Many anti-cancer medications inhibit tubular creatinine excretion, thereby increasing serum creatinine without causing acute kidney damage ("pseudo-kidney injury") including cyclin dependent kinase 4/6, poly ADP ribose polymerase (PARP), and specific tyrosine kinase inhibitors. The long-term effect of this blockade is largely unknown and these same drugs also block growth factors that mediate cell proliferation, resulting in damage of renal tubular epithelium.These medications include first-line therapies for lung, breast, and kidney cancer and once initiated, patients remain on these daily oral medications for years during which time clinicians struggle to distinguish "pseudo-kidney injury" from true nephrotoxicity that may progress to chronic kidney disease (CKD).
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Ziolkowski et al. (2024) studied this question.
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