NDT Plus Advance Access originally published online on March 11, 2008
NDT Plus 2008 1(3):190-192; doi:10.1093/ndtplus/sfn020
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Investigation of the association between oral sodium phosphate use and kidney injury
1 Division of Renal-Electrolyte and Hypertension, Department of Medicine
2 Division of Gastroenterology Department of Medicine
3 Division of General Internal Medicine, Department of Medicine
4 Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania School of Medicine Philadelphia, PA, USA
Correspondence: E-mail: steven.brunelli{at}uphs.upenn.edu
Sir,
Recently we published a report in which we found no apparent association between oral sodium phosphate (OSP) purgative use and incident chronic kidney disease (CKD): OR (95% CI) 0.70 (0.44–1.11) [1]. Published concurrently with our study was another study by Hurst [2] that reported a potent association between OSP use and acute kidney injury (AKI): OR (95% CI) 2.35 (1.51–3.66) [2]. We were intrigued at the dramatic differences in findings, and undertook additional sensitivity analyses of our data in order to explore possible explanations. Potential sources for discrepancy include differences in timing of post-colonoscopy creatinine considered, case definition and population under study.
In order to determine the impact of case definition on findings, we conducted analysis 1 in which case status was reassigned according to Hurst's criterion (50% rise in serum creatinine [2]). The adjusted OR (95% CI) was 0.75 (0.32–1.73) (Table 1).
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In order to examine the association between OSP and AKI, Hurst defined outcome based on the most proximate post-colonoscopy serum creatinine [2]. Thus, we conducted analysis 2 in which case status was defined according to the change between baseline and earliest available post-colonoscopy creatinine. Adjusted ORs (95% CIs) were 0.87 (0.52–1.46) and 1.15 (0.43–3.07) using 25% and 50% serum creatinine rise as case definition, respectively (Table 1).
Hurst limited inclusion to subjects over the age of 50 undergoing colonoscopy for screening purposes, and considered as controls only subjects receiving polyethylene glycol [2]. Thus, we conducted analysis 3 in which we restricted observation to those subjects meeting Hurst's criteria (n = 281). The adjusted ORs (95% CIs) were 0.76 (0.37 to 1.56) and 0.96 (0.25–3.79) based on case definitions of 25% and 50% rise in serum creatinine, respectively.
Multiple case reports and series suggest an association between OSP use and ‘acute phosphate nephropathy.’ The issue here is whether these represent rare, idiosyncratic reactions or a more generalized risk to the population at large. The only prior controlled study of the renal consequences of OSP exposure suggests that there is not a predisposition toward systematic CKD [3], consistent with our present (and past) findings.
These analyses suggest that timing of post-colonoscopy creatinine considered, case definition and certain characteristics of the subjects studied do not account for the dramatic differences between Hurst's findings and our own. Our study included a much higher proportion of patients who were non-white, had diabetes or congestive heart failure; it is possible that differences result from as yet unrecognized effect modification on these bases.
Some limitations of the present analyses bear note. In reassigning case/control status, there was diminution of the number of available cases and statistical power; thus, we cannot exclude the possibility of type II error. As AKI was not our original outcome of interest, we lack data on certain exposures that potentially confound the association between OSP and AKI (e.g. iodinated contrast exposure and non-steroidal anti-inflammatory use), and, therefore, we could not adjust on these bases.
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Acknowledgements |
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This study was supported in part by the National Institutes of Health institutional training grant for clinical nephrology T32-DK-07785 and by the American Heart Association Fellow-to-Faculty transition award 0775021N (S.M.B.).
Conflict of interest statement. S.M.B. had full access to all of the data and takes responsibility for the integrity and accuracy of the data analysis. This work has not been presented elsewhere in manuscript or abstract form.
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References |
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 Top References |
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- Brunelli SM, Lewis JD, Gupta M, et al. Risk of kidney injury following oral phosphosoda bowel preparations. J Am Soc Nephrol (2007) 18:3199–3205.
[Free Full Text] - Hurst FP, Bohen EM, Osgard EM, et al. Association of oral sodium phosphate purgative use with acute kidney injury. J Am Soc Nephrol (2007) 18:3192–3198.
[Abstract/Free Full Text] - Chan A, Depew W, Vanner S. Use of oral sodium phosphate colonic lavage solution by Canadian colonoscopists: pitfalls and complications. Can J Gastroenterol (1997) 11:334–338.[Web of Science][Medline]
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