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Abstract: PO1884

An Elevated Serum Creatinine in a Patient Receiving Palbociclib

Session Information

Category: Onco-Nephrology

  • 1500 Onco-Nephrology

Authors

  • Bonilla, Marco A., Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, Hempstead, New York, United States
  • Bashir, Khawaja Arsalan, Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, Hempstead, New York, United States
  • Jhaveri, Kenar D., Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, Hempstead, New York, United States
Introduction

Serum Creatinine (SCr) is the most widely used parameter in clinical practice to estimate glomerular filtration rate (GFR). Various drugs have been reported to cause a reversible and transient elevation in SCr without a true reduction in overall kidney function

Case Description

A 66-year-old woman with a past medical history of metastatic right breast poorly differentiated invasive ductal carcinoma, hormone receptor-positive, and HER2 negative. Who received treatment with fulvestrant and palbociclib, the dose of Palbociclibwas was 100mg orally a day. Presented for evaluation of elevated serum creatinine with decreased eGFR. On initial evaluation sCr was 1.6mg/dl, blood urea nitrogen of 21mg/dl, eGFR of 33ml/min/1.73m2, her baseline eGFR was ranging from 42 to 52 ml/min/1.73m2 in the past one year. An estimated glomerular filtration rate by cystatin C was performed and showed a value of 47ml/min with a cystatin-C level of 1.36mg/dl, which was at her baseline kidney function for the past year.

Discussion

Creatinine is freely filtered by the glomerulus and actively secreted by the proximal tubule from the peritubular capillaries, which accounts for 10-40% of creatinine clearance. The organic cation transporter 2 (OTC2), multidrug and toxin extrusion protein (MATE) 1 and MATE2-K, are the solute carrier transporters in the kidney that mediate this active tubular secretion. Clinical studies of abemaciclib, another selective inhibitor of CDK 4/6, have shown a reversible increase in creatinine of about 15-40% over baseline of patients with cancer and healthy subjects. This effect has been seen in about 25% of patients treated with abemaciclib however none of the clinical trials on palbociclib have reported an increase in serum creatinine. In our case, the difference between eGFR by cystatin C and by serum creatinine demonstrated not a true decrease in kidney function. We have attributed these events to inhibition of the tubular secretion of creatinine by palbociclib and decided to continue treatment with palbociclib. Physicians should be aware that patients undergoing therapy with palbociclib require monitoring of kidney function and an increase in serum creatinine from baseline, might represent an inhibitory effect of the secretion of creatinine and not an actual decrease in kidney function.