# Maternal hyperuricemia and adverse neonatal outcomes in normotensive pregnancies: Evidence from a prospective cohort study in Eastern Uganda

**Authors:** Hassan Abdullahi Hafsa, Marie Pascaline Sabine Ishimwe, Musa Kasujja, Geoffrey Okot, Sawda Abdikarim Sheikh Isse, Hussein Mire Hamdi, Mohamud Mohamed Sadia, Ramlo Abdi Ali, Adam Abdrahim Suliman Ebaid, Maxwell Okello, Ahmed Kiswezi Kazigo, Theodore Nteziyaremye, Ibrahim Bwaga, Theoneste Hakizimana

PMC · DOI: 10.1371/journal.pone.0342913 · PLOS One · 2026-03-02

## TL;DR

High uric acid levels in pregnant women without high blood pressure are linked to poor baby outcomes like preterm birth and stillbirth in Uganda.

## Contribution

Shows maternal hyperuricemia predicts adverse neonatal outcomes in normotensive pregnancies in a low-income setting.

## Key findings

- Hyperuricemic women had a 4.32x higher risk of adverse neonatal outcomes.
- Hyperuricemia independently predicted preterm birth, SGA, and stillbirth.
- 37.5% of participants experienced adverse neonatal outcomes.

## Abstract

Maternal hyperuricemia is a potential biomarker of adverse pregnancy outcomes, but evidence among normotensive women in low- and middle-income countries is limited. We aimed to assess the association between elevated maternal serum uric acid (SUA) levels and adverse neonatal outcomes.

We conducted a prospective cohort study at Jinja Regional Referral Hospital, Uganda, from 1st October 2024–1st February 2025, enrolling 352 normotensive women in latent labor. SUA was measured using gestational-age–specific cutoffs, classifying women as hyperuricemic or normouricemic. Outcomes included preterm birth, small-for-gestational-age (SGA) birth, stillbirth, and low Apgar score. Poisson regression with robust standard errors estimated adjusted relative risks (aRR) and 95% confidence intervals.

Adverse neonatal outcomes occurred in 37.5% of participants. Hyperuricemic women had significantly higher composite risk (62.5% vs. 12.5%; aRR = 4.32, 95% CI 2.92–6.39). Hyperuricemia independently predicted preterm birth (aRR = 3.63, 95% CI 1.70–7.72), SGA (aRR = 2.80, 95% CI 1.61–4.86), and stillbirth (aRR = 5.00, 95% CI 1.47–16.99). Maternal age ≥ 40 years, low education, < 4 antenatal visits, previous preterm birth, previous stillbirth, and obesity were also associated with adverse outcomes. Conclusions.

Maternal hyperuricemia is a strong predictor of preterm birth, SGA, and stillbirth. Routine SUA screening during antenatal care, combined with closer monitoring of high-risk women, could help improve neonatal outcomes.

## Full-text entities

- **Genes:** IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, SYNE2 (spectrin repeat containing nuclear envelope protein 2) [NCBI Gene 23224] {aka EDMD5, KASH2, NUA, NUANCE, Nesp2, Nesprin-2}, MTOR (mechanistic target of rapamycin kinase) [NCBI Gene 2475] {aka FRAP, FRAP1, FRAP2, RAFT1, RAPT1, SKS}, PTBP1 (polypyrimidine tract binding protein 1) [NCBI Gene 5725] {aka HNRNP-I, HNRNPI, HNRPI, PTB, PTB-1, PTB-T}, PRPH2 (peripherin 2) [NCBI Gene 5961] {aka AOFMD, AVMD, CACD2, DS, MDBS1, RDS}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}
- **Diseases:** Hyperuricemia (MESH:D033461), premature labor (MESH:D007752), maternal (MESH:D000079262), restriction (MESH:D002313), Stillbirth (MESH:D050497), type 1 or type 2 diabetes (MESH:D003924), renal disease (MESH:D007674), fetal distress (MESH:D005316), systemic (MESH:D015619), prematurity (MESH:C536271), infections (MESH:D007239), gestational hypertension (MESH:D046110), hypoglycemia (MESH:D007003), Preterm birth (MESH:D047928), chronic kidney failure (MESH:D007676), placental dysfunction (MESH:D010922), vascular and (MESH:D057772), placental insufficiency (MESH:D010927), LBW (MESH:D001724), hypothermia (MESH:D007035), JRRH (MESH:D003428), deaths (MESH:D003643), hypertension (MESH:D006973), neonatal death (MESH:D066087), metabolic dysregulation (MESH:D021081), Respiratory Distress Syndrome (MESH:D012128), preeclamptic (MESH:C538543), hypoxia (MESH:D000860), obesity (MESH:D009765), Intraventricular Hemorrhage (MESH:D000074042), SGA (MESH:D016640), diabetes (MESH:D003920), endothelial dysfunction (MESH:D014652), preeclampsia (MESH:D011225), chronic kidney disease (MESH:D051436), inflammation (MESH:D007249), Hyperuricemic (MESH:C537696), fetal growth restriction (MESH:D005317), gout (MESH:D006073)
- **Chemicals:** glucose (MESH:D005947), purine (MESH:C030985), amino acid (MESH:D000596), Maternal Uric Acid (-), insulin (MESH:D007328), methotrexate (MESH:D008727), Uric Acid (MESH:D014527)
- **Species:** Homo sapiens (human, species) [taxon 9606], Human immunodeficiency virus 1 (no rank) [taxon 11676]
- **Cell lines:** -1 — Mus musculus (Mouse), Hybridoma (CVCL_C7RB)

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC12952601/full.md

## Figures

1 figure with captions in the complete paper: https://tomesphere.com/paper/PMC12952601/full.md

## References

22 references — full list in the complete paper: https://tomesphere.com/paper/PMC12952601/full.md

---
Source: https://tomesphere.com/paper/PMC12952601