gfhletters-20.7. 1509..1521

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Feb 12, 2016 - Rene´ Mellat, Chalma Badouraly and Linda Delbreil, for their great expertise in all technical aspects of ... Albert Bensman. 75571 Paris Cedex 12. France. Email: [email protected]. 1. Miner LJ, Faix RG. Large vancomycin ...
Nephrol Dial Transplant (2005) 20: 1517

Department of Nephrology and Marc Decupere Renal Transplantation Vanessa Ooms University Hospitals Raymond Oyen Leuven Dirk R. J. Kuypers Belgium Kathleen Claes Email: [email protected] 1. Doorenbos CJ, Ozyilmaz A, van Wijnen M. Severe pseudohypocalcemia after gadolinium-enhanced magnetic resonance angiography. N Engl J Med 2003; 349: 817–818 2. Prince MR. More on pseudohypocalemia and gadoliniumenhanced MRI. N Engl J Med 2004; 350: 87–88 3. Emerson J, Kost G. Spurious hypocalcemia after Omnisanor OptiMARK-enhanced magnetic resonance imaging. Arch Pathol Lab Med 2004; 128: 1151–1156 4. Prince MR, Erel HE, Lent RW et al. Gadodiamide administration causes spurious hypocalcemia. Radiology 2003; 227: 639–646 doi:10.1093/ndt/gfh902

Advance Access publication 10 May 2005

Large-pore haemodialysis membranes: an efficient tool for rapid removal of vancomycin after accidental overdose Sir, The usual dosage of vancomycin is 40–60 mg/kg per day divided into four 1 h infusions. Its elimination is mainly renal. An overdose can be responsible for severe ototoxicity and nephrotoxicity, especially if combined with other nephrotoxic drugs such as aminoglycoside antibiotics. As long as renal

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Fig. 1. Time course of serum creatinine (closed circles) and vancomycin levels (closed triangles) in relation to vancomycin overdose (260 mg/kg per day) over 9 days (grey arrows) and haemodialysis sessions (black arrows) using a high-flux large pore size haemodialysis membrane.

function remains normal, vancomycin plasma t1/2 is 4–6 h, suggesting forced diuresis alone to reduce drug serum levels rapidly [1]. Renal failure provoked by a vancomycin overdose is responsible for an increase in plasma t1/2 suggesting the necessity of efficient extracorporal drug removal. Standard haemodialysis with cuprophane and cellulose acetate membranes has a limited capacity to remove substances larger than 500 Da. As vancomycin has a molecular weight of 1500 Da it is only marginally removed by standard HD or peritoneal dialysis [2], whereas continuous haemodiafiltration [3], charcoal haemoperfusion [4] and haemodialysis with high flux polysulfone membranes [5] have been shown to clear vancomycin successfully from the circulation. The patient, a 9-year-old girl (17 kg, 90 cm), was suffering from cystic fibrosis (homozygous F508del mutation) with chronic airway obstruction and multiple infectious episodes. She accidentally received toxic doses of vancomycin (260 mg/kg/day in four daily doses) over 9 days and usual doses of gentamycin (3 mg/kg/day) in an outside hospital. No controls of vancomycin and gentamycin serum levels were performed until the ninth day. The girl developed progressive malaise and acute generalized exanthematous pustulosis (AGEP) associated with fever of 38 C. On day 10 the vancomycin serum level was 420 mg/l and antibiotic treatment was interrupted. She developed non-oliguric renal failure. Serum creatinine increased to 650 mmol/l and BUN to 42.6 mmol/l 8 days after discontinuation of vancomycin (Figure 1), whereas serum potassium, phosphorus and calcium levels remained in the normal range. She was then transferred to our hospital. On arrival she presented with weight loss of 2 kg, severe anorexia and irritability. The vancomycin serum level was 96 mg/l (calculated t1/2 ¼ 216 h). She had normal blood pressure and a constant diuresis without volume overload. Vascular access was obtained via a femoral 9.0-Fr MedComp dual lumen catheter. A Gambro AK-100 haemodialysis machine was used with a high flux large pore-size polymethylmethacrylate dialysis membrane (BK-F 1.3; Toray, Tokyo, Japan) and paediatric lines giving an extracorporal volume of 150 ml. The filter was prepared using NaCl 0.9% containing heparin 1000 UI/l. Low molecular weight heparin (1 mg/kg) was administered at the onset of haemodialysis. Blood flow was 6 ml/kg per min (100 ml/min); duration of treatment was 4 h using standard dialysis baths. Ultrafiltration was 1000 ml/h compensated by a continuous infusion of NaCl 0.9% at 1000 ml/h.

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Conflict of interest statement. None declared.

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normal ionized calcium level and the absence of symptoms, it was concluded that this had to be a laboratory error. Gadolinium-related spurious hypocalcaemia in colorimetric assays, such as the Arsenazo Dye III and OCP assays, is caused by binding of gadolinium ions to the colorimetric agent, removing the gadolinium from the chelate [3]. The free chelate then binds to serum calcium thereby causing it to be falsely low. The administration of gadodiamide or gadoversetamide in higher doses, in particular when given to patients with chronic renal insufficiency, increases measurement inaccuracy and prolongs the duration of artifactual hypocalcaemia [4]. Since the use of colorimetric assays to determine total calcium levels is widespread, this laboratory ‘artifact’ is a potentially dangerous cause of unnecessary and possibly harmful medical interventions. Due to the nature of their illness, patients with renal disease face the double risk of being injected with higher doses of contrast agent (i.e. for vascular MRI) while being least able to excrete it. Based on our own experience, we feel that, certainly among clinicians, this cause of spurious hypocalcaemia is still largely unknown. We suggest drawing the attention of clinicians and radiologists to the potential interference of gadodiamide with total calcium measurement, especially when high drug doses are used, or when it is administered to patients with impaired renal function.

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Acknowledgements. We are grateful to all members of our paediatric haemodialysis team, in particular Nathalie Bouvet, MarieRene´ Mellat, Chalma Badouraly and Linda Delbreil, for their great expertise in all technical aspects of paediatric haemodialysis. Conflict of interest statement. None declared.

Department of Pediatric Nephrology Hoˆpital Trousseau 26, avenue du Docteur Arnold-Netter 75571 Paris Cedex 12 France Email: [email protected]

Tim Ulinski Georges Descheˆnes Albert Bensman

1. Miner LJ, Faix RG. Large vancomycin overdose in two premature infants with minimal toxicity. Am J Perinatol 2004; 21: 433–438 2. Pai AB, Pai MP. Vancomycin dosing in high flux hemodialysis: a limited-sampling algorithm. Am J Health Syst Pharm 2004; 61: 1812–1816

3. Akil IO, Mir S. Hemodiafiltration for vancomycin overdose in a patient with end-stage renal failure. Pediatr Nephrol 2001; 16: 1019–1021 4. Panzarino VM, Feldstein TJ, Kashtan CE. Charcoal hemoperfusion in a child with vancomycin overdose and chronic renal failure. Pediatr Nephrol 1998; 12: 63–64 5. Bunchman TE, Valentini RP, Gardner J et al. Treatment of vancomycin overdose using high-efficiency dialysis membranes. Pediatr Nephrol 1999; 13: 773–774 doi:10.1093/ndt/gfh900

Renal failure following bowel cleansing with a sodium phosphate purgative Sir, VisicolÕ Tablets (InKine Pharmaceutical Co., Inc.) have been used in >1.2 million patients as a bowel preparation for colonoscopy. To date, InKine Pharmaceuticals has received one report of nephrocalcinosis following use of VisicolÕ . This case was described by Markowitz et al. in the April 2005 issue of the journal along with 15 cases associated with the use of oral sodium phosphate solution (OSPS, FleetÕ PhosphoÕ -Soda, C.B. Fleet). Data reported to InKine indicate that this patient had at least three important risk factors for the development of acute renal failure (ARF) and nephrocalcinosis. First, the patient had a history of renal insufficiency with a rising creatinine (1.7 mg/dl) and had been on meloxicam (MobicÕ , Boehringer Ingelheim) for years. This was discontinued just prior to colonoscopy, but was restarted within 1 month for shoulder pain. VisicolÕ should be used with caution in patients with impaired renal function since they may have difficulty excreting large phosphate loads. It should be noted that the post-colonoscopy creatinine level was much smaller in this patient (2.6 mg/dl 2 months postcolonoscopy) than in the patients receiving OSPS (mean of 4.9 mg/dl 3 days to 2 months post-colonoscopy). It is unknown how much the meloxicam may have contributed to the rising creatinine. In January 2005, the patient’s creatinine was 2.2 mg/dl. Secondly, since 2002, the patient was taking 10 mg of ramipril (AltaceÕ , Monarch Pharmaceutical), an angiotensinconverting enzyme inhibitor (ACEI), which is twice the recommended daily dose for patients with renal insufficiency. Because ACEIs limit the kidneys’ normal capacity to compensate for the stress of volume depletion, patients on these drugs can experience a decrease in glomerular filtration rate and possible renal failure when in a volume-depleted state, e.g. following the use of a purgative. Thirdly, this 44-year-old patient presented with a 1 week history of abdominal pain, bloody stools and no relevant family history. The patient underwent colonoscopy within 2 days of presentation. A diagnosis of acute and chronic colitis was made. Patients with acute colitis are at risk for excess phosphate absorption [1]. Since patients who take a purgative experience diarrhoea and in some cases vomiting, every patient is at risk for developing dehydration and hypovolaemia, which can result in renal failure. Physicians should assess patients’ hydration status prior to beginning any bowel purgative. In this case, there was no information provided on the hydration status of the patient although the patient was prescribed a 3 day bowel preparation regimen consisting

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The post-run vancomycin level was 26 mg/l demonstrating a 73% intravascular vancomycin removal (calculated vancomycin t1/2 ¼ 2.0 h), BUN was 13 mmol/l and serum creatinine 205 mmol/l. A second haemodialysis session was initiated 24 h later resulting in a vancomycin plasma level of 12 mg/l after 2 h (t1/2 ¼ 1.8 h). The skin lesions disappeared progressively. Renal function recovered rapidly 3 days after admission and the patient left the hospital in a good general condition 7 days after discontinuation of haemodialysis with a serum creatinine of 80 mmol/l. One month later serum creatinine was 40 mmol/l, proteinuria was negative and blood pressure was normal. This case demonstrates efficient removal of vancomycin using a high-flux, large pore size haemodialysis membrane (cut off 70 000 Da). Despite the relatively high extracorporal volume (150 ml), no blood priming was necessary and haemodialysis was well tolerated. Once renal function decreased, vancomycin plasma t1/2 increases and resulted in an asymptotic kinetic of drug plasma levels (Figure 1). Earlier reports discuss the benefits of charcoal haemoperfusion or haemodialysis with high efficiency membranes in the treatment of vancomycin overdose. Both methods have been shown to remove vancomycin efficiently. However, charcoal haemoperfusion exposes to the potential risk of excessive calcium and phosphate removal, hypothermia or thrombocytopaenia. In order to avoid such electrolyte disturbances, a haemodialysis filter is placed in line after the charcoal circuit. In order to obtain an efficient toxine clearance, charcoal haemoperfusion requires high blood flow rates. This may cause difficulties concerning the prevention of the above-mentioned potential risks, which are aggravated by higher blood flow. Direct comparison of continuous haemofiltration, charcoal haemoperfusion and haemodialysis with either high efficiency or high flux membranes is not possible because the efficiency of each technique depends on multiple variables such as blood/dialysate flow rates, age of patients and the exact type of haemodialysis filter. The choice of technique should take into consideration the availability and experience in the medical centre as well as the patient’s age. In conclusion, haemodialysis with high-flux, large pore size membranes should be considered rapidly in patients with toxic vancomycin serum levels and concomitant or pre-existing renal failure.