Key result
Urinary peptide profiles in HF reveal altered collagen turnover and immune response versus controls.
Why the study?
The diversity of heart failure makes it challenging to decipher underlying complex pathological processes using single biomarkers.
Does the urinary peptide profile differ between patients with heart failure and matched non-heart failure controls?
Does the urinary peptide profile differ between patients with heart failure and matched non-heart failure controls?
Heart failure, regardless of ejection fraction subtype, is associated with distinct urinary peptide profiles that primarily reflect alterations in collagen turnover and inflammation.
Answers are grounded in this paper and cite their sources.
Should not change practice yet; leaves open whether urinary peptide profiling aids HF diagnosis or monitoring.
Aims Heart failure (HF) is a major public health concern worldwide. The diversity of HF makes it challenging to decipher the underlying complex pathological processes using single biomarkers. We examined the association between urinary peptides and HF with reduced (HFrEF), mid‐range (HFmrEF) and preserved (HFpEF) ejection fraction, defined based on the European Society of Cardiology guidelines, and the links between these peptide biomarkers and molecular pathophysiology. Methods and results Analysable data from 5608 participants were available in the Human Urinary Proteome database. The urinary peptide profiles from participants diagnosed with HFrEF, HFmrEF, HFpEF and controls matched for sex, age, estimated glomerular filtration rate, systolic and diastolic blood pressure, diabetes and hypertension were compared applying the Mann–Whitney test, followed by correction for multiple testing. Unsupervised learning algorithms were applied to investigate groups of similar urinary profiles. A total of 577 urinary peptides significantly associated with HF were sequenced, 447 of which (77%) were collagen fragments. In silico analysis suggested that urinary biomarker abnormalities in HF principally reflect changes in collagen turnover and immune response, both associated with fibrosis. Unsupervised clustering separated study participants into two clusters, with 83% of non‐HF controls allocated to cluster 1, while 65% of patients with HF were allocated to cluster 2 ( P < 0.0001). No separation based on HF subtype was detectable. Conclusions Heart failure, irrespective of ejection fraction subtype, was associated with differences in abundance of urinary peptides reflecting collagen turnover and inflammation. These peptides should be studied as tools in early detection, prognostication, and prediction of therapeutic response.
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He et al. (2021) studied Heart Failure (n=5,608). Urinary peptide profiling vs. Non-HF controls was evaluated on Differences in abundance of urinary peptides reflecting collagen turnover and inflammation between heart failure patients and controls. (p=<0.0001). Urinary peptide profiling in patients with heart failure showed significant differences in peptide abundance compared to non-HF controls, indicating alterations in collagen turnover and immune response.
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