Higher serum phosphorus is associated with catabolic/anabolic imbalance in heart failure

Abstract

BackgroundA higher serum phosphate level is associated with worse outcome. Energy-demanding intracellular transport of phosphate is needed to secure anion bioavailability. In heart failure (HF), energy starvation may modify intracellular and serum levels of phosphate. We analysed determinants of serum phosphates in HF and assessed if catabolic/anabolic balance (CAB) was associated with elevation of serum phosphate.MethodsWe retrospectively reviewed data from 1029 stable patients with HF and have calculated negative (loss) and positive (gain) components of weight change from the onset of HF till index date. The algebraic sum of these components was taken as CAB. The univariate and multivariable predictors of serum phosphorus were calculated. In quintiles of CAB, we have estimated odds ratios for serum phosphorus above levels previously identified to increase risk of mortality. As a reference, we have selected a CAB quintile with similar loss and gain.ResultsApart from sex, age, and kidney function, we identified serum sodium, N-terminal fragment of pro-brain-type natriuretic peptide, and CAB as independent predictors of serum phosphorus. The odds for serum phosphorus above thresholds found in literature to increase risk were highest in more catabolic patients. In most catabolic quintile relative to neutral balance, the odds across selected phosphorus thresholds rose, gradually peaking at 1.30 mmol/L with a value of 3.29 (95% confidence interval: 2.00–5.40, P < 0.0001) in an unadjusted analysis and 2.55 (95% confidence interval: 1.38–2.72, P = 0.002) in a fully adjusted model.ConclusionsMetabolic status is an independent determinant of serum phosphorus in HF. Higher catabolism is associated with serum phosphorus above mortality risk-increasing thresholds.

Protein energy-wasting associated with nephrotic syndrome – the comparison of metabolic pattern in severe nephrosis to different stages of chronic kidney disease

“…We suppose that hypercatabolism may be an additional mechanism responsible for hyperphosphatemia in severe NS. Similarly, hPi as an effect of increased catabolism has been described by Rozentryt et al in patients with heart failure [27]. It is probable that the same pathogenetic way is associated with hyperuricemia in nephrotic patients.…”

Clinical and laboratory determinants of 25-hydroxyvitamin D deficiency during pharmacotherapeutic escalation in heart failure patients

“…The association between 25(OH)D deficiency and higher phosphate concentrations constitutes another argument for this interpretation because, in a CHF patient, the catabolic profile is an independent determinant of phosphate concentration [ 27 ]. Alternatively, the increased phosphate concentration may be a reflection of relative hypoparathyroidism and resulting reduced phosphaturia.…”

Casting the net broader to confirm our imaginations: the long road to treating wasting disorders

“…These authors found that a catabolic/anabolic imbalance, N‐terminal pro‐B‐type natriuretic peptide values, serum sodium, kidney function, age, and sex were independent predictors of serum phosphorus. Thus, the authors concluded that metabolic status is an independent determinant of serum phosphorus in heart failure …”