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Saudi Journal of Kidney Diseases and Transplantation
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ORIGINAL ARTICLE Table of Contents   
Year : 2009  |  Volume : 20  |  Issue : 1  |  Page : 102-105
Renal involvement in children with spina bifida


1 Princesss Al-jawhara Center of Excellence in Research of Hereditary Disorders, King Abdul Aziz University Hospital, Jeddah, Saudi Arabia
2 Department of Pediatrics, King Abdul Aziz University Hospital, Jeddah, Saudi Arabia

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   Abstract 

Renal scarring and renal failure remain life-threatening for children born with spinal dysraphism. An early start of therapy helps to safeguard renal function for such children and avoid end-stage renal disease. However, optimal care is not always available in developing countries. We reviewed our data on all newborns with spina bifida who were born at King Abdulaziz University Hospital between 1997 and 2006. Thirty-three children with myelomeningocele (MMC) were eva­luated; MMC site was thoracolumbar in 26 patients (77.1%) and in the lumbosacral area in 7 patients (22.9%). The mean age at the time of evaluation was 5.4 ± 2.3 years. Thirty (90%) patients presented with neurogenic bladder, and 26(78%) with vesico-uretral reflux (VUR). Only 8 patients (group A) received clean intermittent catheterization (CIC), while the rest (group B) were either non-complaint or not on any therapy. Urinary tract infections overall were 4.5 ± 3.8 per year. Patient undergoing CIC had a lower number of UTI (mean per year) 3.3 ± 1.2 vs 6.6 ± 2.3. Sixty two percent of group A had VUR compared with 93% in group B. The mean creatinine was 46 ± 39 µmol/L for the whole group. However, group A had a lower mean creatinine 38 ± 11 compared to 50 ± 34 in group B. In conclusion, early intervention to relieve urinary retention in children born with spina bifida resulted in preserving renal function and less incidence of VUR and UTI. There is a need of more awareness about the importance of starting proactive treatment of risks of upper urinary tract disease and development of renal failure in babies with spina bifida.

Keywords: Spina bifida, VUR, Reflux, Infection, Urinary, Renal failure

How to cite this article:
Kari JA, Safdar O, Jamjoom R, Anshasi W. Renal involvement in children with spina bifida. Saudi J Kidney Dis Transpl 2009;20:102-5

How to cite this URL:
Kari JA, Safdar O, Jamjoom R, Anshasi W. Renal involvement in children with spina bifida. Saudi J Kidney Dis Transpl [serial online] 2009 [cited 2019 Nov 17];20:102-5. Available from: http://www.sjkdt.org/text.asp?2009/20/1/102/44714

   Introduction Top


Neuropathic bladder caused by spina bifida re­mains an important cause of chronic renal fai­lure in developing countries. [1],[2],[3] In contrast, re­cent reports from western countries showed that children born with spina bifida can avoid such complication if they are provided adequate uro­logical intervention. [4] Early therapy with clean intermittent catheterization to decrease intrave­sical pressure is the preferred treatment, and antimuscarinic agents to counteract detrusor ins­tability [5],[6] help in safe guarding renal function for such children.

Optimal therapy is not usually available for children living in developing or underdeveloped countries. Furthermore, the incidence of spina bifida is still high in the kingdom of Saudi Arabia despite the recent fortification of flour with folic acid. [7],[8],[9]

In this study, we aim to investigate the uro­logical complications in spina bifida children who were born and followed up at our ins­titution, and discuss the possible causes for high percentage of renal complications.


   Patients and Methods Top


All babies born with spina bifida at King Abdulaziz University hospital (KAUH) between 1997 and 2006 were included in the study. Referred patients were not included.

The clinical notes of the babies were re­viewed. We have studied the type of treatment, antimuscarinic agents, clean intermittent cathe­terisation (CIC), and antibiotic prophylaxis. Re­nal function, ultrasound, micturating cystoure­throgram (MCUG), DMSA scan, serum crea­tinine, and bladder function (urodynamic studies) were evaluated.


   Results Top


Data of 33 children with myelomeningocele (MMC) were evaluated. MMC site was thora­columbar in 26 (77.1%) patients and in the lumbosacral area in 7 (22.9%).

The mean age at the time of evaluation was 5.4 ± 2.3 years. Sixteen (48%) children were Saudi and the rest (52%) were non-Saudi. Most of the non-Saudi group was from poor socio­economic background. Fourteen children were from outside the city

Ninety percent (30 patients) were diagnosed as neurogenic bladder and 26(78%) patients diagnosed to have vesico-uretral reflux (VUR). Ten children had unilateral VUR and the re­maining 16 had bilateral VUR. Only 8 (24%) patients (group A) received clean intermittent catheterization (CIC), while the rest (group B) were either non-complaint or did not receive it. Oxybutinin was used only by 18 children (55%) and the rest were not prescribed any medication to reduce the intravesical pressure.

The mean number of urinary tract infections per year was 4.5 ± 3.8. Patient who received CIC had a lower number of UTI of a mean 3.3 ± 1.2 compared with 6.6 ± 2.3. Sixty-two per­cent of group A had VUR compared with 93% in group B. Twelve (36%) patients had evi­dence of renal scars (10 in one kidney and 2 had scars in both kidneys). Children with scared kidneys (92%) were all except one from group B. One child had a single left kidney.

The mean creatinine was 46 ± 39 µmol/L. Group A had a lower mean creatinine 38 ± 11 compared to 50 ± 34 µmol/L in group B. One patient progressed to chronic renal failure at 6 years of age (creatinine was 146 µmol/L). Seven patients were lost to follow-up.


   Discussion Top


Our results demonstrate that our studied spina bifida children developed a considerable renal damage at an early age. This is different from reports from western countries; 36% of our cohort had scared kidneys at 5 years of age, while Dik et al have reported recently that only 6 out of 144 (4%) children with spina bifida had evidence of renal scars at the age of six years. [4] Lewis et al in 1994, reported that the prevalence of renal parenchymal damage was 19.4% with higher prevalence of parenchymal damage in children over 10 year of age ( 27.3%), twice that of the 13.3% under 5 years of age. [10]

The cause of higher incidence of renal damage in our cohort could be explained by the delay in proper management, as regular emptying of the bladder was not commenced early and anti­cholinergic drugs were not instituted in con­siderable number of the children. Furthermore, the lack of good medical follow-up and ma­nagement including early diagnosis and treat­ment of acute pyelonephritis could also have contributed to the worse outcome in these patients. This is caused by the lack of multidisciplinary specialized spina bifida clinics where children have an easy access. Establishing such clinics, would help to reduce this observed delay in commencing the appropriate manage­ment to protect the kidneys. However, our cohort is rather disadvantaged group as many of them came from poor socio-economic back­ground resulting in non-compliance issues.

Early investigation and management of neu­rogenic bladder is crucial to protect the kid­neys. [4],[11] Early start of CIC is the most important factor to avoid renal damage. It was reported that the prognosis of children with upper renal tract changes at birth did not seem to be any worse than children developing changes later in life. [12] Five of the 6 patients with renal scarring in Dik et al report, were started on therapy with intermittent catheterization and antimuscarinic therapy several months after birth.

CIC is not accepted by many families as modality of therapy. It has psychosocial impact on the treated children and their families [13],[14] and probably the rejection to this form of treatment is more common in Arab cultures like ours. Furthermore, advice from the practitioners of alternative medicine and lack of update knowledge of health care professionals to delay the CIC was also a major factor.

Our Group B patients, who were not receiving CIC, had a higher incidence of VUR, UTI and renal scars.One patient from this group pro­gressed to renal failure at an early age.

One patient of our cohort was reported to have a single kidney. Whitaker et al, reported three decades ago the prevalence of renal anomalies in spina bifida patients to be around 8.9%. [15] They observed also that renal agenesis was associated with a sensory level in the derma­tomes T5-8, horseshoe kidneys with T9-L1 and duplications predominantly with the sacral der­matomes. However, Hulton et al, reported few year later similar prevalence of renal abnorma­lities, but a consistent pattern was not con­firmed. [16] It was also shown by previous inves­tigators that children with spina bifida, but with­out a history of intrinsic renal disease, have small kidneys when compared with age-matched standard renal growth charts. [17],[18] This further stresses the need for an aggressive approach for optimal care of the bladder to protect already compromised kidneys.

In conclusion, we have shown that the lack of an early therapy in form of CIC resulted in a considerable morbidity at young age in children born with spina bifida. Children with poor compliance had higher incidence of VUR and UTI. There is a need of more awareness about the importance of starting proactive treatment to prevent renal damage in babies with spina bifida.

 
   References Top

1.Kari JA. Neuropathic bladder as a cause of chronic renal failure in children in developing countries. Pediatr Nephrol 2006;21(4):517-20.  Back to cited text no. 1    
2.Hamed RM. The spectrum of chronic renal failure among Jordanian children. J Nephrol 2002;15(2):130-5.  Back to cited text no. 2    
3.Sirin A, Emre S, Alpay H, Nayir A, Bilge I, Tanman F. Etiology of chronic renal failure in Turkish children. Pediatr Nephrol 1995;9(5): 549-52.  Back to cited text no. 3    
4.Dik P, Klijn AJ, van Gool JD, de Jong-de Vos van Steenwijk CC, de Jong TP. Early start to therapy preserves kidney function in spina bifida patients. Eur Urol 2006;49(5):908-13.  Back to cited text no. 4    
5.Jimenez J, Orueta I, Areses R, Pena B, Arrue­barrena D, Tovar J. Prevention of renal injury by means of intermittent catheterization in children with neurogenic bladder secondary to spina bifida. An Esp Pediatr 1985;23(5):347-53.  Back to cited text no. 5    
6.Ab E, Dik P, Klijn AJ, van Gool JD, de Jong TP. Detrusor overactivity in spina bifida: How long does it need to be treated? Neurourol Urodyn 2004;23(7):685-8.  Back to cited text no. 6    
7.Murshid WR. Spina bifida in Saudi Arabia: Is consanguinity among the parents a risk factor? Pediatr Neurosurg 2000;32(1):10-2.  Back to cited text no. 7    
8.Asinidi AA. Neural tube defects in the Asir region of Saudi Arabia. Ann Saudi Med 2001; 21(1-2):26-9.  Back to cited text no. 8    
9.Safdar OY, Al-Dabbagh AA, Abuelieneen WA, Kari JA. Decline in the incidence of neural tube defects after the national fortification of flour (1997-2005). Saudi Med J 2007;28(8):1227-9.  Back to cited text no. 9    
10.Lewis MA, Webb NJ, Stellman-Ward GR, Bannister CM. Investigative techniques and renal parenchymal damage in children with spina bifida. Eur J Pediatr Surg 1994;4(Suppl 1): 29-31.  Back to cited text no. 10    
11.Perez LM, Khoury J, Webster GD. The value of urodynamic studies in infants less than 1 year old with congenital spinal dysraphism. J Urol 1992;148(2.2):584-7.  Back to cited text no. 11    
12.Greig JD, Young DG, Azmy AF. Follow-up of spina bifida children with and without upper renal tract changes at birth. Eur J Pediatr Surg 1991;1(1):5-9.  Back to cited text no. 12    
13.Edwards M, Borzyskowski M, Cox A, Badcock J. Neuropathic bladder and intermittent cathete­rization: social and psychological impact on children and adolescents. Dev Med Child Neurol 2004;46(3):168-77.  Back to cited text no. 13    
14.Borzyskowski M, Cox A, Edwards M, Owen A. Neuropathic bladder and intermittent cathete­rization: Social and psychological impact on families. Dev Med Child Neurol 2004;46(3): 160-7.  Back to cited text no. 14    
15.Whitaker RH, Hunt GM. Incidence and distri­bution of renal anomalies in patients with neural tube defects. Eur Urol 1987;13(5):322-3.  Back to cited text no. 15    
16.Hulton SA, Thomson PD, Milner LS, Isdale JM, Ling J. The pattern of congenital renal ano­malies associated with neural tube defects. Pediatr Nephrol 1990;4(5):491-2.  Back to cited text no. 16    
17.Gross GW, Thornburg AJ, Bellinger MF. Normal renal growth in children with myelo­dysplasia. AJR Am J Roentgenol 1986;146(3): 615-7.  Back to cited text no. 17    
18.Gross GW, Boal DK. Sonographic assessment of normal renal size in children with myelo­dysplasia. J Urol 1988;140(4):784-6.  Back to cited text no. 18    

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Correspondence Address:
Jameela A Kari
Princesss Al-jawhara Center of Excellence in Research of Hereditary Disorders, King Abdul Aziz University Hospital, P.O. Box 80215, Jeddah 21589
Saudi Arabia
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PMID: 19112226

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    Abstract
    Introduction
    Patients and Methods
    Results
    Discussion
    References
 

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