Hyperphosphatemia is associated with mortality in patients with chronic kidney disease, and is common in critically ill patients with acute kidney injury (AKI); however, its clinical implication in these patients is unknown. We conducted an observational study in 1144 patients (mean age, 63.2 years; male, 705 [61.6%]) with AKI who received continuous renal replacement therapy (CRRT) between January 2009 and September 2016. Phosphate levels were measured before (0 h) and 24 h after CRRT initiation. We assessed disease severity using various clinical parameters. Phosphate at 0 h positively correlated with the Acute Physiology and Chronic Health Evaluation II (APACHE II; P < 0.001) and Sequential Organ Failure Assessment (SOFA; P < 0.001) scores, and inversely with mean arterial pressure (MAP; P = 0.02) and urine output (UO; P = 0.01). In a fully adjusted linear regression analysis for age, sex, Charlson comorbidity index (CCI), MAP, and estimated glomerular filtration rate (eGFR), higher 0 h phosphate level was significantly associated with high APACHE II (P < 0.001) and SOFA (P = 0.04) scores, suggesting that phosphate represents disease severity. A multivariable Cox model also showed that hyperphosphatemia was significantly associated with increased 28-day (HR 1.05, 95% CI 1.02–1.08, P = 0.001) and 90-day (HR 1.05, 95% CI 1.02–1.08, P = 0.001) mortality. Furthermore, patients with increased phosphate level during 24 h were at higher risk of death than those with stable or decreased phosphate levels. Finally, c-statistics significantly increased when phosphate was added to a model that included age, sex, CCI, body mass index, eGFR, MAP, hemoglobin, serum albumin, C-reactive protein, and APACHE II score. This study shows that phosphate is a potential biomarker that can reflect disease severity and predict mortality in critically ill patients receiving CRRT.

Background: High‐density lipoprotein cholesterol ( HDL ‐C) levels are generally decreased in patients with chronic kidney disease ( CKD ). However, studies on the relationship between HDL ‐C and CKD progression are scarce. Methods and Results: We studied the association between serum HDL ‐C levels and the risk of CKD progression in 2168 participants of the KNOW ‐ CKD (Korean Cohort Study for Outcome in Patients With Chronic Kidney Disease). The primary outcome was the composite of a 50% decline in estimated glomerular filtration rate from baseline or end‐stage renal disease. The secondary outcome was the onset of end‐stage renal disease. During a median follow‐up of 3.1 (interquartile range, 1.6–4.5) years, the primary outcome occurred in 335 patients (15.5%). In a fully adjusted Cox model, the lowest category with HDL ‐C of <30 mg/dL (hazard ratio, 2.21; 95% CI, 1.30–3.77) and the highest category with HDL ‐C of ≥60 mg/dL (hazard ratio, 2.05; 95% CI , 1.35–3.10) were associated with a significantly higher risk of the composite renal outcome, compared with the reference category with HDL ‐C of 50 to 59 mg/dL. This association remained unaltered in a time‐varying Cox analysis. In addition, a fully adjusted cubic spline model with HDL ‐C being treated as a continuous variable yielded similar results. Furthermore, consistent findings were obtained in a secondary outcome analysis for the development of end‐stage renal disease. Conclusions: A U‐shaped association was observed between serum HDL ‐C levels and adverse renal outcomes in this large cohort of patients with CKD . Our findings suggest that both low and high serum HDL ‐C levels may be detrimental to patients with nondialysis CKD .