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2012 ; 35
(3
): 279-86
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Renal adaptation to gentamicin-induced mineral loss
#MMPMID22378246
Lee CT
; Chen HC
; Ng HY
; Lai LW
; Lien YH
Am J Nephrol
2012[]; 35
(3
): 279-86
PMID22378246
show ga
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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