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Ranitidine has no influence on tubular creatinine secretion
J G van den Berg1, M G Koopman, L Arisz
1Department of Internal Medicine, Academic Medical Center, Amsterdam, The Netherlands.
Nephron
|January 1, 1996
Summary
Oral ranitidine does not block creatinine secretion in healthy individuals. This study found no significant changes in kidney function markers after ranitidine administration, unlike cimetidine.
Area of Science:
- Nephrology
- Pharmacology
Background:
- Cimetidine, an H2-receptor antagonist, is known to inhibit tubular creatinine secretion.
- Ranitidine is a comparable H2-receptor antagonist, prompting investigation into its effect on creatinine secretion.
Purpose of the Study:
- To investigate whether oral ranitidine inhibits the tubular secretion of creatinine.
- To compare the effect of ranitidine with cimetidine on creatinine handling by the kidneys.
Main Methods:
- Simultaneous measurement of inulin clearance (glomerular filtration rate) and endogenous creatinine clearance in 10 healthy subjects.
- Administration of a single oral dose of 300 mg ranitidine to all subjects.
- An additional study with 1,200 mg ranitidine in 7 subjects with high tubular secretion.
Main Results:
- Neither 300 mg nor 1,200 mg of oral ranitidine significantly altered glomerular filtration rate (inulin clearance).
- No significant changes were observed in mean plasma creatinine or mean creatinine clearance after ranitidine administration.
- Ranitidine did not inhibit tubular secretion of creatinine in healthy subjects.
Conclusions:
- Oral ranitidine, at doses of 300-1,200 mg, does not inhibit tubular creatinine secretion in normal subjects.
- This lack of inhibition is likely due to ranitidine's lower affinity for the tubular membrane transport carrier compared to cimetidine.