Renal Outcomes in Children with Neurogenic Bladder: Anatomical and Urodynamic Determinants Beyond Uropathogen Type Renale Outcomes bei Kindern mit neurogener Blase: Anatomische und urodynamische Determinanten jenseits des Uropathogentyps
Klinische Padiatrie, 2026 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Basım Tarihi: 2026
- Doi Numarası: 10.1055/a-2907-7807
- Dergi Adı: Klinische Padiatrie
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, EMBASE, MEDLINE
- Anahtar Kelimeler: detrusor pressure, estimated glomerular filtration rate, neurogenic bladder, renal scarring, urinary tract infection, urine culture
- Sivas Cumhuriyet Üniversitesi Adresli: Evet
Özet
Background In children with neurogenic bladder, urine cultures and uropathogen patterns often guide treatment decisions. Whether these patterns add to renal risk beyond established anatomical and urodynamic factors is unclear. Patients Retrospective cohort of 151 children with neurogenic bladder followed between November 2023 and March 2025. Contaminated urine cultures were excluded from primary multivariable analyses. Method Uropathogen category (E. coli, Proteus spp., other Gram-negative organisms) was modelled together with high-grade vesicoureteral reflux, ultrasonographic megaureter, bladder wall thickness, and maximum filling detrusor pressure (Pdet). Renal injury was defined as advanced DMSA scarring (score ≥ 3) and reduced function (eGFR < 90 mL/min/1.73 m2). Multivariable logistic regression was used. Results Megaureter independently predicted advanced scarring (OR 5.86; 95 % CI 1.73–19.87; p = 0.005). Higher Pdet was independently associated with reduced eGFR (OR 1.41 per 10 mmHg; 95 % CI 1.10–1.82; p = 0.007). Uropathogen category was not independently associated with renal injury. Discussion In pediatric neurogenic bladder, renal vulnerability is driven mainly by pressure and by upper tract anatomy rather than by uropathogen identity. Conclusion The findings suggest that pressure-related factors may contribute more strongly to renal injury than the isolated pathogen itself. Long-term renal protection should prioritize storage pressure control and upper tract drainage.