Elevated admission serum calcium phosphate product as an independent risk factor for acute kidney injury in hospitalized patients

Abstract

ABSTRACTBackground: Increased serum calcium-phosphate product (CaP) can result in acute kidney injury (AKI) due to tubular and interstitial calcium phosphate deposits. CaP of > 55 mg2/dL2 is also associated with systemic calcification. However, the risk of AKI development among hospitalized patients with different admission calcium-phosphate product levels remains unclear.Methods: All adult hospitalized patients who had both admission serum calcium and phosphate levels available from 2009 through 2013 were enrolled. Admission CaP was categorized based on its distribution into six groups (<22, 22- < 27, 27- < 32, 32- < 37, 37- < 42 and ≥42 mg2/dL2). The odds ratio (OR) of in-hospital mortality by admission CaP, using the CaP category of < 22 mg2/dL2 as the reference group, was obtained by logistic regression analysis.Results: After excluding patients with end-stage renal disease, without serum creatinine measurement, and those who presented with AKI at the time of admission, a total of 9,864 patients were studied. In-hospital AKI occurred in 1,478 patients (15.0%). The incidence of AKI among patients with admission CaP < 22, 22 to < 27, 27 to < 32, 32 to < 37, 37 to < 42, and ≥42 mg2/dL2 was 11.1%, 12.4%, 14.9%, 15.2%, 17.5%, and 19.9%, respectively. After adjusting for potential confounders, a CaP ≥37 mg2/dL2 was associated with an increased risk of developing AKI with OR of 1.53 (CI 1.19–1.96) and 1.63 (CI 1.25–2.14) in patients with admission CaP 37- < 42 and ≥42, respectively. Subgroup analysis based on eGFR consistently demonstrated that CaP ≥37 mg2/dL2 was associated with an increased risk of developing AKI in both chronic kidney disease (CKD) and non-CKD patients.Conclusion: Elevated admission CaP was independently associated with an increased risk for in-hospital AKI.