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Abstract: FR-PO235

Olaparib Associated AKI: Real or Fake?

Session Information

Category: Onconephrology

  • 1700 Onconephrology


  • Clay, Tyler W., MedStar Georgetown University Hospital, Washington, District of Columbia, United States
  • Kirby, Madeline, MedStar Georgetown University Hospital, Washington, District of Columbia, United States
  • Pourafshar, Negiin, MedStar Georgetown University Hospital, Washington, District of Columbia, United States

Olaparib is a chemotherapy drug used in the treatment of metastatic ovarian and breast cancer. Olaparib, an inhibitor of human Poly-(ADP-ribose)-polymerase (PARP), is the first PARPi approved for the treatment of metastatic ovarian cancer. Olaparib has been associated with increases in serum creatinine thought to be due to a non-pathologic mechanism. As the renal function of oncology patients can affect their course of care, distinguishing pathologic kidney injury from non-pathologic laboratory changes is important.

Case Description

A 61-year-old woman with non-insulin dependent type II diabetes and hypertension was receiving chemotherapy for metastatic ovarian cancer with carcinomatosis. Baseline creatinine was 0.8 mg/dl with eGFR 67 ml/min. She received paclitaxel and then was started on Olaparib. Her creatinine rose over the course of several months to a peak of 2.0 mg/dl and eGFR of 28 ml/min. Urinalysis was negative. Urine protein-creatinine ratio was 55 mg/gm. Renal imaging was negative. Subsequent serum cystatin C was normal at 1.11 mg/l and eGFR of 63ml/min. This suggested Olaparib caused a non-pathologic increase in serum creatinine. Patient continued therapy and future kidney function evaluation used cystatin C.


This case showcases the importance of distinguishing between pathologic and non-pathologic increases in serum creatinine in cancer patients. As kidney damage can alter the pharmacodynamics of chemotherapy drugs and alter the available pharmacologic options for individuals undergoing cancer treatment, determining the cause of alterations in serum creatinine is critical.

Olaparib's effect on serum creatinine is thought to be due to interactions with creatinine secreting transporter proteins on the apical membrane of the proximal tubule. Interactions with these transporters can falsely increase the serum creatinine without intrinsically altering renal function. Cystatin C is freely filtered by the glomerulus without utilizing transporter proteins, therefore it is not affected by the use of Olaparib. A recent case series showed a 14% increase in creatinine in 66 patients receiving Olaparib without significant changes in cystatin-C measurements. In this patient with sustained elevation in creatinine but normal cystatin C following Olaparib treatment, the likely mechanism of an elevated creatinine was non-pathologic effects of Olaparib.