SP211EVALUATION OF MINERAL BONE DISEASE IN PATIENTS WITH ACUTE KIDNEY INJURY

Abstract

INTRODUCTION AND AIMS: FGF23 was identified as a phosphaturic hormone in 2000. FGF23, produced in bone, controls renal phosphate reabsorption, modulates the production of parathyroid hormone (PTH) and 1,25-(OH)2-vitamin D3, and participates in mineral homeostasis. Since its discovery, the study of its role in mineral homeostasis has been the main focus of FGF23 research. FGF23 is dramatically increased in chronic kidney disease (CKD) and end-stage renal disease (ESRD) and has been proposed as a biomarker for adverse outcomes in patients with CKD and ESRD. However, in patients with acute kidney injury (AKI) who abruptly lose kidney function; bone mineral disease has not yet been investigated. In addition, because these are hospitalized in intensive care units, the classic characterization of sarcopenia by measuring skeletal muscle mass is not possible; requiring the use of serum biomarkers that represent the loss of muscle mass. Aim: Objective of this study was to investigate sarcopenia through serum markers of muscle mass loss in AKI patients. METHODS: We included 77 severe patients without AKI and 83 severe AKI patients 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 sarcopenia: growth factor like insulin-1 (IGF-1), myostatin, interleukin-6, TNF-a and IL-15 were studied by enzyme-linked immunosorbent assay (ELISA). Results are expressed as median. Mann-Whitney test was used to analyze the groups. RESULTS: All AKI patients presented serum creatinine> 3.1 mg / dL (reference value 0.8-1.3 mg / dL). We observed increased serum IL-6 levels [AKI 21 (11-32) vs. No-AKI 12 (7-19); p<0.001], TNF-a [AKI 8.2 (6.7-10.5) vs. No-AKI 7.0 (6.2-7.9); p <0.001], IL-10 [AKI 1.1 (0.8-1.6) vs. No-AKI 0.8 (0.7-1.0); p<0.001], and IL-15 [AKI 5.8 (3.3-7.7) vs. No-AKI 4.5 (2.8-6.1); p= 0.04] and we did not observe differences in IGF-1 [AKI 0.3 (0.1-0.5) vs. No-AKI 0.3 (0.2-0.4); p =0.53] and myostatin. [AKI 33 (19-57) vs. No-AKI 37 (20-59); p =0.30]. CONCLUSIONS: AKI patients presented higher inflammation characterized by increased serum levels of IL-6, TNF-a and IL-15, which may contribute to sarcopenia. However, myostatin and IGF-1 did not behave as a marker of muscle loss in AKI Patients.