Clinical Case Discussion
Spinal Cord (2005) 43, 269–277. doi:10.1038/sj.sc.3101713 Published online 18 January 2005
Recurrent vesical calculi, hypercalciuria, and biochemical evidence of increased bone resorption in an adult male with paraplegia due to spinal cord injury: is there a role for intermittent oral disodium etidronate therapy for prevention of calcium phosphate bladder stones?
S Vaidyanathan1, I D Watson2, O Jonsson3, A Z Buczynski4, F Grases5, I P Heilberg6, T Yasui7, J J Wyndaele8, K Tozawa7, K Kohri7, B Schurch9, P L Hughes10, G Singh11, B M Soni1, P Sett1 and W D Fraser11
- 1Regional Spinal Injuries Centre, District General Hospital, Southport, UK
- 2Department of Biochemistry, District General Hospital, Southport, UK
- 3Department of Urology, Sahlgrenska University Hospital, Göteborg, Sweden
- 4Metropolitan Rehabilitation Centre, Department of Neuro-Urology, Konstancin, Poland
- 5Laboratory of Renal Lithiasis Research, Institute of Health Sciences Research (IUNICS), University of Balearic Islands, Palma de Mallorca, Spain
- 6Nephrology Division, Universidade Federal de São Paulo, São Paulo – SP, Brazil
- 7Department of Nephro-Urology, Nagoya City University Graduates School of Medical Sciences, Nagoya, Japan
- 8Centrum Urologische Revalidatie, Universitair Zieckenhuis Antwerpen, Edgem, Belgium
- 9Department of Neuro-Urology, Spinal Cord Injury Centre, University Hospital Balgrist, Zurich, Switzerland
- 10Department of Radiology, District General Hospital, Southport, UK
- 11Department of Clinical Chemistry, Royal Liverpool and Broadgreen University Hospital, Liverpool, UK
Correspondence: S Vaidyanathan, Regional Spinal Injuries Centre, Southport, Merseyside PR8 6PN, UK
Abstract
Study design:
Clinical case report with comments by colleagues from Sweden, Poland, Spain, Brazil, Japan, Belgium and Switzerland.
Objectives:
To discuss the role of disodium etidronate therapy for prevention of calcium phosphate vesical calculi in persons with spinal cord injury, who have hypercalciuria and biochemical evidence of increased bone resorption.
Setting:
Regional Spinal Injuries Centre, Southport, UK.
Methods:
A 21-year-old male sustained paraplegia (T-10; ASIA scale: A) in a road traffic accident in June 2001. He had an indwelling urethral catheter until the end of August 2001, when he started self-catheterisation. He developed bladder stones and electrohydraulic lithotripsy (EHL) was performed in May 2002. All stone fragments were removed. Recurrence of vesical calculi was noted in October 2002. These stones were fragmented by lithoclast lithotripsy in two sessions, in December 2002 and February 2003; all stone fragments were removed at the end of the second session. This patient reverted to indwelling catheter drainage when vesical calculi recurred. In September 2003, X-ray of the abdomen showed recurrence of vesical calculi. By February 2004, the stones had increased in size and number. EHL of vesical calculi was again performed in April 2004. Complete clearance was achieved.
Results:
A 24-h urinalysis detected hypercalciuria – 18.7 mmol/day (reference range: 2.5–7.5). Biochemical analysis of vesical calculus revealed calcium phosphate (85%) and magnesium ammonium phosphate (15%). Plasma C-terminal telopeptide (CTX) was increased – 1.06 ng/ml (reference range: 0.1–0.5 ng/ml). Free deoxypyridinoline/creatinine ratio (fDPD/Cr) in urine was also increased – 20.2 (reference range: 2.3–5.4). In April 2004, this patient was prescribed disodium etidronate 400 mg day. Nearly 3 months after commencing therapy with etidronate, plasma CTX decreased to 0.87 ng/ml. fDPD/Cr in urine also decreased to 12.4. After 4 months of etidronate therapy, 24-h urinary calcium excretion had decreased to 6.1 mmol/day.
Conclusion:
Etidronate (400 mg daily) is a very effective inhibitor of calcium phosphate crystallisation. Etidronate decreased urinary excretion of calcium, an important factor in prevention of calcium phosphate bladder stones. Etidronate therapy is not a substitute for other well-established methods for prevention of vesical calculi in spinal cord injury patients, for example, large fluid intake, avoiding long-term catheter drainage. Intermittent therapy with etidronate may be considered in selected patients, in whom hypercalciuria persists after instituting nonpharmacological therapy for an adequate period, for example, early mobilisation, weight-bearing exercises, and functional electrical stimulation. However, possible side effects of etidronate, and the fact that etidronate is not licensed in United Kingdom for prevention of urolithiasis, should be borne in mind.
Keywords:
hypercalciuria, urinary bladder, calculi, etidronate
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