Gentamicin Induced Hypomagnesemia

Finton, Chris K.; Chernow, Bart; Bjorkland, S; Zaloga, Gary P.

doi:10.1097/00003246-198203000-00080

Cited by 6 publications

(4 citation statements)

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“…Thus, mitochondrial dysfunction in the proximal tubule is the expected consequence of AG toxicity, and this is, indeed, concordant with the clinical findings: AG-induced kidney failure is typically non-oliguric, with evidence of proximal tubular dysfunction and damage (reviewed in [8]) and occasionally frank renal Fanconi syndrome [9]. Occasionally, more distant tubular segments are affected with a Bartter-like syndrome [10] or renal magnesium wasting [11].…”

Section: Aminoglycosides and The Kidneysupporting

confidence: 65%

Cystic fibrosis, aminoglycoside treatment and acute renal failure: the not so gentle micin

2009

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Aminoglycosides have a wide spectrum of gramnegative anti-bacterial activities and are available at low cost, which makes them commonly used drugs, especially for patients with cystic fibrosis (CF), who often suffer from chronic lung infections from Pseudomonas aeruginosa. Unfortunately, this treatment seems to have resulted in an increased incidence of acute renal failure (ARF) in patients with CF. A recent case-control study investigated risk factors for ARF in CF patients and suggested intravenous use of gentamicin as the prime culprit. Moreover, in most cases, at least one other risk factor, such as CF-related diabetes, pre-existing renal failure, dehydration or concurrent use of other nephrotoxic drugs, was present. We comment on the renal handling of aminoglycosides and the possible mechanisms of toxicity, as well as strategies for risk minimisation.

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Section: Aminoglycosides and The Kidneysupporting

confidence: 65%

Cystic fibrosis, aminoglycoside treatment and acute renal failure: the not so gentle micin

2009

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“…This results in hypokalemic metabolic alkalosis with hypermagnesuria and hypercalciuria and a normal serum creatinine (Bartter-like syndrome) [172,173]. Furthermore, gentamicin might cause Mg 2+ wasting; animal experiments have shown a causal relationship between gentamicin administration and Mg 2+ wasting [174]. In healthy people, gentamicin causes immediate and transient renal calcium (Ca 2+ ) and Mg 2+ wasting (Fig.…”

Section: Aminoglycosidesmentioning

confidence: 99%

Drug-induced acid-base disorders

et al. 2014

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The incidence of acid-base disorders (ABDs) is high, especially in hospitalized patients. ABDs are often indicators for severe systemic disorders. In everyday clinical practice, analysis of ABDs must be performed in a standardized manner. Highly sensitive diagnostic tools to distinguish the various ABDs include the anion gap and the serum osmolar gap. Drug-induced ABDs can be classified into five different categories in terms of their pathophysiology: (1) metabolic acidosis caused by acid overload, which may occur through accumulation of acids by endogenous (e.g., lactic acidosis by biguanides, propofol-related syndrome) or exogenous (e.g., glycol-dependant drugs, such as diazepam or salicylates) mechanisms or by decreased renal acid excretion (e.g., distal renal tubular acidosis by amphotericin B, nonsteroidal antiinflammatory drugs, vitamin D); (2) base loss: proximal renal tubular acidosis by drugs (e.g., ifosfamide, aminoglycosides, carbonic anhydrase inhibitors, antiretrovirals, oxaliplatin or cisplatin) in the context of Fanconi syndrome; (3) alkalosis resulting from acid and/or chloride loss by renal (e.g., diuretics, penicillins, aminoglycosides) or extrarenal (e.g., laxative drugs) mechanisms; (4) exogenous bicarbonate loads: milk-alkali syndrome, overshoot alkalosis after bicarbonate therapy or citrate administration; and (5) respiratory acidosis or alkalosis resulting from drug-induced depression of the respiratory center or neuromuscular impairment (e.g

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“…The frequency of use of diuretics and presence of diabetes mellitus before HSCT did not differ between the two groups (Tables 1 and 2). Hypomagnesemia also occurs due to urinary Mg excretion, which may result from the use of aminoglycoside antibiotics (20), amphotericin B (21), and foscarnet (22). But again, there was no difference in the duration of aminoglycoside administration between the two groups, and no recipients received amphotericin B or foscarnet within 28 days after HSCT (Table 2).…”

Section: Figurementioning

confidence: 99%