EVALUATION OF SARCOPENIA IN PATIENTS WITH ACUTE KIDNEY INJURY: USE OF SERUM BIOMARKERS
Authors: Lanzoni Luís Gustavo , Morales Armando , Silveira Cylmara Gargalak Aziz , Grabulosa Caren Cristina , Tinucci Taís , Moysés Rosa Maria Affonso , Quinto Beata Marie Redublo , Batista Marcelo Costa , Dalboni Maria Aparecida 
Published: June 2021

Introduction

Sarcopenia is a syndrome characterized by progressive loss of skeletal muscle mass, decreased strength, decreased physical performance, increased risk of falls, fractures, hospitalization, and mortality. In patients with chronic renal disease on dialysis (CKD) approximately 40% present sarcopenia due to the effect of toxic substances that are not excreted and induce activation of the inflammatory response that contributes to muscle catabolism, mitochondrial alterations, decrease of satellite cells, changes hormones and loss of neuromuscular junctions. Sarcopenia is well documented in patients with CKD, where the diagnosis is made by measuring the skeletal muscle index, measuring the strength of the wrist and low speed in walking.

However, in patients with acute kidney injury (AKI) who abruptly lose kidney function; sarcopenia 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.

Objective

Objective of this study was to investigate sarcopenia through serum markers of muscle mass loss in AKI patients.

Material and 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 (IL‐6), tumor necrosis factor alpha (TNF‐α) and interleukin‐15 (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 (pg/mL) levels [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], and IL‐15 (pg/mL) [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 (ng/mL) [AKI 0.3 (0.1 – 0.5) vs. No‐AKI 0.3 (0.2 – 0.4); p = 0.53] and myostatin (ng/mL) [AKI 33 (19 – 57) vs. No‐AKI 37 (20–59); p = 0.30].

Conclusion

AKI patients presented higher inflammation characterized by increased serum levels of IL‐6, TNF‐α and IL‐15, which may contribute to sarcopenia. However, myostatin and IGF‐1 did not behave as a marker of muscle loss in this population studied.

This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.