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.

The Evidence of Acute Kidney Injury in the Community and for Primary Care Interventions

“…In a large retrospective cohort, volume depletion was the most frequent etiology (58.5% of cases) for CA H -AKI with infection, either sepsis, urinary tract infection, or pneumonia, being present in over 40% of cases [6] . Another recent study revealed similar results with 38.5% of patients with CA H -AKI having sepsis compared to 24% without AKI [7] . Confounding infection with AKI results in poorer outcomes; in community-acquired pneumonia, the presence of CA H -AKI has been shown to increase the likelihood of mechanical ventilation, vasopressor support, and results in higher 30-day mortality increasing according to RIFLE class [8] .…”

“…Talabani et al [5] reported 45% 3-year mortality for CA H -AKI compared to 15.7% ( p < 0.01) in the control cohort with similar figures reported at 5 years (44.6% in Soto et al [7] ). As expected the need for renal replacement therapy (RRT) is significantly higher for patients with CA H -AKI compared to non-AKI [7] .…”

“…Talabani et al [5] reported 45% 3-year mortality for CA H -AKI compared to 15.7% ( p < 0.01) in the control cohort with similar figures reported at 5 years (44.6% in Soto et al [7] ). As expected the need for renal replacement therapy (RRT) is significantly higher for patients with CA H -AKI compared to non-AKI [7] . Alarmingly however the progression to CKD (estimated glomerular filtration rate <60 mL/min/1.73 m 2 , persisting for >3 months) following an episode of CA H -AKI has been reported as high as 73.8% at 5 years [7] .…”

“…As expected the need for renal replacement therapy (RRT) is significantly higher for patients with CA H -AKI compared to non-AKI [7] . Alarmingly however the progression to CKD (estimated glomerular filtration rate <60 mL/min/1.73 m 2 , persisting for >3 months) following an episode of CA H -AKI has been reported as high as 73.8% at 5 years [7] . All AKI, including CA H -AKI and AKI identified and managed in primary care, showed similar and very poor long-term outcomes in a recent Scottish population cohort study [12] .…”

Acute kidney injury: still misunderstood and misdiagnosed

“…This standardized approach has utility in epidemiological studies, for coding and billing purposes, and triggering electronic medical record alerts for ‘best practice’ guidelines; however, such an approach fails to account for the myriad clinical scenarios in which SCr is elevated due to incidental non-renal or even artefactual conditions, or as a normal physiologic response to a reduction in extracellular fluid volume (ECFV). In the majority of patients entering emergency departments or hospitals worldwide, any increase in SCr is often fleeting, and usually reversed within 72 h of fluid therapy, suggesting a depletion in ECFV as the primary culprit and a concomitant absence of intrinsic structural kidney injury 2–4 . More than a century of experimental and human studies have elucidated physiologic neurohormonal mechanisms that transiently decrease renal excretory function while conserving salt and water in ECFV depletion, resulting in the clinical condition classically denoted as ‘functional pre-renal AKI’ or even as ‘acute renal success’.…”