Mitochondrial viability in neurogenic bladder urothelium after sigmoidocolocystoplasty. Implications for persistent vesicoureteral reflux
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In brief
In brief
This study examines why vesicoureteral reflux persists in some neurogenic bladder patients after sigmoidocolocystoplasty, finding that compromised mitochondrial viability in bladder tissue—indicated by elevated GDF15 and reduced HSP60—correlates with persistent reflux. The research suggests mitochondrial dysfunction and associated fibrosis may play a key role in surgical treatment failure.
- Compromised mitochondrial viability (GDF15+/weak HSP60) in neurogenic bladder urothelium correlates with persistent VUR after sigmoidocolocystoplasty.
- Dense fibrosis and inflammatory infiltration are significantly associated with mitochondrial stress markers in neurogenic bladder tissue.
- VUR resolved with SCP alone in only 11% of cases; 45% required additional ureteroneocystostomy, and 45% had persistent reflux.
- Mitochondrial dysfunction may be an underlying mechanism preventing VUR resolution despite adequate neobladder compliance and capacity.
- Urothelial mitochondrial health assessment via GDF15/HSP60 may help predict which patients need concurrent ureteral reimplantation at SCP.
Written by the GCMD Library team from the article.
Abstract
Purpose
We investigated whether inflammatory cell infiltration (ICI), fibrosis, and mitochondrial viability of the neurogenic bladder urothelium are involved in the mechanism of persistent vesicoureteral reflux (VUR) after sigmoidocolocystoplasty (SCP).
Methods
Bladder biopsies obtained 1994–2023 from 62 neurogenic bladder patients were examined by hematoxylin and eosin for ICI, Masson’s trichrome for fibrosis, and immunofluorescence for urothelial growth differentiation factor 15 (GDF15; a mitochondrial stress-responsive cytokine) (positive/negative) and heat shock protein 60 (HSP60; a mitochondrial matrix marker) (strong ≥ 50%/weak≤ 50%) expression. GDF15 + /weak HSP60 indicated compromised mitochondrial viability. Cystometry measured neobladder compliance/capacity.
Results
Mean ages (years) at SCP and bladder biopsies were 9.4 ± 4.6 and 14.2 ± 7.1, respectively. VUR was present in 38/62 patients (51 ureters) at SCP and resolved with SCP alone in 4/38 patients, with SCP and ureteroneocystostomy in 17/38, and persisted in 17/38. Fibrosis was significantly denser in GDF15 + (n = 24)/weak HSP60 (n = 31) compared with GDF15- (n = 38)/strong HSP60 (n = 31) (p < 0.001 and p < 0.01, respectively). Differences in ICI were significant for GDF15 + vs. GDF15- (p < 0.05) but not for HSP60. Patients with VUR after SCP had higher incidence of GDF15 + /weak HSP60 compared with cases without VUR (p < 0.05 and p < 0.001, respectively).
Conclusion
Viability of mitochondria appears to be compromised with possible etiologic implications for VUR persisting after SCP.