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Comment
. 2025 Oct 8;29(1):428.
doi: 10.1186/s13054-025-05703-1.

Reconsidering the urea-to-creatinine ratio as a signal of muscle catabolism in patients with cirrhosis

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Comment

Reconsidering the urea-to-creatinine ratio as a signal of muscle catabolism in patients with cirrhosis

Abderrahim Oussalah et al. Crit Care. .
No abstract available

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Conflict of interest statement

Declarations. Ethical approval and consent to participate: Not applicable. Consent for publication: Not applicable. Competing interests: The authors declare no competing interests.

Figures

Fig. 1
Fig. 1
Impact of cirrhosis on the interpretation of the urea-to-creatinine ratio (UCR). A In patients without cirrhosis, ammonia generated in the gut is efficiently converted to urea via the hepatic urea cycle and excreted by the kidneys, while creatinine production remains stable. Under these conditions, the UCR has been proposed as a helpful index of protein catabolism in critically ill patients [1]. B In patients with cirrhosis, both components of the UCR are altered by disease-specific mechanisms. On the creatinine side, sarcopenia and reduced hepatic creatine synthesis lower creatinine generation, while increased tubular secretion and analytical underestimation in hyperbilirubinemia further decrease measured levels. On the urea side, hepatocellular dysfunction and portosystemic shunting impair ureagenesis, resulting in lower plasma urea levels and increased systemic ammonia; the ammonia-to-urea ratio reflects this reduced cycle efficiency. Gastrointestinal bleeding delivers an exogenous nitrogen load that increases urea independently of proteolysis. Renal dysfunction, particularly hepatorenal syndrome, further increases creatinine levels. The combined effect is that both the numerator (urea) and the denominator (creatinine) are altered by processes unrelated to muscle catabolism, resulting in UCR values that may misrepresent metabolic state in patients with cirrhosis. Created with BioRender.com

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