Open AccessEverolimus worsening chronic proteinuria in patient with diabetic nephropathy post liver transplantation
Author(s) -
Ramy M Hanna,
Beshoy Yanny,
Farid Arman,
Marina Barsoum,
Mira Mikhail,
Maha Al Baghdadi,
Anjay Rastogi,
W. Dean Wallace,
Sammy Saab
Publication year - 2019
Publication title -
saudi journal of kidney diseases and transplantation/našrat amraḍ wa zira'aẗ al-kulaẗ
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.268
H-Index - 30
eISSN - 2320-3838
pISSN - 1319-2442
DOI - 10.4103/1319-2442.265481
Subject(s) - medicine , proteinuria , everolimus , thrombotic microangiopathy , sirolimus , urology , diabetic nephropathy , creatinine , calcineurin , renal biopsy , transplantation , gastroenterology , glomerulosclerosis , endocrinology , renal function , kidney , disease
Mammalian target of rapamycin (mTOR) inhibitors are used in renal sparing protocols and transplant immunosuppression in patients with solid organ and stem cell transplants. They cause various side effects, including proteinuria, which is mediated by blockade of the vascular endothelial growth factor receptor pathway. There have been various reports of mTOR inhibitors causing proteinuria or worsening proteinuria form preexisting renal glomerulo-pathies. We report a 73-year old male with diabetic glomerulosclerosis, acute liver failure due to Budd-Chiari syndrome, chronic low platelets, and worsening proteinuria from 0.46 g protein/g creatinine to 2.2 g protein/g creatinine. Workup revealed no thrombotic microangiopathy through skin biopsy, and a renal biopsy confirmed only clinically suspected diabetic and hypertensive glomerulosclerosis and possible calcineurin inhibitors. On discontinuation of everolimus urine protein decreased back to 0.6 g/g creatinine. We review the mechanism of mTOR-induced proteinuria and how this may affect diabetic nephropathy secondarily. We also consider the clinical implications of this in transplant patients receiving these agents.