ArticleBritish journal of cancer2025
Pseudo acute kidney injury in patients receiving CDK4/6 inhibitors.
Article in British journal of cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Overview of pseudo-acute kidney injury.Renal failure · 2026Review
- Creatinine-Cystatin C Discrepancy and Renal Transporter Polymorphisms in Japanese Patients with Breast Cancer Receiving Abemaciclib.Clinical pharmacology and therapeutics · 2026Article
- Young Investigator Award 2026: Extent and incidence of pseudo-worsening of kidney function due to oral antitumor therapeutics in the AMBORA cohort: an analysis of real-world data.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Pilot Study of Diagnostic Performance of Serum Creatinine/Cystatin C Ratio for Pseudo-AKI.Kidney international reports · 2026Article
- Role of solute carrier transporters in the biodistribution and toxicity of chemotherapeutic drugs.Pharmacological reviews · 2026Review
- Extent and Incidence of Pseudo-Worsening of Kidney Function Due to Oral Antitumor Therapeutics in the AMBORA Cohort: An Analysis of Real-World Data.Clinical pharmacology and therapeutics · 2026Article
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8 authors.
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Abstract
introductionCDK4/6 inhibitors (CDK4/6i) improve progression-free survival in patients with advanced oestrogen-receptor-positive breast cancer. However, all CDK4/6i may increase creatinine levels, which can indicate kidney injury. In vitro research has shown that CDK4/6i can also inhibit tubular secretion of creatinine, thereby causing the phenomenon 'pseudo-acute kidney injury (pseudo-AKI)'. The incidence of pseudo-AKI is, however, unknown. We aimed to determine this incidence by assessing cystatin C, a protein filtered in the glomerulus without being subject to tubular secretion, in patients with creatinine increase during CDK4/6i treatment.
methodsIn this retrospective single-centre cohort study patients with breast cancer who received CDK4/6 inhibitors between January 1st 2017 and December 29th 2023 were screened for the incidence of creatinine increases suggesting potential kidney injury in the first six months of treatment. A significant creatinine increase was defined as 1) a creatinine plasma level of >90 µmol/L in women or >115 µmol/L in men and >10% increase from baseline creatinine plasma level or 2) a creatinine plasma level >1.5 times baseline creatinine or 3) an increase in creatinine plasma level from baseline with >26 µmol/L. Pseudo-AKI was diagnosed if the estimated glomerular filtration rate (eGFR) using cystatin C at the moment of creatinine increase was 1) equal or higher than eGFR using creatinine at baseline and/or 2) at least 25% higher than eGFR using creatinine at the moment of creatinine increase. The primary endpoint was the percentage of patients with pseudo-AKI analysed by means of the binomial probability test.
resultsOf the 234 patients treated with a CDK4/6i, 41 (17.5%) had creatinine levels indicating an AKI. From 22 of these 41 patients, cystatin C could be determined in retrospectively available serum. Pseudo-AKI was found in 16 out of 22 patients (73%, 95% CI 50-89%). In 5 out of 41 patients (12%) the CDK4/6i dose was unjustly adjusted or the drug was stopped due to creatinine increase.
conclusionPseudo-AKI has a high incidence in patients treated with CDK4/6i. Determining an eGFR based on the cystatin C value should therefore be considered as the first step when creatinine increases during CDK4/6i treatment.
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