Are urinary biomarkers better than acute kidney injury duration for predicting readmission?
Brown JR, Philbrook HT, Goodrich CA, Bohm AR, Alam SS, Coca SG, McArthur E, Garg AX, Parikh CR. Ann Thorac Surg. 2019; 107(6):1699-705. Epub 2019 Mar 14. DOI: 10.1016/j.athoracsur.2019.02.005.
Background — Acute kidney injury (AKI) is a common complication of cardiac surgery. Postprocedural AKI is a risk factor for 30-day readmission. We sought to examine the association of AKI and kidney injury biomarkers with readmission after cardiac surgery.
Methods — Patients alive at discharge who underwent cardiac surgery from the Translational Research Investigating Biomarker Endpoints-AKI cohort were enrolled from six medical centers in the United States and Canada. AKI duration was defined as the total number of days AKI was present during index admission (no AKI, 1-2, 3-6, and 7+ days). Preoperative and postoperative urinary levels were collected for interleukin-18, neutrophil gelatinase-associated lipocalin, kidney injury molecule-1, liver-fatty-acid-binding protein, cystatin C, microalbumin, creatinine, and albumin-to-creatinine ratio. Readmission and death events were identified through US (Medicare) and Canadian administrative databases at 30 days and 365 days after discharge.
Results — Of 968 patients, 15.9% were readmitted or died within 30 days of discharge and 35.9% were readmitted or died within 365 days. AKI duration of 3 to 6 days was significantly associated with 30-day readmission or mortality (adjusted odds ratio, 1.82%; 95% confidence interval, 1.08-3.05). Patients with AKI duration ≥7 days had increased odds of readmission or death at both 30 days (adjusted odds ratio, 2.49%; 95% confidence interval, 1.15-5.43) and 365 days (adjusted odds ratio, 3.67%; 95% confidence interval,1.73-7.79). Urinary biomarkers had no association with readmission and death.
Conclusions — AKI duration ≥3 days, and not kidney biomarkers, was strongly associated with readmission or death. These clinical outcomes are potentially due to cardiovascular or hemodynamic causes rather than intrinsic injury to the kidney parenchyma.