School of Medicine

Introduction : Acute kidney injury (AKI) is commonly observed during the treatment of acute decompensated heart failure. During aggressive diuresis in hospitalized patients, neurohormonal antagonists are often reduced or withheld when a decrement in renal function as indicated by rising creatinine is observed. Neutrophil gelatinase-associated lipocalin (NGAL) is released by tubular epithelial cells of the nephron upon injury and has been detected in the serum much earlier than creatinine. We sought to reproduce previous data supporting the fact that NGAL is an early biomarker of AKI hypothesizing that it would be predictive of the onset or worsening of acute kidney injury. Additionally, we identified specific patient scenarios in which the idea of NGAL-guided changes in neurohormonal blockade may be instituted. Methods : Serial serum and urine NGAL levels were measured from 53 patients with acute decompensated heart failure admitted through the emergency department at the Veterans Affairs San Diego Healthcare System (VASDHS). Serum and urine NGAL levels were obtained on admission and daily up to five days of hospitalization. Patient demographics, laboratory values, medication regimens, physical exam information, and other tests or imaging results were recorded on case report forms. Primary and secondary diagnoses given during hospitalization were also recorded. Study protocols did not influence clinical care decision-making. Results : Of the 53 patients in our study cohort, 24 developed AKI as defined by the AKIN criteria. Serum NGAL was significantly elevated on time point 2 in those who developed AKI versus those who did not (201.9ng/ml, IQR 122.6-287.8 versus 141.2ng/ml, IQR 98.55-168.9, p=0.039). Additionally, the maximum serum NGAL across all five time points for each patient was significantly elevated in the AKI group (507.5ng/ml) versus the non AKI group (242.1ng/ml), p=0.007. Per logistic regression the log-odds of having AKI increases by 0.003997 (p=0.024) for each unit of increase in maximum NGAL. Incr.