Gentamicin-induced Bartter-like syndrome

Landau, Daniel; Kher, Kanwal K.

doi:10.1007/s004670050378

Cited by 47 publications

(20 citation statements)

References 20 publications

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“…Only sporadically has a syndrome similar to Bartter syndrome type 5 (gain of function mutation of CSR) with hypokalemia, hypomagnesemia and hypercalciuria been reported in gentamicin-treated patients [12,13]. In the present study, we conducted an animal study to investigate the renal adaptation of calcium and magnesium handling during gentamicin administration, and gentamicin effects on the gene expression of calcium and magnesium transport molecules in the DCT.…”

Section: Introductionmentioning

confidence: 99%

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: Introductionmentioning

confidence: 99%

Renal Adaptation to Gentamicin-Induced Mineral Loss

Lee

Chen

et al. 2012

Am J Nephrol

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“…Apart from reducing glomerular filtration, aminoglycosides may cause enzymuria, proteinuria, amino aciduria, glycosuria and diverse electrolytic alterations including hypomagnesemia, hypocalcemia and hyperkalemia, and may even cause Fanconi's-like [51] or Bartter-like syndrome [52]. Urine examinations are little characteristic; sometimes with leukocyturia, proteinuria and cylindruria [53].…”

Section: Clinical Aspectsmentioning

confidence: 99%

Nefrotoxicidade dos aminoglicosídeos

Oliveira¹,

Cipullo²,

Burdmann³

2006

Rev Bras Cir Cardiovasc

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Aminoglycoside are frequently used due to its high efficacy against gram-negative bacteria and positive synergism with other antibiotics against gram-positive organisms. They are commonly used for prevention and treatment of infection complications after cardiothoracic surgery. The principal side effect of this class of antibiotics is nephrotoxicity, which may occur in up to 20% of the exposed patients. Although usually reversible, aminoglycosideinduced renal injury prolongs hospitalization time and increase patients cost. Even more important, the occurrence of nephrotoxicity is associated with higher patient mortality. There are some known risk factors for nephrotoxicity development and some measures that may prevent it. This review will cover the most relevant aspects of this important side effect of aminoglycoside therapy. Descriptors 445OLIVEIRA, JFP ET AL -Aminoglycoside nephrotoxicity Braz J Cardiovasc Surg 2006; 21(4): 444-452

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“…The extent of the tubular dysfunction ranges from clinically undetectable enzymuria to substantial wasting of electrolytes and minerals [3]. Two types of renal tubular damage have been reported: a Fanconi-like syndrome of a rather generalized proximal tubular damage and a syndrome of hypokalemic metabolic alkalosis associated with hypomagnesemia [4][5][6][7][8][9][10][11][12][13][14][15][16]. We report 2 representative cases of a reversible tubular damage related to chronic aminoglycoside administration.…”

Section: Introductionmentioning

confidence: 99%

Aminoglycoside-Induced Reversible Tubular Dysfunction

Alexandridis

Liberopoulos

Elisaf³

2003

Pharmacology

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Nonoliguric renal insufficiency is a well-known nephrotoxic consequence of aminoglycosides, although reversible tubular damage in the absence of any change in the renal function has been occasionally found. Reported herein are 2 representative cases of a reversible tubular damage due to prolonged aminoglycoside administration: a patient with a Fanconi-like syndrome of proximal tubular dysfunction and a patient with a syndrome of hypokalemic metabolic alkalosis associated with hypomagnesemia.

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Gentamicin-induced Bartter-like syndrome

Cited by 47 publications

References 20 publications

Renal Adaptation to Gentamicin-Induced Mineral Loss

Renal Adaptation to Gentamicin-Induced Mineral Loss

Nefrotoxicidade dos aminoglicosídeos

Aminoglycoside-Induced Reversible Tubular Dysfunction

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