Williams JC Jr et al, 2012: Fragility of brushite stones in shock wave lithotripsy: absence of correlation with computerized tomography visible structure

Monday, 17 September 2012

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Williams JC Jr, Hameed T, Jackson ME, Aftab S, Gambaro A, Pishchalnikov YA, Lingeman JE, McAteer JA.
Department of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, Indiana, USA

Abstract

PURPOSE: Brushite stones were imaged in vitro and then broken with shock wave lithotripsy to assess whether stone fragility correlates with internal stone structure visible on helical computerized tomography.

MATERIALS AND METHODS: A total of 52 brushite calculi were scanned by micro computerized tomography, weighed, hydrated and placed in a radiological phantom. Stones were scanned using a Philips® Brilliance iCT 256 system and images were evaluated for the visibility of internal structural features. The calculi were then treated with shock wave lithotripsy in vitro. The number of shock waves needed to break each stone to completion was recorded.

RESULTS: The number of shock waves needed to break each stone normalized to stone weight did not differ by HU value (p 0.84) or by computerized tomography visible structures that could be identified consistently by all observers (p 0.053). Stone fragility correlated highly with stone density and brushite content (each p [1]0.001). Calculi of almost pure brushite required the most shock waves to break. When all observations of computerized tomography visible structures were used for analysis by logistic fit, computerized tomography visible structure predicted increased stone fragility with an overall area under the ROC curve of 0.64.

CONCLUSIONS: The shock wave lithotripsy fragility of brushite stones did not correlate with internal structure discernible on helical computerized tomography. However, fragility did correlate with stone density and increasing brushite mineral content, consistent with clinical experience with patients with brushite calculi. Thus, current diagnostic computerized tomography technology does not provide a means to predict when brushite stones will break well using shock wave lithotripsy.

J Urol. 2012 Sep;188(3):996-1001. doi: 10.1016/j.juro.2012.04.097. Epub 2012 Jul 21.
PMID: 22819106 [PubMed - indexed for MEDLINE] PMCID: PMC3418465. FREE ARTICLE

Comments 1

Peter Alken on Monday, 17 September 2012 10:53

A properly performed basic research study.

Whenever I read a publication from this group on brushite stones I eagerly wait for some remarks on the fatal consequences of EWSL. The ESWL-Brushite story was iniatetd at least in 1991 (Klee LW, Brito CG, Lingeman JE: The clinical implications of brushite calculi. J Urol 145:715–718, 1991). It continued to 2004 (Parks JH, Worcester EM, Coe FL, Evan AP, Lingeman JE. Clinical implications of abundant calcium phosphate in routinely analyzed kidney stones. Kidney Int. 2004 Aug;66(2):777-85) with the conclusion: " ... Are the ESWL procedures a cause or an effectof CaP stones, especially of the brushite variety? ... The present work cannot further resolve these matters." And it went on to 2010 (Krambeck AE, Handa SE, Evan AP, Lingeman JE. Brushite stone disease as a consequence of lithotripsy? Urol Res. 2010 Aug;38(4):293-9) with the conclusion:" It is possible that external injury to the nephron either by natural obstruction or iatrogenic forces, such as alkalinization therapy or SWL, is the initiating factor for this conversion. Further research in the areas of SWL induced nephron damage and brushite stone disease is necessary to draw definite conclusions."

In the present publication the story continues at the very end: „It has been suggested that kidney injury caused by SWL may induce this transformation to brushite stone formation (Krambeck et al.). It is far from certain that there is a real connection between SW injury and the induction of brushite stones. Also, to our knowledge there are no data on whether further SW injury might worsen brushite stone disease. Nevertheless, it might be wise to avoid SW treatment of known brushite calculi since the chance of successful treatment is small (Klee et al.) and this would avoid possibly exacerbating stone disease."

After 20 years of suspicion at least the senior author should be able to abandon the hypothesis and end the quotation of the old publications.

Peter Alken

A properly performed basic research study.

Whenever I read a publication from this group on brushite stones I eagerly wait for some remarks on the fatal consequences of EWSL. The ESWL-Brushite story was iniatetd at least in 1991 (Klee LW, Brito CG, Lingeman JE: The clinical implications of brushite calculi. J Urol 145:715–718, 1991). It continued to 2004 (Parks JH, Worcester EM, Coe FL, Evan AP, Lingeman JE. Clinical implications of abundant calcium phosphate in routinely analyzed kidney stones. Kidney Int. 2004 Aug;66(2):777-85) with the conclusion: "  ... Are the ESWL procedures a cause or an effectof CaP stones, especially of the brushite variety? ... The present work cannot further resolve these matters." And it went on to  2010 (Krambeck AE, Handa SE, Evan AP, Lingeman JE. Brushite stone disease as a consequence of lithotripsy? Urol Res. 2010 Aug;38(4):293-9) with the conclusion:" It is possible that external injury to the nephron either by natural obstruction or iatrogenic forces, such as alkalinization therapy or SWL, is the initiating factor for this conversion. Further research in the areas of SWL induced nephron damage and brushite stone disease is necessary to draw definite conclusions."

In the present publication the story continues at the very end: „It has been suggested that kidney injury caused by SWL may induce this transformation to brushite stone formation (Krambeck et al.). It is far from certain that there is a real connection between SW injury and the induction of brushite stones. Also, to our knowledge there are no data on whether further SW injury might worsen brushite stone disease. Nevertheless, it might be wise to avoid SW treatment of known brushite calculi since the chance of successful treatment is small (Klee et al.) and this would avoid possibly exacerbating stone disease."

After 20 years of suspicion at least the senior author should be able to abandon the hypothesis and end the quotation of the old publications.

Peter Alken

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