Does vancomycin cause kidney damage?
Vancomycin has been shown have nephrotoxicity, which can lead to acute kidney injury (AKI). This is most likely caused by the drug stopping blood flow and oxygen from reaching the kidneys. Patients are at a higher risk for developing AKI if they have underlying renal function impairment, use other nephrotoxic medications, are elderly, or are dehydrated.
Does Levaquin cause thrombocytopenia?
Thrombocytopenia is found among people who take Levofloxacin, especially for people who are male, 60+ old, have been taking the drug for < 1 month. The phase IV clinical study analyzes which people take Levofloxacin and have Thrombocytopenia.
Can linezolid cause nephrotoxicity?
Can linezolid cause nephrotoxicity? Because of side effects of linezolid, i.e. nephrotoxicity, we recommend close monitoring of kidney function tests when linezolid therapy is attempted. Clinicians should be aware of these potential life- threatening adverse reactions and monitor kidney function while patients are using linezolid.
Can amphotericin B cause nephrotoxicity?
The association of amphotericin B with nephrotoxicity is well known, but risk factors for this complication are not well characterized. One hundred and seventy-eight patients who received > 3 days of intravenous amphotericin B and a minimal total cumulative dose >100 mg were reviewed retrospectively.
Can vancomycin damage the kidneys?
Vancomycin has been shown have nephrotoxicity, which can lead to acute kidney injury (AKI). This is most likely caused by the drug stopping blood flow and oxygen from reaching the kidneys.
Which antibiotic is most nephrotoxic?
Two antibiotics associated with nephrotoxicity that are used to treat dangerous resistant infections are vancomycin and colistin.
Is vancomycin-induced nephrotoxicity reversible?
Although most vancomycin nephrotoxic events are deemed reversible, available data support there is prolonged hospitalization, increased mortality rate and higher incidence of ESKD from AKI of any cause [Prendecki et al. 2016].
Can vancomycin cause a kidney infection?
Results of a small Johns Hopkins Children's Center study show that hospitalized children given high-dose IV infusions of the antibiotic vancomycin to treat drug-resistant bacterial infections face an increased risk for kidney damage — an often reversible but sometimes serious complication.
Which antibiotics are safest for kidneys?
Penicillins are generally well tolerated in patients with kidney disease.
Which antibiotics damage kidneys?
Aminoglycoside antibiotics are known for causing kidney injury—even at low doses. People with chronic kidney disease, dehydration, or those who have been taking these antibiotics for a long time are at particularly high risk. The most toxic aminoglycoside is neomycin, followed by gentamicin, tobramycin, and amikacin.
What are signs of nephrotoxicity?
If severe enough, nephrotoxicity can show signs of other types of decreased kidney function, such as decreased urination, swelling from fluid retention and high blood pressure. In some patients, nephrotoxicity can also affect other body systems such as the liver or the skin and show signs in those areas as well.
What level of vancomycin is toxic?
In patients receiving vancomycin, a greater risk of nephrotoxicity occurs when doses exceed 4 grams per day and trough levels are higher than 15mcg/mL and an AUC above 600 mg-h/L is present.
What are the symptoms of vancomycin toxicity?
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Who should not take vancomycin?
Vancomycin (Vancocin) can cause kidney damage, including kidney failure. Your risk of this is higher if you have or have had kidney problems, if you're over 65 years old, or if you take medications that are tough on the kidneys (NSAIDs, certain blood pressure medications, water pills).
Is vancomycin safe in CKD?
Infectious Diseases Society of America guidelines recommend achieving vancomycin trough levels of 10 to 20 μg/mL. Usage of vancomycin in high dosages especially ≥ 4 g/d has led to an increase in the incidence of vancomycin-induced nephrotoxicity, particularly in patients with chronic kidney disease (CKD).
What are contraindications of vancomycin?
The following conditions are contraindicated with this drug....Conditions:systemic mastocytosis.low levels of a type of white blood cell called neutrophils.hearing loss.kidney disease with likely reduction in kidney function.
Which penicillin is most nephrotoxic?
The most nephrotoxic beta-lactams available for study are cephaloridine, cephaloglycin, and imipenem; panipenem, which is comparably nephrotoxic, is currently available only in Japan.
Which antibiotics cause nephrotoxicity and ototoxicity?
The aminoglycoside antibiotic gentamicin can cause both ototoxicity and nephrotoxicity, the severity of which varies with circadian time of daily treatment.
Is ciprofloxacin nephrotoxic?
Nephrotoxic reactions to ciprofloxacin appear to be unusual but potentially serious. It has previously been reported that fluoroquinolones could cause acute renal failure (ARF) after the ingestion of large quantities, but it is now recognized that therapeutic doses of fluoroquinolones can also cause renal injury.
Are cephalosporins nephrotoxic?
All cephalosporins are thought to be potentially nephrotoxic at high doses, and the usual site of damage is the renal tubule. Interstitial nephritis would appear to be much less common. The pathogenesis of nephrotoxicity is therefore thought to be directly dose-related rather than due to hypersensitivity.
What are the risk factors for nephrotoxicity?
Risk factors for nephrotoxicity are enumerated, including the potential synergistic nephrotoxicity of vancomycin and piperacillin-tazobactam. Suggestions for clinical practice and future research are given.
Is vancomycin nephrotoxic?
The Nephrotoxicity of Vancomycin. Vancomycin use is often associated with nephrotoxicity. It remains uncertain, however, to what extent vancomycin is directly responsible, as numerous potential risk factors for acute kidney injury frequently coexist.
Why is vancomycin used in intensive care?
Larger doses of vancomycin are often required in patients in intensive care unit because the offending pathogens are less susceptible to the antibiotic. There is multiplefold greater MIC compared with the noncritically ill controls [Roberts et al. 2014]. In addition, apart from renal hypoperfusion in these patients, altered volume of distribution of vancomycin, a hydrophilic compound, aggravates susceptibility to renal injury [Roberts et al. 2014; Bagshaw et al. 2008]. In severe sepsis, increase in the volume of distribution ultimately results from widespread endothelial injury and excess administration of resuscitative fluids. Furthermore, as evident in animal experiments, endotoxemia per seincreases the intrarenal distribution of vancomycin while there is a reduction in its elimination kinetics [Ngeleka et al. 1989]. Finally, due to the variability of pharmacokinetic parameters and the greater susceptibility to renal injury, therapeutic drug monitoring has been recommended in critically ill patients [Roberts et al. 2011].
What is the clinical issue encountered in patients with end stage kidney disease?
The clinical issue encountered in patients with end-stage kidney disease (ESKD) is different. It is principally driven by the common use of a central line for vascular access. Seventy-seven percent of these patients had sepsis compared with 23% recorded for those dialyzed with either arteriovenous fistulas or grafts [Decker et al. 2010]. Case fatality rate from septicemia is quite high, about 20%. This is partly because MRSA accounts for more than 40% of the bacterial infection in this population [Klevens et al. 2008]. Given its common use as empirical treatment, there are reports of resistant pathogens: Vancomycin resistant enterococcus (VRE), Vancomycin intermediate staphylococcus aureus (VISA) and Vancomycin resistant staphylococcus aureus (VRSA) in the dialysis population [Pai and Pai, 2006; Fridkin, 2001; Centers for Disease Control and Prevention, 2002]. Hence a diligent dosing regimen of vancomycin is important to avoid compromise of the residual renal function. A fixed loading dose (1 g of intravenous vancomycin) given at the end of initial HD, and 0.5–1 g maintenance dose after subsequent dialysis provides adequate pre-HD drug level in 96% of patients (5–20 ug/ml) [Decker et al. 2010]. Other studies have found a relative advantage with a weight-based calculation of the loading doses [Brown et al. 2011]. This may be facilitated by the use of a preprogramed dose calculator [Vandecasteele et al. 2011].
Is vancomycin nephrotoxic?
Although most vancomycin nephrotoxic events are deemed reversible, available data support there is prolonged hospital ization, increased mortality rate and higher incidence of ESKD from AKI of any cause [Prendecki et al. 2016]. For this reason, awareness of these complications particularly in critically ill patients may allow prompt intervention. Customized dosing of vancomycin on the basis of patient characteristics, baseline creatinine clearance, pattern of microbial resistance, MIC of the pathogen involved, and specific population pharmacokinetics may be advantageous [Roberts et al. 2014]. However, there is need for comprehensive studies on the decision-making process for customized vancomycin dose adjustment on the basis of these parameters [van Hal et al. 2013].
Does vancomycin increase blood volume?
Due to increases in both adipose tissue and skeletal muscle mass, there is a greater volume of distribution of vancomycin in patients with obesity compared with the healthy controls [Grace, 2012]. In addition, the increase in blood volume and cardiac output results in augmented renal delivery. Studies have examined the impact of greater drug exposure imposed by the use of unadjusted body weight to calculate the dose of vancomycin in patients with obesity [Davies et al. 2015; Matson et al. 2015]. Apparently influenced by the retrospective design, the results of such studies are inconsistent. Few studies showed higher vancomycin trough concentration in the absence of weight adjustment but most data found no difference in comparison with the controls [Heble et al. 2013; Le et al. 2015; Eiland and Sonawane, 2014]. Because sample sizes of the studies are often small, there may be a lack of adequate power to detect a significant difference. In addition, study outcome may reflect the imperfection of body mass index (deduced from height and weight) in the determination of adiposity. In a retrospective study of 530 patients stratified by body mass index (>30 kg/m2), APACHE II score greater than 21 was the only variable associated with nephrotoxicity in a regression analysis [Davies et al. 2015]. There was no significant relationship between obesity and a higher risk of nephrotoxicity [Davies et al. 2015; Matson et al. 2015]. However, a different outcome was obtained in another study: there was fivefold greater likelihood of attaining a serum vancomycin greater than 20 mg/l in patients with exogenous obesity [Richardson et al. 2015].
Does vancomycin cause kidney damage?
Although there is a low rate of renal toxicity with modest doses, vancomycin reduces the threshold for kidney injury while using other agents with potential nephrotoxicity. Such synergism has been observed with the combination of vancomycin and piperacillin–tazobactam [Burgess and Drew, 2014]. In a retrospective cohort, 8% of 99 adults treated with vancomycin had AKI while combination with piperacillin–tazobactam accounted for 16.3%. Similarly, there is a threefold greater occurrence of AKI when this combination was compared with the controls who were treated with a concurrent cefepime [Gomes et al. 2014]. Furthermore, in a pediatric study, concurrent use of vancomycin with acyclovir, amphotericin B and piperacillin–tazobactam significantly increased the risk of AKI respectively [Knoderer et al. 2015]. A major limitation of retrospective data is the uncertainty of the adverse renal impact while using other agents that were not part of the study. However, a similar pattern of results was realized in a prospective trial of 168 patients that compared three therapeutic modalities: AKI occurred in 5% of those treated with vancomycin, 22% of those who had vancomycin and aminoglycoside, and 11% of those treated with gentamicin only [Rybak et al. 1990].
Does vancomycin cause AKI?
Furthermore, in a study by Lodise and colleagues, a daily dose of vancomycin in excess of 4 g increases the likelihood of AKI by more than threefold [Lod ise et al. 2008 ]. Perhaps demonstrating the strength of the dose–toxicity relationship, there are several case reports of inadvertent use of a supranormal dose of vancomycin that led to severe AKI [Stidham et al. 2011; Barraclough et al. 2007; Wicklow et al. 2006]. In such events, the water solubility and the low protein binding of vancomycin facilitate its rapid removal by acute hemodialysis (HD) procedures. The author has two anecdotal experiences of teenage surgical patients with normal underlying renal function who were inadvertently given high doses of vancomycin that led to plasma trough levels of 54 and 115 mg/l respectively (not published). The former also received a nonsteroidal anti-inflammatory agent for analgesia. In both cases, due to the severity of azotemia, discontinuation of vancomycin and prompt institution of daily HD sessions led to restoration of serum creatinine to the normal baseline values.
Is vancomycin a rash?
Apparently due to a rising frequency of use, vancomycin is increasingly recognized as a major etiological factor in Drug Rash with Eos inophilia and Systemic Symptoms (DRESS syndrome), a distinct but severe hypersensitivity reaction. Characteristic features include skin rash, fever, eosinophilia, atypical lymphocytes, lymphadenopathy and visceral involvement [Zuliani et al. 2005]. As part of the visceral components, acute interstitial nephritis occurs in about 10%. In a review of inpatient consultation at a Boston tertiary hospital over an 18-month period, six patients fulfilled the clinical criteria for DRESS syndrome [Blumenthal et al. 2012]. Eighty-three percent of these events were attributed to vancomycin, and there was elevated human herpesvirus 6 immunoglobulin G titer in 60% of the patients. Outcome is favorable with prompt withdrawal of the offending drugs and early institution of steroids but case fatality rate was close to 10% [Zuliani et al. 2005].
Why is vancomycin used in intensive care?
Larger doses of vancomycin are often required in patients in intensive care unit because the offending pathogens are less susceptible to the antibiotic. There is multiplefold greater MIC compared with the noncritically ill controls [ Roberts et al. 2014 ]. In addition, apart from renal hypoperfusion in these patients, altered volume of distribution of vancomycin, a hydrophilic compound, aggravates susceptibility to renal injury [ Roberts et al. 2014; Bagshaw et al. 2008 ]. In severe sepsis, increase in the volume of distribution ultimately results from widespread endothelial injury and excess administration of resuscitative fluids. Furthermore, as evident in animal experiments, endotoxemia per se increases the intrarenal distribution of vancomycin while there is a reduction in its elimination kinetics [ Ngeleka et al. 1989 ]. Finally, due to the variability of pharmacokinetic parameters and the greater susceptibility to renal injury, therapeutic drug monitoring has been recommended in critically ill patients [ Roberts et al. 2011 ].
What is the AUC of vancomycin?
Recent studies on vancomycin-related AKI frequently suggest that increase in the total amount of drug exposure as measured by plasma trough concentration; area under the curve (AUC) or duration of treatment is the principal determinant of nephrotoxicity. Other risk factors are pre-existing renal impairment, concurrent administration of nephrotoxic agents and its use in high-risk populations including those with obesity, and in the treatment of deep visceral infections.
What is the clinical issue encountered in patients with end stage kidney disease?
The clinical issue encountered in patients with end-stage kidney disease (ESKD) is different. It is principally driven by the common use of a central line for vascular access. Seventy-seven percent of these patients had sepsis compared with 23% recorded for those dialyzed with either arteriovenous fistulas or grafts [ Decker et al. 2010 ]. Case fatality rate from septicemia is quite high, about 20%. This is partly because MRSA accounts for more than 40% of the bacterial infection in this population [ Klevens et al. 2008 ]. Given its common use as empirical treatment, there are reports of resistant pathogens: Vancomycin resistant enterococcus (VRE), Vancomycin intermediate staphylococcus aureus (VISA) and Vancomycin resistant staphylococcus aureus (VRSA) in the dialysis population [ Pai and Pai, 2006; Fridkin, 2001; Centers for Disease Control and Prevention, 2002 ]. Hence a diligent dosing regimen of vancomycin is important to avoid compromise of the residual renal function. A fixed loading dose (1 g of intravenous vancomycin) given at the end of initial HD, and 0.5–1 g maintenance dose after subsequent dialysis provides adequate pre-HD drug level in 96% of patients (5–20 ug/ml) [ Decker et al. 2010 ]. Other studies have found a relative advantage with a weight-based calculation of the loading doses [ Brown et al. 2011 ]. This may be facilitated by the use of a preprogramed dose calculator [ Vandecasteele et al. 2011 ].
Does vancomycin increase blood volume?
Due to increases in both adipose tissue and skeletal muscle mass, there is a greater volume of distribution of vancomycin in patients with obesity compared with the healthy controls [ Grace, 2012 ]. In addition, the increase in blood volume and cardiac output results in augmented renal delivery. Studies have examined the impact of greater drug exposure imposed by the use of unadjusted body weight to calculate the dose of vancomycin in patients with obesity [ Davies et al. 2015; Matson et al. 2015 ]. Apparently influenced by the retrospective design, the results of such studies are inconsistent. Few studies showed higher vancomycin trough concentration in the absence of weight adjustment but most data found no difference in comparison with the controls [ Heble et al. 2013; Le et al. 2015; Eiland and Sonawane, 2014 ]. Because sample sizes of the studies are often small, there may be a lack of adequate power to detect a significant difference. In addition, study outcome may reflect the imperfection of body mass index (deduced from height and weight) in the determination of adiposity. In a retrospective study of 530 patients stratified by body mass index (>30 kg/m 2 ), APACHE II score greater than 21 was the only variable associated with nephrotoxicity in a regression analysis [ Davies et al. 2015 ]. There was no significant relationship between obesity and a higher risk of nephrotoxicity [ Davies et al. 2015; Matson et al. 2015 ]. However, a different outcome was obtained in another study: there was fivefold greater likelihood of attaining a serum vancomycin greater than 20 mg/l in patients with exogenous obesity [ Richardson et al. 2015 ].
Does vancomycin cause kidney damage?
Although there is a low rate of renal toxicity with modest doses, vancomycin reduces the threshold for kidney injury while using other agents with potential nephrotoxicity. Such synergism has been observed with the combination of vancomycin and piperacillin–tazobactam [ Burgess and Drew, 2014 ]. In a retrospective cohort, 8% of 99 adults treated with vancomycin had AKI while combination with piperacillin–tazobactam accounted for 16.3%. Similarly, there is a threefold greater occurrence of AKI when this combination was compared with the controls who were treated with a concurrent cefepime [ Gomes et al. 2014 ]. Furthermore, in a pediatric study, concurrent use of vancomycin with acyclovir, amphotericin B and piperacillin–tazobactam significantly increased the risk of AKI respectively [ Knoderer et al. 2015 ]. A major limitation of retrospective data is the uncertainty of the adverse renal impact while using other agents that were not part of the study. However, a similar pattern of results was realized in a prospective trial of 168 patients that compared three therapeutic modalities: AKI occurred in 5% of those treated with vancomycin, 22% of those who had vancomycin and aminoglycoside, and 11% of those treated with gentamicin only [ Rybak et al. 1990 ].
Is vancomycin trough level associated with AKI?
The major shortcoming of these studies is the inability to deduce if there is causal association given that data on trough level of vancomycin were obtained in parallel with the incidence of AKI. However, these findings were corroborated by studies in which trough concentration was measured prior to the estimation of serum creatinine [ Cano et al. 2012; van Hal et al. 2013 ]. After accounting for the temporal effect, the incidence of AKI was 21–28% in patients with other risk profiles compared with 7% in those lacking additional renal risk [ Wong-Beringer et al. 2011 ]. In two similar studies corrected for this variable, the odds ratio for AKI among patients with vancomycin trough level at least 15 mg/l was 3.1 and 5.0 respectively [ Cano et al. 2012; van Hal et al. 2013 ].
Does vancomycin cause AKI?
Furthermore, in a study by Lodise and colleagues, a daily dose of vancomycin in excess of 4 g increases the likelihood of AKI by more than threefold [ Lodise et al. 2008 ]. Perhaps demonstrating the strength of the dose–toxicity relationship, there are several case reports of inadvertent use of a supranormal dose of vancomycin that led to severe AKI [ Stidham et al. 2011; Barraclough et al. 2007; Wicklow et al. 2006 ]. In such events, the water solubility and the low protein binding of vancomycin facilitate its rapid removal by acute hemodialysis (HD) procedures. The author has two anecdotal experiences of teenage surgical patients with normal underlying renal function who were inadvertently given high doses of vancomycin that led to plasma trough levels of 54 and 115 mg/l respectively (not published). The former also received a nonsteroidal anti-inflammatory agent for analgesia. In both cases, due to the severity of azotemia, discontinuation of vancomycin and prompt institution of daily HD sessions led to restoration of serum creatinine to the normal baseline values.
What are the side effects of vancomycin?
Check with your doctor immediately if any of the following side effects occur while taking vancomycin: More common. Bladder pain. bloating or swelling of the face, arms, hands, lower legs, or feet. bloody or cloudy urine. decreased urine.
Does vancomycin need immediate medical attention?
Side effects not requiring immediate medical attention. Some side effects of vancomycin may occur that usually do not need medical attention. These side effects may go away during treatment as your body adjusts to the medicine.
Is vancomycin nephrotoxic?
Vancomycin is a glycopeptide antibiotic excreted by the kidney and has been used extensively, especially for methicillin-resistant staphylococcus aureus (MRSA) and for many strains of pathogenic staphylococcus epidermis. The nephrotoxic potential of vancomycin is neither fully appreciated nor well characterized. Previously, most reports of acute kidney injury (AKI) associated with vancomycin had blamed the acute renal failure (ARF) on early, relatively impure formulations of vancomycin (impurities popularly known as Mississippi mud). This conventional belief and the ensuing ambiguity if not controversy in the literature about its nephrotoxic potential have led to common notion that it is rather innocuous. Its popularity as an inexpensive and effective anti-staph medication and its widespread use had contributed to the increased incidence of AKI. But the impurity theory no longer holds because the modern purified preparations are devoid of additives.
Is vancomycin a cause and effect?
The issue of Van-AKI has been controversial due to the difficulty in establishing a cause-and-effect relationship between vancomycin and the alleged ARF. This is true among the affected patients reported in large epidemiologic surveys or drug toxicity monitoring studies because they generally provide little details on individual patients for an objective review or independent determination (Table 1). Similarly, among the two dozen or so reported cases of Van-AKI (Table 2), fewer than 10 had unequivocally excluded the usual confounding variables like sepsis, bacteremia, hemodynamic factors and concurrent nephrotoxins. Many also failed to provide serial vancomycin levels to show the temporal evolution with the ARF. Thus, to date, the existence of Van-AKI has been intensely debated and at times categorically dismissed. Our first objective was to more firmly establish this clinical entity by performing a vigorous and comprehensive review of the existing literature and by reporting our own experience. We have obtained and presented three lines of evidence to argue for the entity of Van-AKI. First, the drug toxicity monitoring studies in the aggregate have offered a substantial body of indirect evidence to support the existence of Van-AKI, mainly based on the close correlations between increased blood levels and/or increased dosage on the one hand and increased incidence on the other hand (Rybak et al, 2009) (Table 1). Typically, there was observed a very low incidence of Van-AKI with low trough vancomycin levels like < 10 mg/L (Sorrel et al, 1985), but increased incidence with higher trough levels like >14 (Pritchard et al, 2008) or >15-20 mg/L (Hidayat et al, 2006), or with
What are the side effects of vancomycin?
Nausea, abdominal pain, vomiting, diarrhea, flatulence, and low potassium levels are the most common side effects associated with vancomycin capsules. Edema, back pain, urinary tract infection, and a headache may also occur .
What medications interact with vancomycin?
Common medications that may interact with vancomycin include: amikacin. aminoglycosides, such as gentamicin or tobramycin. bile acid sequestrants, such as colestipol or cholestyramine. lactobacillus. NSAIDs such as ibuprofen, diclofenac, or naproxen. piperacillin. sirolimus or tacrolimus. sodium picosulfate.
How long does vancomycin last?
The usual duration of therapy is seven to ten days. 7. Interactions. Medicines that interact with vancomycin may either decrease its effect, affect how long it works for, increase side effects, or have less of an effect when taken with vancomycin.
What class of antibiotics is vancomycin?
Vancomycin belongs to the class of medicines known as glycopeptide antibiotics.
Is vancomycin absorbed into the bloodstream?
difficile -associated diarrhea or enterocolitis when given orally, or other severe infections when given intravenously (IV). Oral dosages are not typically absorb ed into the bloodstream; however, people with inflammatory diseases of the colon may be at risk. Higher dosages and IV use of vancomycin increase the risk of ear and kidney side effects.
Can you take vancomycin for diarrhea?
difficile -associated diarrhea or enterocolitis, take it exactly as directed by your doctor and finish the course. Do not use vancomycin capsules to treat any other type of infection.
Can vancomycin cause red man syndrome?
Rarely, "Red Man Syndrome" has been associated with vancomycin IV.
