After correcting serum creatinine for fluid balance and adjusting for surgical complexity, LFR performs fairly at 2 hours, whereas at 6 hours, LFR is a good AKI predictor. Prospective studies are needed to validate whether diuretic responsiveness predicts AKI.

Beta-2-microglobulin (B2M) is a marker of proximal tubular injury and glomerular filtration. Analyses using older/non-standardized definitions have shown low efficacy of B2M to predict acute kidney injury (AKI). We assessed if elevated levels of B2M would associate with either the diagnosis of AKI [under current Kidney Disease: Improving Global Outcomes (KDIGO) criteria] or recovery from AKI. We performed a retrospective study, including children who had urine B2M (uB2M) and/or serum B2M (sB2M) measured by immunoturbidimetry in our clinical laboratory between January 2011 and December 2015. We defined AKI based on KDIGO criteria [increase of serum creatinine (sCr) 0.3 mg/dL over 48 h or >50% baseline over 7 days] or urine output <0.5 mL/kg/h for 24 h. Recovery from AKI was defined as a return to baseline sCr within 6 months. We calculated receiver operating characteristics (ROC) area under the curve (AUC). Of 529 patients, 245 developed AKI. Serum and uB2M associated with AKI development (AUCs 0.84 and 0.73, respectively). Patients had a graded higher median sB2M and uB2M with each higher AKI stage. sB2M differentiated Stage I from Stage III AKI (P < 0.001) and Stage II from Stage III AKI (P = 0.004). However, neither uB2M nor sB2M levels associated with recovery from AKI. Only older age {hazard ratio [HR] 0.97, [95% confidence interval (CI) 0.94–0.99]} and need for dialysis [HR 0.39 (95% CI 0.23–0.61)] predicted incomplete recovery after AKI. Using KDIGO criteria, sB2M and uB2M associate with the severity of AKI. Given its relative ease and lower cost, we suggest more widespread use of B2M for AKI detection.

Chronic kidney disease (CKD) has become a significant public health concern, as it is associated with substantial morbidity. Prior research has evaluated multiple novel CKD biomarkers to supplement serum creatinine and proteinuria. The ultimate goal of this research is to find biomarkers that can be used to accurately predict CKD progression and to better time outpatient follow-up, and referral for transplant. Also, an optimal panel of biomarkers can augment the predictive value of proteinuria and serum creatinine by enriching patient enrollment in clinical trials. In this review, we discuss salient findings on 12 candidate plasma and urine biomarkers and their reported association with CKD. We explore the common pathways of CKD progression and the pathophysiologic processes of tubulointerstitial injury, inflammation, repair, and fibrosis that are potentially classified by specific biomarkers. We describe both pediatric and adult findings and highlight the paucity of pediatric research in CKD progression. It will be important for cohorts with longitudinal follow-up to evaluate these CKD biomarkers for potential use in pediatric clinical trials and routine CKD management.

Background Clotting of continuous renal replacement therapy (CRRT) circuits leads to inadequate clearance, decreased ultrafiltration, and increased resource use. We identified factors associated with premature clotting of circuits during CRRT in children. Methods In a retrospective cohort of 26 children (median age 11.8 years) receiving 79 CRRT circuits (51 heparin, 22 citrate, 6 using no anticoagulation), we captured hourly pressure, flow, and fluid removal rates along with all activated clotting time (ACT) and circuit ionized calcium measurements. Cox and logistic regression models were used to examine factors associated with premature circuit clotting before the scheduled 3-day circuit change. Results Of the 79 circuits, 51 (64.6%) underwent unplanned filter change due to filter clotting (median duration 18.25 h, interquartile range [IQR] 9.25, 33.5 h), and 28 (35.4%) underwent scheduled change (median duration 66 h, IQR 61.00, 69.00 h). Patient age, catheter size and location, blood flow rate, and the percentage of pre-filter replacement fluid were not associated with premature clotting. Heparin circuits were less likely than citrate circuits to clot prematurely. Each 1-mmHg increase in the transmembrane or filter pressure was independently associated with a 1.5% (95% confidence interval [CI] 1.0–2.0%) and 1.5% (95% CI 1.0–2.0%) higher risk of clotting, respectively. Higher ACTs were associated with lower transmembrane (p = 0.03) and filter (p < 0.001) pressures. Conclusions The majority of circuits in our cohort were subject to unplanned filter changes. Elevated transmembrane and filter pressures were associated with clotting. Our results suggest that maintaining higher ACT may decrease the risk of circuit clotting. Larger studies are needed to examine other factors that may prolong the lifespan of the CRRT circuit in this high-risk population.