The risk of chronic kidney disease and mortality are increased after community-acquired acute kidney injury

Abstract

We investigated whether community-acquired acute kidney injury encountered in a tertiary hospital emergency department setting increases the risk of chronic kidney disease (CKD) and mortality, and whether plasma biomarkers could improve the prediction of those adverse outcomes. In a prospective cohort study, we enrolled 616 patients at admission to the emergency department and followed them for a median of 62.1 months. Within this cohort, 130 patients were adjudicated as having acute kidney injury, 159 transient azotemia, 15 stable CKD, and 312 normal renal function. Serum cystatin C and plasma neutrophil gelatinase-associated lipocalin (NGAL) were measured at index admission. After adjusting for clinical variables, the risk of developing CKD stage 3, as well as the risk of death, were increased in the acute kidney injury group (hazard ratio [HR], 5.7 [95% confidence interval, 3.8-8.7] and HR, 1.9 [95% confidence interval, 1.3-2.8], respectively). The addition of serum cystatin C increased the ability to predict the risk of developing CKD stage 3, and death (HR, 1.5 [1.1-2.0] and 1.6 [1.1-2.3], respectively). The addition of plasma NGAL resulted in no improvement in predicting CKD stage 3 or mortality (HR, 1.0 [0.7-1.5] and 1.2 [0.8-1.8], respectively). The risk of developing CKD stage 3 was also significantly increased in the transient azotemia group (HR, 2.4 [1.5-3.6]). Thus, an episode of community acquired acute kidney injury markedly increases the risk of CKD, and moderately increases the risk of death. Our findings highlight the importance of follow-up of patients with community acquired acute kidney injury, for potential early initiation of renal protective strategies.

Keywords: NGAL; acute kidney injury; biomarkers; chronic kidney disease; cystatin C.

Figure 1

Study profile. Flow chart of patients during follow-up. ⁽¹⁾n=86, and ⁽²⁾n=171 with missing GFR values.

Figure 2

Figure 2A. Evolution of chronic kidney disease by estimated GFR. Kidney function by estimated GFR at baseline, discharge, 1^st follow-up (median 19.9 months), and 2^nd follow-up (median 62.1 months), in each clinical group. AKI, acute kidney injury; TAz, transient azotemia; sCKD, stable chronic kidney disease; NF, normal function. p<0.05 for all groups, comparing baseline to 2^nd follow up. Figure 2B. Change in eGFR between baseline and last follow-up time (F2). AKI, acute kidney injury; TAz, transient azotemia; sCKD, stable chronic kidney disease; NF, normal function. p<0.001 when comparing AKI and TAz with NF.

Figure 2

Figure 2A. Evolution of chronic kidney disease by estimated GFR. Kidney function by estimated GFR at baseline, discharge, 1^st follow-up (median 19.9 months), and 2^nd follow-up (median 62.1 months), in each clinical group. AKI, acute kidney injury; TAz, transient azotemia; sCKD, stable chronic kidney disease; NF, normal function. p<0.05 for all groups, comparing baseline to 2^nd follow up. Figure 2B. Change in eGFR between baseline and last follow-up time (F2). AKI, acute kidney injury; TAz, transient azotemia; sCKD, stable chronic kidney disease; NF, normal function. p<0.001 when comparing AKI and TAz with NF.

Figure 3

Percent of eGFR ≤60 mL/min/1.73m² at baseline, discharge, 1^st follow-up (median 19.9 months), and 2^nd follow-up (median 62.1 months), in each clinical group. AKI, acute kidney injury; TAz, transient azotemia; NF, normal function. *p<0.001 compared to baseline.

Figure 4

Cumulative incidence of chronic kidney disease during follow-up time. The figure on the left shows Kaplan Meier curves estimates (p < 0.001 for both Taz and AKI compared to normal function) for the entire follow up period. Figure on the right shows cumulative incidence rates during the five years of follow-up. AKI, acute kidney injury; TAz, transient azotemia; NF, normal function.