The Marker of Tubular Injury, Kidney Injury Molecule-1 (KIM-1), in Acute Kidney Injury Complicating Acute Pancreatitis: A Preliminary Study

• Main Authors: Justyna Wajda, Paulina Dumnicka, Witold Kolber, Mateusz Sporek, Barbara Maziarz, Piotr Ceranowicz, Marek Kuźniewski, Beata Kuśnierz-Cabala
• Format: Article
• Language: English
• Published: MDPI AG 2020-05-01
• Series: Journal of Clinical Medicine
• Subjects: kidney injury molecule-1; acute pancreatitis; acute kidney injury; biomarkers of acute kidney injury
• Online Access: https://www.mdpi.com/2077-0383/9/5/1463

Acute pancreatitis (AP) may be associated with severe inflammation and hypovolemia leading to organ complications including acute kidney injury (AKI). According to current guidelines, AKI diagnosis is based on dynamic increase in serum creatinine, however, creatinine increase may be influenced by nonrenal factor and appears late following kidney injury. Kidney injury molecule-1 (KIM-1) is a promising marker of renal tubular injury and it has not been studied in AP. Our aim was to assess if urinary KIM-1 may be used to diagnose AKI complicating the early stage of AP. We recruited 69 patients with mild to severe AP admitted to a secondary care hospital during the first 24 h from initial symptoms of AP. KIM-1 was measured in urine samples collected on the day of admission and two subsequent days of hospital stay. AKI was diagnosed based on creatinine increase according to Kidney Disease: Improving Global Outcomes 2012 guidelines. Urinary KIM-1 on study days 1 to 3 was not significantly higher in 10 patients who developed AKI as compared to those without AKI and did not correlate with serum creatinine or urea. On days 2 and 3, urinary KIM-1 correlated positively with urinary liver-type fatty acid-binding protein, another marker of tubular injury. On days 2 and 3, urinary KIM-1 was higher among patients with systemic inflammatory response syndrome, and several correlations between KIM-1 and inflammatory markers (procalcitonin, urokinase-type plasminogen activator receptor, C-reactive protein) were observed on days 1 to 3. With a limited number of patients, our study cannot exclude the diagnostic utility of KIM-1 in AP, however, our results do not support it. We hypothesize that the increase of KIM-1 in AKI complicating AP lasts a short time, and it may only be observed with more frequent monitoring of the marker. Moreover, urinary KIM-1 concentrations in AP are associated with inflammation severity.