Τόμος 20 (2006) – Τεύχος 2 – Άρθρο 39 – Επιθεώρηση Κλινικής Φαρμακολογίας και Φαρμακοκινητικής-Διεθνής Έκδοση – Volume 25 (2006) – Issue 2 – Article 39 – Epitheorese Klinikes Farmakologias και Farmakokinetikes-International Edition

Title Assessment of vancomycin induced nephrotoxicity by determination of urinary alpha and pi glutathione S-transferase
Authors E. Haliassos¹,², S. Markantonis-Kyroudis¹, G. Papatheodorou² and N. Drakoulis¹

1. University of Athens, School of Pharmacy, Greece

2. 401 General Military Hospital of Athens, Greece

Citation Haliassos, E., Markantonis-Kyroudis, S., Papatheodorou, G., Drakoulis, N.: Assessment of vancomycin induced nephrotoxicity by determination of urinary alpha and pi glutathione S-transferase, Epitheorese Klin. Farmakol. Farmakokinet. 20(2): 168-170 (2006)
Publication Date Accepted for publication: 19-20 May 2006
Full Text Language English
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Keywords Vancomycin, nephrotoxicity, glutathione S-transferase, renal tubular damage.
Other Terms review article
Summary The aim of the study was (a) to assess the effect of vancomycin on the structural integrity of renal tubules by determination of alpha and pi glutathione S-transferase (αGST and πGST) in urine and (b) to evaluate the predictive value of αGST and πGST for vancomycin induced nephrotoxicity. Ten hospitalized patients, treated with intravenously administered vancomycin, without other nephrotoxic agents present, were included in the study. Serum creatinine, αGST and πGST urinary levels and serum vancomycin concentrations were quantitatively determined. The effect of vancomycin on renal tubular integrity was evaluated by observing the change in urinary excretion rates with respect to baseline values on the first day of treatment. Significant changes in αGST and πGST urinary excretion rates from baseline were noted throughout vancomycin treatment. The observed increase in the urinary excretion rate of αGST and πGST support the idea that structural damage occurred in tubular cells during treatment. The statistical significance of the results allows us to conclude that intravenously administered vancomycin induces renal tubular damage while its concentrations lie within the therapeutic range and serum creatinine is normal. Vancomycin induced nephrotoxicity could not be evaluated using GSTs because no study patients presented renal insufficiency (change in serum creatinine >0.5 mg/dl).
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