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Kidney‐function assessment supports drug dosing in critical illness but does not directly measure drug clearance. Reduced creatinine generation, fluid shifts and rapidly changing filtration can make creatinine‐based estimates misleading, whereas genuinely augmented renal clearance can cause insufficient drug exposure. These processes can coexist. This narrative review distinguishes estimated glomerular filtration rate from estimated or measured creatinine clearance and explains how equation version, body‐surface‐area indexing and sampling time affect interpretation. It separates the 2021 creatinine, 2012 cystatin C and 2021 creatinine–cystatin C equations of the Chronic Kidney Disease Epidemiology Collaboration (CKD‐EPI) and considers when each can inform a clinical decision. Cystatin C provides complementary information, not an intensive‐care reference standard; timed urinary creatinine clearance is also vulnerable to collection error and changing physiology. We present a resource‐adapted assessment framework rather than a validated dosing algorithm. It accommodates delayed cystatin C results, unavailable or unreliable urine collections, non‐steady‐state kidney function and access to therapeutic drug monitoring. Augmented renal clearance is treated as a continuum, with drug‐specific thresholds distinguished from research definitions. Examples involving antibiotics, levetiracetam and gabapentin show why a kidney‐function estimate must match the metric used in the relevant label or pharmacokinetic model. The practical objective is a documented, revisable dosing decision that integrates estimated kidney function, drug exposure and the consequences of under‐ or over‐treatment, without assuming that biomarker discordance identifies its own cause.
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Liao et al. (2026) studied this question.
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