EVALUATION OF MINERAL BONE DISEASE IN PATIENTS WITH ACUTE KIDNEY INJURY

Abstract

IntroductionPatients with end‐stage renal disease (ESRD) develop various kinds of abnormalities in bone and mineral metabolism, widely known mineral bone disease (MBD). The MBD is one of the main cause of vascular calcification (VC) and mortality in this patients. This abnormalities are a consequence of the glomerular filtration rate declined and retention of a large number of compounds which under normal conditions are excreted by healthy kidneys. In the last years, Fibroblast Growth Factor 23 (FGF‐23) a phosphaturic hormone, Sclerostin (SOST) (a protein that inhibit bone formation ) and inflammation markers have been described as a important axis of the physiopathology of MBD and VC in ESRD. The early detection of MBD can reduced the VC and its complications. However, patients with acute kidney injury (AKI) which abruptly lose kidney function; have not been yet investigated to MBD. Thus, the objective of this study was to investigate markers of MBD in AKI patients.Material and MethodsWe included 77 severe patients without AKI and 83 severe AKI patients (ageing‐ 77 (60–84) all admitted to the Intensive Care Unit. Patients with AKI were characterized by AKIN criteria that used a 0.3 mg/dL increase in serum creatinine within seven days of admission in the hospital. Serum markers of MBD and inflammation investigated were: FGF‐23, SOST, Interleukin‐6 (IL‐6), Tumor Necrosis Factor Alpha (TNF‐α) and Interleukin‐10 (IL‐10) (by enzyme‐linked immunosorbent assay (ELISA). Results are expressed as median. Mann‐Whitney test was used to analyze the groups.ResultsAll AKI patients presented serum creatinine >3.1 mg/dL (reference value 0.8 – 1.3 mg/dL). We observed increased serum levels of SOST (pg/mL) [AKI 1.74 (1.74–46.40) vs. No‐AKI 1.74 (1.74–1.74); p=0.009)], IL‐6 (pg/mL) [AKI 21 (11–32) vs. No‐AKI 12 (7–19); p<0.001], TNF‐α (pg/mL) [AKI 8.2 (6.7–10.5) vs. No‐AKI 7.0 (6.2–7.9); p<0.001], IL‐10 (pg/mL) [AKI 1.1 (0.8–1.6) vs. No‐AKI 0.8 (0.7–1.0); p<0.001]. We did not observe difference in FGF‐23 (pg/mL) [AKI 48.3 (1.5–141.3) vs. No‐AKI 48.0 (1.5–188.5); p=0.35].ConclusionAKI patients presented higher inflammation state characterized by increased serum levels of IL‐6, TNF‐α and IL‐10. Additionally, as SOST was higher in AKI patients, is possible used it as a marker of early bone disease in this population. In summary, this is the first study that detected high levels of SOST in AKI patients.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.