogEngelsk
TidsskriftNephrology
Vol/bind26
Udgave nummer12
Sider (fra-til)1007-1017
ISSN1320-5358
DOI
StatusUdgivet - 2021

Bibliografisk note

Funding Information:
Ministry of Research, Innovation and Digitization, CNCS/CCCDI‐UEFISCDI, Grant/Award Number: PN‐III‐P4‐ID‐PCE‐2020‐2393; Comunidad de Madrid en Biomedicina, Grant/Award Number: B2017/BMD‐3686 CIFRA2‐CM; Sociedad Española de Nefrología; FIS/Fondos FEDER, Grant/Award Numbers: RD016/0009, AC18/00071, AC18/00064, ERA‐PerMed‐JTC2018, DTS18/00032, PI19/00815, PI19/00588, PI18/01386, PI17/00257; Presidency of Turkey, Presidency of Strategy and Budget Funding information

Funding Information:
M. K. gratefully acknowledges use of the services and facilities of the Koc University Research Center for Translational Medicine (KUTTAM), funded by the Presidency of Turkey, Presidency of Strategy and Budget. The content is solely the responsibility of the authors and does not necessarily represent the official views of the “Presidency of Strategy and Budget.” A. O. researches are supported by FIS/Fondos FEDER (PI17/00257, PI18/01386, PI19/00588, PI19/00815, DTS18/00032, ERA‐PerMed‐JTC2018 (KIDNEY ATTACK AC18/00064 and PERSTIGAN AC18/00071, ISCIII‐RETIC REDinREN RD016/0009), Sociedad Española de Nefrología, FRIAT, Comunidad de Madrid en Biomedicina B2017/BMD‐3686 CIFRA2‐CM. A. C. was supported by a grant of the Ministry of Research, Innovation and Digitization, CNCS/CCCDI‐UEFISCDI, project number PN‐III‐P4‐ID‐PCE‐2020‐2393, within PNCDIII.

Publisher Copyright:
© 2021 Asian Pacific Society of Nephrology.

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