# Higher serum follistatin levels are associated with increased vascular calcification in haemodialysis patients

**Authors:** Conghui Liu, Aihua Zhang, Zhongxin Li

PMC · DOI: 10.3389/fendo.2026.1759582 · 2026-02-03

## TL;DR

Higher levels of follistatin in the blood are linked to more vascular calcification in patients undergoing hemodialysis.

## Contribution

This study is the first to show a clinical association between serum follistatin and vascular calcification in hemodialysis patients.

## Key findings

- HD patients had significantly higher serum follistatin levels compared to healthy controls.
- Higher follistatin levels were independently associated with increased abdominal aortic calcification scores.
- Pulse pressure, corrected calcium, and total cholesterol were also significant determinants of vascular calcification.

## Abstract

Follistatin is a secreted protein whose main role is antagonizing the activity of transforming growth factor β (TGF-β) superfamily members. Our study aimed to evaluate the serum follistatin levels and establish their relationship with vascular calcification (VC) in haemodialysis (HD) patients.

In total, 206 HD patients and 41 healthy individuals, as controls, were included. Serum concentrations of follistatin, along with various clinical and laboratory parameters, were analyzed and compared. VC was assessed using the abdominal aortic calcification (AAC) scores. HD patients were categorized into a low-AAC-score group (AAC score < 4) and a high-AAC-score group (AAC score ≥ 4).

HD patients had higher serum follistatin levels than the controls (1.25 ± 0.53 ng/ml vs. 0.88 ± 0.30 ng/ml, p < 0.001). Compared with the low-AAC-score group, the high-AAC-score group had a higher serum follistatin concentration (1.37 ± 0.57 ng/ml vs. 1.12 ± 0.46 ng/ml, p < 0.001). Multivariate logistic regression revealed that the higher serum follistatin, pulse pressure, serum total cholesterol (TC), serum sodium, and serum corrected calcium were significant independent determinants of high AAC scores of HD patients.

The results herein provide the first clinical evidence of the association between serum follistatin and VC in HD patients. Higher follistatin, pulse pressure, serum corrected calcium levels, and lower serum sodium and TC levels are independent associated with high AAC scores in HD patients.

## Linked entities

- **Proteins:** LOC5564573 (agrin)

## Full-text entities

- **Genes:** INHBE (inhibin subunit beta E) [NCBI Gene 83729], TGFB1 (transforming growth factor beta 1) [NCBI Gene 7040] {aka CAEND1, CED, DPD1, IBDIMDE, LAP, TGF-beta1}, ALB (albumin) [NCBI Gene 213] {aka FDAHT, HSA, PRO0883, PRO0903, PRO1341}, CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, GLYAT (glycine-N-acyltransferase) [NCBI Gene 10249] {aka ACGNAT, GAT}, FST (follistatin) [NCBI Gene 10468] {aka FS}, BMP1 (bone morphogenetic protein 1) [NCBI Gene 649] {aka OI13, PCOLC, PCP, TLD}, GCG (glucagon) [NCBI Gene 2641] {aka GLP-1, GLP1, GLP2, GRPP}, INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, REN (renin) [NCBI Gene 5972] {aka ADTKD4, HNFJ2, RTD}, BMP4 (bone morphogenetic protein 4) [NCBI Gene 652] {aka BMP2B, BMP2B1, MCOPS6, OFC11, ZYME}, MSTN (myostatin) [NCBI Gene 2660] {aka GDF8, MSLHP}, PTH (parathyroid hormone) [NCBI Gene 5741] {aka FIH1, PTH1}
- **Diseases:** CVD (MESH:D002561), mineral and bone disorder (MESH:D012080), limb mobility impairment (MESH:D014086), malnutrition (MESH:D044342), hypertension (MESH:D006973), polycystic ovary syndrome (MESH:D011085), acute and chronic energy deficiency (MESH:D001930), chronic glomerulonephritis (MESH:D005921), VC (MESH:D061205), hypoproteinemia (MESH:D007019), infectious diseases (MESH:D003141), Medial calcification (MESH:D050380), arteriovenous fistula (MESH:D001164), hyperphosphatemia (MESH:D054559), autosomal dominant polycystic kidney disease (MESH:D016891), diabetic nephropathy (MESH:D003928), coronary artery disease (MESH:D003324), kidney disease (MESH:D007674), congestive heart failure (MESH:D006333), transient ischaemic attack (MESH:D002546), type 2 diabetes (MESH:D003924), peripheral arterial disease (MESH:D058729), CKD (MESH:D051436), cancer (MESH:D009369), calcification (MESH:D002114), diabetes (MESH:D003920), coronary atherosclerotic heart disease (MESH:D003327), bone fractures (MESH:D050723), carotid calcification (MESH:D016893), AAC (MESH:C565230), fibrosis (MESH:D005355), chronic inflammation (MESH:D007249), systemic diseases (MESH:D034721), metabolic dysregulation (MESH:D021081), stroke (MESH:D020521), hypoalbuminemia (MESH:D034141), acute kidney injury (MESH:D058186), wasting (MESH:D019282), bone metabolic disorders (MESH:D001851)
- **Chemicals:** bicarbonate (MESH:D001639), urea (MESH:D014508), sodium (MESH:D012964), potassium (MESH:D011188), Chromogen (-), calcium (MESH:D002118), creatinine (MESH:D003404), calcitriol (MESH:D002117), iPTH (MESH:C041952), tCO2 (MESH:C561418), carbon dioxide (MESH:D002245), aldosterone (MESH:D000450), TG (MESH:D014280), uric acid (MESH:D014527), cinacalcet (MESH:D000069449), phosphorus (MESH:D010758), phosphate (MESH:D010710), cholesterol (MESH:D002784), biotin (MESH:D001710)
- **Species:** Homo sapiens (human, species) [taxon 9606], Mus musculus (house mouse, species) [taxon 10090]

## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12909218/full.md

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Source: https://tomesphere.com/paper/PMC12909218