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A rise in plasma creatinine that is not a sign of renal failure: which drugs can be responsible?
. Andreev E, Koopman M, Arisz L (Medical University‐Sofia, Sofia, Bulgaria and University of Amsterdam, Amsterdam, The Netherlands). A rise in plasma creatinine that is not a sign of renal failure: which drugs can be responsible? (Review.) J Intern Med 1999; 246: 247–252. This is a review of the ava...
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Published in: | Journal of internal medicine 1999-09, Vol.246 (3), p.247-252 |
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Main Authors: | , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | . Andreev E, Koopman M, Arisz L (Medical University‐Sofia, Sofia, Bulgaria and University of Amsterdam, Amsterdam, The Netherlands). A rise in plasma creatinine that is not a sign of renal failure: which drugs can be responsible? (Review.) J Intern Med 1999; 246: 247–252.
This is a review of the available information about drugs which cause an increase in plasma creatinine concentration without decreasing glomerular filtration rate (GFR). The GFR is the main, but not the single, determinant of the plasma creatinine levels. Several drugs, such as cimetidine, trimethoprim, corticosteroids, pyrimethamine, phenacemide, salicylates and active vitamin D metabolites, have been reported to increase plasma creatinine without influencing its glomerular filtration. Cimetidine, trimethoprim, pyrimethamine and salicylates can inhibit secretion of creatinine by the proximal tubule. Corticosteroids and vitamin D metabolites probably modify the production rate and the release of creatinine. The exact mechanism of phenacemide–creatinine interaction is not fully explained. These drug‐induced alterations in plasma creatinine concentration have clinical significance when GFR is estimated by using plasma creatinine. |
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ISSN: | 0954-6820 1365-2796 |
DOI: | 10.1046/j.1365-2796.1999.00515.x |