Bendamustine induced tumor lysis syndrome with acute renal failure in chronic lymphocytic leukemia

2014 ◽  
Vol 51 (3) ◽  
pp. 380 ◽  
Author(s):  
R Naithani ◽  
A Bhat ◽  
A Bhasin
PEDIATRICS ◽  
1990 ◽  
Vol 85 (5) ◽  
pp. 819-823
Author(s):  
Nancy A. Bishof ◽  
Thomas R. Welch ◽  
C. Frederic Strife ◽  
Frederick C. Ryckman

Continuous arteriovenous hemofiltration is a form of renal replacement therapy whereby small molecular weight solutes and water are removed from the blood via convection, alleviating fluid overload and, to a degree, azotemia. It has been used in many adults and several children. However, in patients with multisystem organ dysfunction and acute renal failure, continuous arteriovenous hemofiltration alone may not be sufficient for control of azotemia; intermittent hemodialysis or peritoneal dialysis may be undesirable in such unstable patients. Recently, the technique of continuous arteriovenous hemodiafiltration has been used in many severely ill adults. We have used continuous arteriovenous hemodiafiltration in four patients at Children's Hospital Medical Center. Patient 1 suffered perinatal asphyxia and oliguria while on extracorporeal membrane oxygenation. Patients 2 and 4 both had Burkitt lymphoma and tumor lysis syndrome. Patient 3 had septic shock several months after a bone marrow transplant. All had acute renal failure and contraindications to hemodialysis or peritoneal dialysis. A blood pump was used in three of the four patients, while spontaneous arterial flow was adequate in one. Continuous arteriovenous hemodiafiltration was performed for varying lengths of time, from 11 hours to 7 days. No patient had worsening of cardiovascular status or required increased pressor support during continuous arteriovenous hemodiafiltration. The two survivors (patients 2 and 4) eventually recovered normal renal function. Continuous arteriovenous hemodiafiltration is a safe and effective means of renal replacement therapy in the critically ill child. It may be ideal for control of the metabolic and electrolyte abnormalities of the tumor lysis syndrome.


2007 ◽  
Vol 25 (31) ◽  
pp. 5047-5047 ◽  
Author(s):  
Laure A. Moutouh-de Parseval ◽  
Lilia Weiss ◽  
Robert J. DeLap ◽  
Robert D. Knight ◽  
Jerome B. Zeldis

1998 ◽  
Vol 16 (7) ◽  
pp. 2313-2320 ◽  
Author(s):  
B D Cheson ◽  
J N Frame ◽  
D Vena ◽  
N Quashu ◽  
J M Sorensen

PURPOSE To quantify the incidence and severity of tumor lysis syndrome (TLS) as a consequence of fludarabine therapy in patients with advanced chronic lymphocytic leukemia (CLL). PATIENTS AND METHODS A retrospective review and questionnaire follow-up of clinical and laboratory data were performed on patients with intermediate or high-risk CLL on the National Cancer Institute Group C protocol or special exception mechanisms, or phase II trials of fludarabine, for whom adverse drug reports of TLS were available. Fludarabine was administered at a dose of 20 to 40 mg/m2 per day for 5 days at monthly intervals. RESULTS Among the 6,137 patients, TLS was suspected in 26 (0.42%), with clinical and laboratory features consistent with TLS present in 20 (0.33%). Prophylaxis against TLS had been administered to 60% of these patients. Clinical or laboratory features were similar to patients who did not develop TLS. Of the patients with TLS, 90% had high-risk CLL, 60 months of prior disease duration, with a median pretreatment WBC of 109 x 10(9)/L, two prior regimens, lymphadenopathy in 89%, splenomegaly and/or hepatomegaly in 90%. TLS developed on approximately day 7 and lasted a median of 9.5 days. Dialysis was required in 30% during the TLS episode; 20% of patients died during cycle one of fludarabine therapy with renal failure, and another 20% died of infection or congestive heart failure. Six patients were retreated with fludarabine without recurrent TLS. CONCLUSION TLS after fludarabine therapy is extremely uncommon, but may be associated with significant morbidity and mortality.


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