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Early measurement of KIM-1 predicts outcomes for APAP-induced liver injury

Kidney function, more specifically the kidney injury molecule 1, was found to be a predictor of outcomes in patients with acetaminophen-induced liver injury, according to study data.

Researchers analyzed data of 74 adult patients with and without acute liver injury (ALI), secondary to acetaminophen (APAP) ingestion by a single overdose, staggered overdose or therapeutic excess. The researchers used immunoassay to quantify kidney injury molecule 1 (KIM-1) upon admission to a liver transplant clinic and analyzed its “diagnostic performance” to predict its outcome of the patients compared with serum creatinine concentration. Of the patients, seven did not develop liver or kidney injury and were therefore not included in the final analyses.

“We investigat[ed] the hypothesis that measurement of circulating KIM-1 during APAP hepatotoxicity can represent a more sensitive and specific predictor of patient outcomes than serum creatinine,” the researchers wrote.

Of the 67 patients who developed ALI, 42 survived and 25 either died (n = 16) or underwent liver transplant (n = 9; LT). KIM-1 plasma was slightly more elevated on day 1 in patients that died or required LT compared to the survivors (1,182 ± 251 pg/mL vs. 214 ± 45 pg/mL; P < .005).

KIM-1 was found to be superior to serum creatinine (area under the curve (AUC): 0.87; 95% CI, 0.78-0.95 vs. 0.76; 95% CI, 0.64-0.87) and other indicators on day 1, according to the receiver operator characteristic analysis.

In addition, a multivariable logistic regression model showed KIM-1 to be an independent predictor for outcome at the 5% level (P < .0386), even when considering all factors such as gender, encephalopathy grade and creatinine. The model also accounted for “approximately 89.5% variability in patients’ response (pseudo-R^2 = 0.895),” according to the research.

“The present study adds a novel, translational biomarker of kidney injury into this panel, and further clinical development may result in prognostic models that are superior to current tools to aid management of patients and provide additional mechanistic insights into development of APAP-induced hepatotoxicity,” the researchers concluded.

Disclosures: Antoine reports no relevant financial disclosures. Please see the full study for a list of all other authors’ relevant financial disclosures.