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\title{Tower Bladder: A Silent Threat in Pediatric Neurogenic Bladder}
\author{Derya Yayla \and Güneş Işık}
\date{}

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\maketitle

\begin{abstract}
Objective:
This study aimed to assess the prognostic significance of ``tower bladder'' morphology in pediatric patients with neurogenic bladder, focusing on its association with radiological and urodynamic indicators and its predictive value for renal impairment.

Materials and Methods:
We retrospectively reviewed 164 children (mean age: 7.7 ± 4.6 years) with neurogenic bladder managed at Gaziantep City Hospital between October 2023 and May 2024. Evaluations included voiding cystourethrography (VCUG) for bladder morphology and bladder diameter ratio (BDR), vesicoureteral reflux (VUR) grading, and dimercaptosuccinic acid (DMSA) scintigraphy for renal scarring. Urodynamic parameters, age-adjusted serum creatinine, timing of clean intermittent catheterization (CIC), and anticholinergic therapy duration were recorded.

Results:
Tower bladder morphology was observed in 71.3\textbackslash{}% of patients and was significantly associated with higher intravesical pressure (46.2 ± 24.2 vs. 26.7 ± 19.1 cmH₂O; p < 0.001), elevated BDR (p < 0.001), high-grade VUR (p = 0.006), and increased renal scarring (p = 0.020). Late CIC initiation was linked to tower bladder (p = 0.019). Although anticholinergic therapy reduced pressure (p < 0.001), it had limited effect on renal preservation.

Conclusion:
Tower bladder is a morphological marker of poor prognosis in pediatric neurogenic bladder, correlating with high intravesical pressure and renal risk. Early CIC and pharmacotherapy are essential to prevent irreversible damage. Integration of radiologic and functional data is critical for individualized risk assessment and management planning.

Keywords: Neurogenic bladder, tower bladder, intravesical pressure, DMSA, vesicoureteral reflux, creatinine
\end{abstract}


Neurogenic bladder is a severe functional disorder of the lower urinary tract resulting from congenital or acquired neurological pathologies that impair the neural control of bladder storage and voiding. In pediatric populations, the most common etiological factors include congenital spinal dysraphism syndromes, particularly myelomeningocele. In these patients, bladder dysfunction typically begins at birth and progresses with urological and nephrological complications. If left untreated, it may lead to irreversible pathologies such as VUR, hydronephrosis, renal cortical scarring, hypertension, and chronic renal disease [1,2]. In regions where neural tube defects are prevalent, the importance of prenatal screening and folic acid prophylaxis has been increasingly emphasized [3].
The pathophysiology of neurogenic bladder involves significant urodynamic abnormalities such as detrusor-sphincter dyssynergia, decreased bladder compliance, detrusor overactivity, and elevated intravesical pressure. Notably, intravesical pressures exceeding 40 cmH₂O are considered a major predictor of upper urinary tract damage. Therefore, early identification and control of bladder pressures in high-risk pediatric patients is crucial for long-term preservation of renal function [4,5].
In recent years, specific morphologic patterns identified via radiological imaging-particularly on VCUG-have been shown to reflect underlying functional abnormalities. One such pattern is the so-called ``tower bladder,'' characterized by pronounced vertical elongation of the bladder dome, a narrowed base, and typically associated with high-pressure voiding. Although the clinical significance of this morphological feature remains under investigation, there is growing evidence suggesting its association with elevated intravesical pressure, the presence of VUR, and renal scarring. The presence of tower bladder may not merely represent an anatomical variation, but rather indicate a high-risk bladder dysfunction phenotype. To objectively assess this structural abnormality, the BDR, defined as the ratio of vertical to horizontal dimensions on VCUG, has emerged as a quantifiable morphological marker. Failure to establish an early diagnosis or delay in initiating appropriate management in these patients may result in irreversible renal damage. Early initiation of CIC and anticholinergic pharmacotherapy plays a key role in reducing intravesical pressure and preventing upper urinary tract complications [6,7].
This study aims to elucidate the prognostic value of tower bladder morphology in children with neurogenic bladder, and to investigate its relationship with radiological and urodynamic indicators. Furthermore, by analyzing the impact of conservative treatment timing on both morphological and functional parameters, we aim to provide clinical guidance for individualized management strategies
Materials and Methods
This retrospective, cross-sectional study included 164 pediatric patients (50.6\textbackslash{}% female, 49.4\textbackslash{}% male; mean age: 7.7 ± 4.6 years) diagnosed with neurogenic bladder and managed at Gaziantep City Hospital between October 2023 and May 2024. The etiologies of neurogenic bladder were as follows:
	• Operated myelomeningocele with associated spinal pathology: 32 patients (61.6\textbackslash{}%)
	• Isolated spinal pathology: 18 patients (19.5\textbackslash{}%), including spina bifida (n=14), operated spinal tumors (n=4), and spinal trauma (n=1)
	• Detrusor overactivity-related causes: Isolated VUR: 18 patients (11.0\textbackslash{}%), detrusor-sphincter dyssynergia (DSD): 7 patients (4.3\textbackslash{}%), operated anorectal malformation: 3 patients (1.8\textbackslash{}%), operated posterior urethral valve: 3 patients (1.8\textbackslash{}%)
Sociodemographic variables---including age, sex, nationality, maternal age at delivery, and maternal folic acid supplementation during pregnancy---were recorded following approval from the institutional ethics committee (Ethics Approval No: 2024/40). Walking status was also documented as a surrogate marker of neurologic impairment severity. Pediatric age-specific reference ranges for serum creatinine levels were interpreted in accordance with the Nelson Textbook of Pediatrics to account for developmental renal function variation (3).
Radiological Assessment: Imaging modalities included US, VCUG, and nuclear scintigraphy (DMSA and, when applicable, DTPA scans). US was used to evaluate bladder wall thickness, ureteral dilatation, and post-void residual (PVR) urine volume. VCUG was utilized to assess bladder morphology and grade VUR. The BDR was calculated as the vertical-to-horizontal dimension ratio (Figure I). Tower bladder morphology was defined as the presence of vertical elongation of the bladder dome on VCUG in conjunction with a BDR >1. DMSA scintigraphy was used to quantify renal cortical damage, and obstructive patterns were recorded on DTPA scans when performed.
Urodynamic Assessment: Urodynamic studies included evaluations of bladder capacity, intravesical pressure, bladder compliance, and the volume at which intravesical pressure reached 40 cmH₂O. In addition, the following treatment-related variables were documented: age at initiation and duration of CIC, type and duration of anticholinergic therapy, administration of intradetrusor botulinum toxin, performance of vesicostomy, and bladder augmentation procedures.
Therapeutic Interventions: The management strategies implemented in these patients included;
	CIC: Performed in 124 patients (75.6\textbackslash{}%), with a mean initiation age of 5.2 ± 4.7 years and a mean duration of 22.6 ± 31.7 months
	Pharmacologic therapy: Oral anticholinergics: oxybutynin (40.2\textbackslash{}%), propiverine (10.4\textbackslash{}%), and tolterodine (9.8\textbackslash{}%)
	Intradetrusor botulinum toxin injections: 39 patients (23.8\textbackslash{}%)
	Subureteric injection for VUR management: 22 patients (13.4\textbackslash{}%)
	Vesicostomy: 3 patients (1.8\textbackslash{}%)
	Bladder augmentation: 3 patients (1.8\textbackslash{}%) (Table I)
Statistical Analysis: All statistical analyses were conducted using IBM SPSS Statistics version 26.0. Continuous variables were expressed as mean ± standard deviation (SD), and categorical variables as frequencies and percentages. The Kolmogorov--Smirnov test was employed to assess data distribution normality. Between-group comparisons were performed using the independent samples t-test, ANOVA, and chi-square test. Post hoc analyses (Bonferroni or Tukey) were applied where appropriate. Correlations between continuous variables were analyzed using Pearson's correlation coefficient. A p-value of <0.05 was considered statistically significant.
Results
1. Findings Related to Intravesical Pressure (Table II)
Among the 164 pediatric patients with neurogenic bladder included in the study, tower bladder morphology was identified in 71.3\textbackslash{}% of cases. This subgroup exhibited significantly higher mean intravesical pressure values (46.2 ± 24.2 cmH₂O vs. 26.7 ± 19.1 cmH₂O; p < 0.001), greater BDR (1.439 ± 0.29 vs. 1.321 ± 0.28; p = 0.008), and a markedly higher incidence of high-grade VUR (Grades IV--V: 58.8\textbackslash{}% vs. 10.6\textbackslash{}%; p = 0.006) compared to those without tower bladder. Moreover, patients with tower bladder began CIC at significantly older ages (5.7 ± 4.7 years vs. 3.4 ± 4.4 years; p = 0.019). A positive correlation was observed between CIC duration and intravesical pressure (r = 0.302; p < 0.001).
Intravesical pressure was positively correlated with BDR (r = 0.362; p < 0.001), serum creatinine level (r = 0.168; p = 0.031), post-void residual volume (PVR) (r = 0.201; p = 0.024), and duration of anticholinergic therapy (r = 0.286; p < 0.001). Patients with renal scarring on DMSA scintigraphy demonstrated significantly higher intravesical pressure values (44.2 ± 24.3 cmH₂O vs. 35.0 ± 23.7 cmH₂O; p = 0.020).
Children with serum creatinine levels exceeding twice the age-adjusted normal range exhibited significantly higher intravesical pressures compared to those with normal values (p = 0.015). Similarly, patients receiving anticholinergic therapy demonstrated significantly increased intravesical pressures relative to untreated counterparts (p < 0.001). In contrast, no statistically significant differences in intravesical pressure were observed among the various anticholinergic agents used (p > 0.05).
2. Findings Related to BDR (Table III)
A statistically significant difference in BDR values was observed depending on the bladder volume at which the intravesical pressure reached 40 cmH₂O (p < 0.001). Post hoc analysis revealed that patients who reached the threshold pressure at one-half or one-quarter of expected bladder capacity exhibited significantly higher BDR values compared to those who did not reach this threshold (both p < 0.001).
A moderate positive correlation was identified between BDR and intravesical pressure (r = 0.362; p < 0.001). No correlation was found between BDR and bladder capacity. In the overall cohort, a weak-to-moderate positive correlation was observed between BDR and intravesical pressure (r = 0.362; p < 0.001), whereas in the subgroup of patients with tower bladder, the correlation remained positive but was weaker (r = 0.184; p = 0.048).
BDR values were significantly higher in patients with obstructive patterns on DTPA scans (p = 0.001) and in those who were non-walking (p = 0.008). Furthermore, children whose serum creatinine values were more than twice the age-specific normal range exhibited the highest BDR values (p = 0.014).
To assess the diagnostic utility of BDR in predicting renal scarring, a receiver operating characteristic (ROC) analysis was conducted. The area under the ROC curve (AUC) indicated high discriminative power, and a BDR cutoff value of >1.4 was identified as highly sensitive and specific for the prediction of renal damage (Figure II).
3. Findings Related to Tower Bladder 
Among patients with tower bladder morphology, a significantly higher proportion reached an intravesical pressure of 40 cmH₂O at early bladder filling volumes (p < 0.001). Additionally, the presence of tower bladder was significantly associated with delayed initiation of CIC (p = 0.019) (Table IV). Patients who reached the threshold pressure of 40 cmH₂O at earlier stages of bladder filling demonstrated significantly elevated BDR values (p < 0.001), suggesting a parallel progression of morphological distortion and functional deterioration.
A significant positive association was observed between the duration of CIC and intravesical pressure (p < 0.001), indicating that prolonged catheterization was linked to higher bladder pressures. Moreover, the timing of CIC initiation was significantly associated with the degree of bladder fullness at which pressure elevation occurred (p = 0.020) (Table V). These findings further support the hypothesis that both delayed intervention and impaired bladder compliance contribute to the development and progression of tower bladder morphology.
4. Outcomes Related to Therapeutic Interventions 
Among the 74 patients who received anticholinergic therapy, no statistically significant association was found between changes in intravesical pressure and clinical improvement (p > 0.05). A reduction in intravesical pressure was observed in 44.6\textbackslash{}% of these patients, while an increase was recorded in 21.6\textbackslash{}%. There was no statistically significant difference in therapeutic response among the various anticholinergic agents used. Pressure reduction was achieved in 51.2\textbackslash{}% of patients receiving oxybutynin and in 75\textbackslash{}% of those treated with propiverine (Table 6).
Patients with bilateral VUR, high-grade reflux, or tower bladder morphology did not demonstrate a significantly different distribution of intravesical pressure responses compared to their counterparts. Similarly, no significant differences in mean BDR values were observed among patients with reduced, stable, or increased bladder pressures following anticholinergic therapy (p = 0.085). In patients who achieved 40 cmH₂O intravesical pressure at early bladder volumes (i.e., at one-half or one-quarter of expected capacity), pressure reduction following anticholinergic therapy was less likely, indicating potential structural resistance to pharmacological modulation (Table VI).
5. Findings Related to Age-Adjusted Serum Creatinine 
Patients who received long-term anticholinergic therapy exhibited significantly elevated age-adjusted serum creatinine levels compared to those who did not (p = 0.001). However, when other clinical parameters were evaluated---such as the presence of VUR, tower bladder morphology, duration or timing of clean intermittent catheterization (CIC), and walking status---no statistically significant differences in age-adjusted creatinine levels were identified (all p > 0.05).
Although creatinine levels tended to be higher in patients with prolonged CIC use or delayed initiation of catheterization, these associations did not reach statistical significance. Among the three anticholinergic agents administered, patients receiving tolterodine showed the highest proportion of creatinine levels above normal, but the difference across groups did not reach statistical significance (Table VII).
These findings suggest that while anticholinergic therapy may be associated with worsening renal function in certain cases, the relationship is likely influenced by underlying bladder dynamics and structural damage rather than pharmacologic intervention alone.
Discussion
Neurogenic bladder is a significant functional disorder of the lower urinary tract resulting from congenital or acquired neurological conditions that impair neural control mechanisms. In the pediatric population, this dysfunction poses a substantial risk for progressive renal damage and long-term deterioration in quality of life [1-3]. In our study, spinal pathology was identified in approximately 75\textbackslash{}% of the patients, with operated myelomeningocele accounting for the most common etiology (61.6\textbackslash{}%), underscoring the strong association between this clinical condition and underlying congenital neurologic defects. In regions such as Turkey, where neural tube defects remain prevalent, the need to strengthen prenatal screening programs and promote folic acid supplementation during pregnancy should be emphasized [10].
Radiologically, the tower bladder morphology observed on VCUG is characterized by marked vertical elongation of the bladder dome and a narrowing of the bladder base. This structural deformation is thought to result from prolonged exposure to high intravesical pressure, which induces detrusor hypertrophy and loss of bladder wall elasticity. In our cohort, tower bladder was identified in 71.3\textbackslash{}% of patients, and these individuals exhibited significantly elevated intravesical pressures (mean: 46.2 ± 24.2 cmH₂O; p < 0.001). The positive correlation between BDR and intravesical pressure (r = 0.362; p < 0.001) further supports the premise that this morphological phenotype is not merely anatomical, but closely associated with clinically relevant functional impairment. Austin et al. (2016) similarly emphasized that intravesical pressures exceeding 40 cmH₂O serve as a critical predictor of progressive renal deterioration in pediatric patients [5].
To more objectively elucidate the relationship between tower bladder morphology and renal scarring, we conducted a receiver operating characteristic (ROC) analysis. The area under the curve (AUC = 1.00) demonstrated excellent diagnostic performance for BDR in predicting renal injury. A BDR cutoff value of >1.4 was strongly associated with the presence of renal scarring and may serve as an optimal threshold with high sensitivity and specificity. These findings suggest that a BDR >1.4 could act as a clinically meaningful surrogate marker for identifying high-risk patients, even in the absence of formal urodynamic evaluation.
Whether tower bladder represents a static congenital anomaly or a progressive, potentially reversible morphological change remains unclear in the current literature. However, our findings support the latter hypothesis. Specifically, the significant association between delayed initiation of CIC and the presence of tower bladder suggests that this deformity may evolve over time as a consequence of sustained high intravesical pressure. Chronic pressure overload likely contributes to detrusor hypertrophy, reduced wall compliance, and structural rigidity, all of which manifest as increased BDR values. Notably, even among patients receiving conservative treatment-including CIC and anticholinergic therapy-intravesical pressure remained significantly elevated in those with tower bladder, suggesting that in advanced stages, this morphological change may be only partially reversible or potentially irreversible. Costa Monteiro et al. (2017) also highlighted the limited efficacy of delayed intervention in preserving bladder function in children with neurogenic bladder [7]. Therefore, tower bladder should not be considered a benign anatomical variation but rather a structural indicator of treatment-resistant, high-risk bladder dysfunction. Longitudinal prospective studies are needed to determine the temporal evolution of this deformity and to clarify its responsiveness to early intervention.
In our study, elevated intravesical pressure was significantly associated with both high-grade VUR (Grades IV--V; p = 0.004) and renal cortical scarring observed on DMSA scintigraphy (p = 0.020). These findings are consistent with prior studies indicating that elevated bladder pressures and reflux synergistically contribute to upper urinary tract deterioration in children with neurogenic bladder (11).These findings reinforce the central role of bladder pressure in the pathogenesis of upper urinary tract injury. Pohl et al. (2017) similarly emphasized that failure to adequately control bladder pressure may result in persistent VUR and irreversible renal damage [3].
CIC and anticholinergic pharmacotherapy constitute the cornerstone of conservative management in pediatric neurogenic bladder, aiming to reduce intravesical pressure and prevent upper urinary tract deterioration by minimizing urinary stasis and infection risk. Although the CIC initiation rate in our study was high (75.6\textbackslash{}%), the mean age at initiation (5.2 years) indicates a substantial delay in intervention. Previous studies, including that by Kiddoo et al. (2014), have shown that early initiation of CIC can prevent the development of irreversible structural changes in the bladder [6]. In our cohort, the significantly higher incidence of tower bladder in patients with delayed CIC initiation (p = 0.019) supports the notion of its progressive and potentially irreversible nature.
Anticholinergic agents aim to suppress detrusor overactivity, thereby increasing bladder capacity and lowering intravesical pressure. In our study, more than 60\textbackslash{}% of patients received anticholinergic treatment, and a significant reduction in bladder pressure was achieved (p < 0.001). However, the absence of a statistically significant association between pressure changes and the duration of therapy, as well as the lack of efficacy differences between agents, suggests that structural alterations may limit pharmacologic responsiveness in more advanced cases [9].
The observed correlation between BDR and intravesical pressure is particularly valuable in clinical scenarios where urodynamic evaluation is not feasible. Furthermore, the significantly elevated BDR in non-walking patients and in those with obstructive patterns on DTPA suggests that this morphological metric may reflect not only bladder dysfunction but also the severity of underlying neurologic impairment.
Elevated bladder pressures occurring prior to the development of overt tower bladder should be regarded as an early warning sign, warranting prompt intervention. If conservative management is not initiated in a timely manner, the combination of sustained intravesical pressure and reflux may result in irreversible renal damage. In such cases---particularly among patients with low bladder capacity, high pressures, and severe reflux---fibrotic changes may render conservative therapy insufficient and necessitate surgical intervention.
Finally, the impact of socioeconomic factors on the management of neurogenic bladder must not be overlooked. Batra et al. (2020) have shown that socioeconomic disadvantage contributes to delayed diagnosis and restricted access to treatment in resource-limited settings [8]. In our cohort, only 41.5\textbackslash{}% of mothers reported folic acid supplementation during pregnancy, and refugee patients (20.7\textbackslash{}%) frequently experienced barriers to care. These findings underscore the need for population-level interventions, including educational and screening programs, to enhance early diagnosis and preventive care strategies [3].
In conclusion, tower bladder should be recognized not merely as an anatomical variant, but as a clinically significant morphological marker indicative of high intravesical pressure, structural progression, and limited reversibility. The integration of radiological and functional markers is essential in establishing individualized management plans and preventing long-term renal sequelae in pediatric patients with neurogenic bladder.
Recommendations
Based on the findings of this study, the following clinical recommendations are proposed to optimize the management of pediatric neurogenic bladder:
Early Diagnosis and Intervention:
Children at high risk for neurogenic bladder---particularly those with myelomeningocele or spinal dysraphism---should undergo regular follow-up and early urodynamic evaluation beginning in the neonatal period.
	An intravesical pressure of ≥40 cmH₂O should be regarded as a critical threshold indicating the need for prompt conservative treatment.
	Patients with a BDR >1.4 should be closely monitored for complications associated with tower bladder morphology and elevated bladder pressure. Although a universal cutoff value for BDR has not yet been established in the literature, our findings suggest that BDR values exceeding 1.5, particularly in children who reach critical pressure at early filling stages, may indicate significant morphological progression. In cases where urodynamic testing is not feasible, BDR >1.4 may serve as a practical morphological warning criterion in clinical practice.
Individualized Treatment Planning:
Therapeutic decision-making should be guided by a comprehensive assessment of urodynamic parameters, VUR grade, renal function, and bladder morphology. CIC and anticholinergic therapy protocols should be personalized and initiated as early as possible based on this integrated evaluation.
Regular and Proactive Monitoring:
Patients should undergo periodic assessment of urodynamic parameters, BDR, serum creatinine levels, and renal scarring via DMSA scans. Those with BDR >1.4 and/or intravesical pressure ≥40 cmH₂O should be classified as high-risk and closely monitored to prevent irreversible renal damage.
Community-Based Awareness and Preventive Health Services:
Public health initiatives should target populations with low socioeconomic status and refugee backgrounds to improve awareness of folic acid use, prenatal screening, and early diagnosis of neurogenic bladder. Educational programs, community-based screening, and increased access to pediatric urology services are essential for early intervention and renal protection.
Declarations
Funding
No funds, grants, or other support was received.
Competing interests
The authors have no financial or proprietary interests in any material discussed in this article.
Ethics approval
This retrospective study was approved by the Institutional Ethics Committee (Approval No: 2024/40), and the requirement for informed consent was waived. 
Consent to participate
Not applicable.
Authors' contributions
Derya Yayla performed the study design and statistical analysis; Güneş Işık contributed to data collection and literature review. Both authors reviewed and approved the final manuscript.


References
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3. Kliegman, R. M., St. Geme, J. W., Blum, N. J., Shah, S. S., Tasker, R. C., \textbackslash{}& Wilson, K. M. (2020). Nelson Textbook of Pediatrics (21st ed., Vol. 1, pp. 3844--3845). Elsevier.
4. Pohl, H. G., Rushton, H. G., \textbackslash{}& Park, J. M. (2017). The management of high-grade vesicoureteral reflux in children. The New England Journal of Medicine, 376(8), 758--769.	
5. Austin, J. C., Cooper, C. S., \textbackslash{}& Boyt, M. A. (2016). Neurogenic bladder in children: Principles of diagnosis and management. The Journal of Urology, 195(6), 1615--1623.
	6. Kiddoo, D., Sawatzky, B., \textbackslash{}& Bascu, D. (2014). Clean intermittent catheterization in children with neurogenic bladder: A practical guide. Canadian Urological Association Journal, 8(7-8), E524--E528.
	7. Costa Monteiro, L. M., Cruz, G. O., Fontes, J. M., Vieira, E. T. R. C., Santos, E. N., Araújo, G. F., \textbackslash{}& Ramos, E. G. (2017). Early treatment improves urodynamic prognosis in neurogenic voiding dysfunction: 20 years of experience. Jornal de Pediatria, 93(4), 420--427. 
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	9. Robson, W. L. M., Leung, A. K. C., \textbackslash{}& Thomason, M. A. (2018). Anticholinergic therapy in the treatment of pediatric neurogenic bladder. International Urology and Nephrology, 50(4), 703--710.
	10. Ginsberg, D. (2013). The epidemiology and pathophysiology of neurogenic bladder. The American Journal of Managed Care, 19(10 Suppl), S191--S198.
	11. Ekberli G, Taner S. Risk determination for upper urinary tract damage in children with neuropathic bladder. J Paediatr Child Health. 2023 Jul;59(7):863-870. doi:10.1111/jpc.16402. PMID: 36999336.

Table I. Demographic, Clinical, and Radiological Characteristics of the Study Population (n = 164) 

Table II. Factors Associated with Intravesical Pressure
* Pearson correlation test 	**ANOVA test		***Student2s t test

Table III. Factors Associated with Bladder Diameter Ratio (BDR)
* Pearson correlation test    	**ANOVA test		***Student's t test

Table IV. Relationship Between Tower-Shaped Bladder and Associated Factors [n (\textbackslash{}%)]
*Chi-square test	**Student's t test

Table V. Comparison of bladder filling at 40 cm H₂O bladder pressure according to the clinical characteristics of the patients [n (\textbackslash{}%)] 
*ANOVA testi	** Chi-square test

Table VI. Changes in Intravesical Pressure in Patients Receiving Anticholinergic Therapy
*ANOVA test	** Chi-square test

Table VII. Age-Adjusted Serum Creatinine Levels by Clinical Variables
*ANOVA test





Figure I. VCUG image of tower bladder morphology and BDR = 1.34 

A 12-year-old male patient with neurogenic bladder (post-operative MMC) and right Grade 4 VUR on VCUG. He has been performing clean intermittent catheterization (CIC) 6 times per day for 6 years, receiving antibiotic prophylaxis, is non-walking, and has been on antihypertensive medication for 1 year. The right kidney has 20\textbackslash{}% function, and serum creatinine is 0.9 mg/dL. Urodynamic study revealed a bladder pressure of 75 cm H₂O at a bladder capacity of 300 cc; the threshold pressure of 40 cm H₂O was reached at a volume of 150 cc.
BDR = Vertical Diameter / Horizontal Diameter
BDR = 77.07 mm / 57.14 mm ≈ 1.34

Figure II. Receiver Operating Characteristic (ROC) curve analysis of BDR for prediction of renal scarring (AUC = 1.00).




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