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Abstract: TH-PO066

AKI in a Kidney Transplant Patient Started on Ranolazine

Session Information

Category: Acute Kidney Injury

  • 102 AKI: Clinical, Outcomes, and Trials


  • Howard, Andrew J., Walter Reed National Military Medical Center, Bethesda, Maryland, United States
  • Frankston, Amy J., Walter Reed National Military Medical Center, Bethesda, Maryland, United States

Ranolazine is an antianginal agent only rarely associated with kidney failure (< 1%). We present a case of a kidney transplant recipient who experienced acute kidney injury (AKI) and hyperkalemia after starting ranolazine, and subsequently improved after it was stopped.

Case Description

A 74-year-old man with end-stage kidney disease (ESKD), presumed secondary to diabetic nephropathy, received a deceased-donor kidney transplant in 2014. Post-transplant course was complicated by BK nephropathy with persistent low-grade viremia and atypical hemolytic uremic syndrome treated with ravulizumab. He presented to the Emergency Department at the request of his hematologist for hyperkalemia and acute kidney injury discovered on routine labs. Baseline serum creatinine was 1.3-1.6 mg/dL. At presentation, serum creatinine was 3.23 mg/dL and potassium 7.3 meq/L. After a standard evaluation, there was no obvious etiology for AKI, and an urgent transplant kidney biopsy was performed. Biopsy showed severe tubular injury with interstitial inflammation and focal tubulitis, mild interstitial fibrosis and tubular atrophy (30%). There was no evidence of T-cell or antibody mediated rejection, transplant glomerulopathy, de-novo glomerulonephritis, or recurrent atypical hemolytic uremic syndrome. On review, the only new medication prescribed was ranolazine. This was held and he was treated medically for his hyperkalemia. Renal function subsequently improved, with a new baseline creatinine of 1.8-2.3 mg/dL. Hyperkalemia resolved. He is asymptomatic off ranolazine.


This patient developed AKI and hyperkalemia approximately 6 months after starting ranolazine. This is a rare adverse effect with only a few reported cases in the literature. A previous report implicated ranolazine as a cause of AKI due to drug-induced phospholipidosis, with the finding of zebra bodies on electron microscopy. Our patient’s biopsy did not have zebra bodies present, making drug-induced phospholipidosis less likely. The mechanism is unclear. This case demonstrates that a thorough medication review and cessation of any possibly offending agents is vital in assessing AKI of unclear etiology.

Disclaimer: The views expressed in this Abstract are those of the authors and do not necessarily reflect the official policy of the Department of Defense or the United States Government.