Clinical impact of chronic kidney disease on appendicular skeletal muscle mass and mortality in hospitalized patients with acute heart failure

Heart failure (HF) is a clinical syndrome associated with diverse metabolic disturbances. Recent studies including ours suggest that skeletal muscle plays an important role in the pathogenesis of chronic HF and chronic kidney disease (CKD). However, the effect of renal function on skeletal muscle mass in HF remains unclear.

The purpose of this study was to investigate the impact of chronic kidney disease on appendicular skeletal muscle mass in hospitalized patients with acute HF (AHF).

We assessed lean body mass by dual energy X-ray absorptiometry in 418 hospitalized patients with AHF (age 71±13, left ventricular ejection fraction (LVEF) 39±17%, estimated glomerular filtration rate (eGFR) at discharge 46±19 mL/min/1.73 m²). Low appendicular skeletal muscle mass index (ASMI, appendicular skeletal muscle mass/height2) was defined according to the Asia Working Group for Sarcopenia criteria (<7.0 kg/m² in male, <5.4 kg/m² in female). CKD was defined as eGFR <60 mL/min/1.73 m² at discharge.

CKD was observed in 77% of hospitalized patients with AHF (eGFR ≥60 mL/min/1.73 m², n=96, 23%, eGFR 30–59 mL/min/1.73 m², n=233, 56%, eGFR <30 mL/min/1.73 m², n=89, 21%). ASMI positively correlated with eGFR (r=0.16, P=0.002). ASMI decreased according to CKD categories (eGFR ≥60 mL/min/1.73 m²; ASMI 6.75±0.14 kg/m², eGFR 30–59 mL/min/1.73 m²; ASMI 6.24±0.08 kg/m², eGFR <30 mL/min/1.73 m²; ASMI 6.24±0.13 kg/m², p=0.003, Figure 1). During a median follow-up of 37 months, 92 (22%) of 418 patients died. The combination of ASMI and CKD identified subgroups with a significantly different probability of all-cause death (log-rank test p<0.001, Figure 2).

CKD was associated with decreased skeletal muscle mass in hospitalized patients with AHF. CKD and skeletal muscle mass independently correlated with mortality after AHF episode. The cross link between kidney and skeletal muscle might play an important role in the pathogenesis of AHF.

Type of funding sources: None.