Researchers have demonstrated for the first time that increased calcium-phosphate product at hospital admission is independently associated with an elevated risk of in-hospital acute kidney injury (AKI), according to new report.
Patients admitted with a calcium-phosphate product (in mg2/dL2) of 37 or higher but less than 42 and 42 or higher have significant 1.5-fold and 1.6-fold increased odds of experiencing AKI, respectively, after adjusting for multiple potential confounders, compared with patients who had an admission calcium-phosphate product below 22.
“Patients with elevated calcium-phosphate produce at admission should closely monitored for development of AKI, said lead investigator Charat Thongprayoon, MD, of Mayo Clinic in Rochester, Minnesota.
The findings are based on a retrospective study of 9864 patients admitted to a tertiary referral hospital and who had admission serum calcium and phosphate levels available. AKI developed in 1478 patients (15%). The investigators defined AKI as an absolute increase in serum creatinine of at least 0.3 mg/dL within 48 hours of admission or a 50% or greater increase in serum creatinine level from baseline within 7 days after the admission date.
Dr Thongprayoon’s team found that calcium-phosphate product was associated with a significantly increased AKI risk among patients with and without chronic kidney disease (CKD), which was defined as an estimated glomerular filtration rate (eGFR, in mL/min/1.73 m2) below 60. A calcium-phosphate product of 37 or higher was associated with approximately 1.5-fold increased odds of AKI among patients with an eGFR of 60 or higher and 2-fold increased odds among those with an eGFR below 60.
The investigators offered some possible explanations for how calcium-phosphate product might influence AKI risk. For example, in the setting of acute phosphate nephropathy, studies have demonstrated injuries to distal tubules and collecting ducts due to calcium phosphate deposits, they noted. In addition, as calcium-phosphate product increases, precipitation of calcium phosphate crystals may occur. Elevated serum calcium levels, which can cause renal vasoconstriction that leads to renal ischemia and tubular injury, can result in or exacerbate AKI.
Dr Thongprayoon and his colleagues acknowledged that the study’s single-center retrospective design, as well as the very heterogeneous patient population, limit data interpretation. In addition, the institutional database from which they extracted data lacked important clinical information, such as vital signs or hydration state at admission.
“Future study is needed to investigate if calcium phosphate product can be incorporated in AKI risk prediction model or used along with AKI biomarkers to improve AKI detection and management,” Dr Thongprayoon said.
Thongprayoon C, Cheungpasitporn W, Mao MA et al. Elevated admission serum calcium phosphate produce as an independent risk factor for acute kidney injury in hospitalized patients. Hospital Pract. 2019; published online ahead of print.