Creatinine-Cystatin C Discrepancy and Renal Transporter Polymorphisms in Japanese Patients with Breast Cancer Receiving Abemaciclib.
Gene–drug pair / mechanism
SLC47A1
Abemaciclib raises serum creatinine by inhibiting renal tubular transporters without lowering true glomerular filtration; SLC47A1 rs2289669 GG is associated with a greater rise, consistent with a MATE1-mediated mechanism.
Summary
Abemaciclib raises serum creatinine by inhibiting renal tubular transporters (pseudo-acute kidney injury) without reducing true glomerular filtration. This single-centre prospective study included 63 Japanese patients with breast cancer. Creatinine rose in 62 of them (median change 0.21 mg/dL), with cystatin C-based eGFR exceeding creatinine-based eGFR by a median 54.9 mL/min/1.73 m2. SLC47A1 rs2289669 GG was associated with a greater rise, and the pre-treatment creatinine/cystatin C ratio predicted the on-treatment discrepancy; the SLC22A2 and SLC47A2 variants tested were not reported as associated. The authors conclude that a pre-treatment cystatin C measurement is needed to interpret creatinine elevation.
Synthesis written by Geno'X. For the full original abstract, please refer to the source publication.
Analysis
The main practical contribution is non-genetic: measure cystatin C before treatment so that pseudo-kidney injury is not mistaken for the real thing. The SLC47A1 association rests on 63 patients and is not a predictive test: it supports a mechanism, not an indication for genotyping.
Analysis by Dr Thibaut Benquey
Why this score?
Clinical impact: 1/3 · Evidence strength: 1/3 · Novelty: 1/2 · Sample size: 0/1 · Publication status: 1/1 → Total: 4/10
Keywords
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