Acute effects of gentamicin on urinary electrolyte excretion in neonates

Giapros, Vasileios; Cholevas, Vasileios; Andronikou, Styliani

doi:10.1007/s00467-003-1381-0

Cited by 30 publications

(28 citation statements)

References 13 publications

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“…There are several other factors that may affect serum calcium during the early period after birth. Persistent urinary calcium and magnesium wasting after gentamicin treatment (2.5 mg/kg/ 12 h) in neonates has been reported by Giapros et al [21], although in their study, serum electrolyte levels were normal. Whether the differences in serum calcium levels between these two reports are related to different doses of gentamicin remains unclear.…”

Section: Discussionmentioning

confidence: 62%

“…Both clinical observation and experimental animal studies have demonstrated that acute gentamicin administration produced significant urinary calcium and magnesium wasting [4,20,21]. As mentioned earlier, gentamicin can cause symptoms and signs identical to the Bartter syndrome type 5, which is due to a gain of function mutation of the CSR [22].…”

Section: Discussionmentioning

confidence: 99%

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Renal Adaptation to Gentamicin-Induced Mineral Loss

Lee

Chen

et al. 2012

Am J Nephrol

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Background: Gentamicin, a well-known nephrotoxic drug, affects calcium and magnesium homeostasis. Although gentamicin induces urinary calcium and magnesium wasting immediately, it rarely causes significant hypocalcemia or hypomagnesemia clinically. Methods: We conducted an animal study to investigate the renal adaptation in calcium and magnesium handling after gentamicin treatment and effects on the expression of calcium and magnesium transport molecules in distal tubule. Gentamicin (40 mg/kg) was injected daily in male Sprague-Dawley rats (220–250 g) for up to 7 days. Results: This treatment did not affect serum creatinine, calcium, or magnesium levels. Gentamicin induced significant hypercalciuria (14-fold) and hypermagnesiuria (10-fold) in 6 h, which was associated with upregulation of TRPV5 (175 ± 3%), TRPV6 (170 ± 4%), TRPM6 (156 ± 4%) and calbindin-D28k (174 ± 3%; all p < 0.05 vs. control). This gene upregulation was maintained with daily injection of gentamicin for 7 days. The gentamicin-induced urinary calcium loss was reduced by 80% at days 3 and 7, while magnesium loss was reduced by 52 and 57% at days 3 and 7, respectively. On the other hand, urinary loss of potassium became worse on day 7 (2-fold), and phosphorus loss worse from day 3 to day 7 (3-fold). Conclusion: There is a rapid adaptation to gentamicin-induced hypercalciuria and hypermagnesiuria. The upregulation of distal tubule transport molecules, TRPV5, TRPV6, TRPM6 and calbindin-D28k occurs within 6 h of gentamicin treatment. This renal adaptation prevents further mineral loss due to gentamicin treatment.

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Section: Discussionmentioning

confidence: 62%

Section: Discussionmentioning

confidence: 99%

Renal Adaptation to Gentamicin-Induced Mineral Loss

Lee

Chen

et al. 2012

Am J Nephrol

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“…Gentamicin has been reported to be an effective drug for various applications in neonatal intensive care units [1][2][3][4][5][6][7], but also to be one which is relatively toxic, with indications that it can induce tubular injury in term and preterm neonates [1][2][3][4]. The dosing schedules in this age group are also subject to controversy.…”

Section: Introductionmentioning

confidence: 99%

Acute effects of gentamicin on glomerular and tubular functions in preterm neonates

et al. 2006

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It has been reported that gentamicin causes natriuresis, magnesuria and calciuria in neonates. The aim of this study was to determine the acute effects of trough and peak levels of gentamicin on the values of serum creatinine (SCr), urine albumin/urine creatinine (UA/UCr), fractional excretion of sodium and potassium (FENa, FEK) and urine calcium/urine creatinine (UCa/UCr) in preterm neonates treated with gentamicin for suspected infection. Baseline levels of serum and urine Cr, Na and K and urine albumin and Ca levels together with trough and peak gentamicin levels were measured in 61 preterm neonates at the start of the therapy, on the day of the third gentamicin dose and 48-72 h after the cessation of the gentamicin therapy. Therapeutic trough and peak levels were recorded in 56 (91.8%) and 39 (63.9%) of the preterm neonates, respectively, whereas high trough (>2 mg/dl) and peak (>9.99 mg/dl) levels were recorded in five (8.1%) and 11 (18%) of the 61 preterm neonates, respectively. Trough and peak levels of gentamicin were positively correlated with SCr, UA/UCr, FENa, FEK and UCa/UCr values. The UA/UCr, FENa and UCa/UCr values recorded during treatment were statistically significantly different from sub-therapeutic, therapeutic and high peak gentamicin levels. Gentamicin was found to have a serum peak level-dependent microalbuminuric, natriuric and calciuric effect in preterm neonates. Based on these results, we suggest that when the monitoring of serum gentamicin levels is not possible, the monitoring of UA/UCr, FENa and UCa/UCr can be useful as a noninvasive alternative.

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“…Indeed, a cumulative effect of gentamicin was observed. [10][11][12] We found an increase in urinary calcium excretion after the first dose of gentamicin, and an even higher increase after the second dose of gentamicin. A previous study showed that serum calcium levels were lowest on third day of gentamicin.…”

Section: Discussionmentioning

confidence: 56%