Marie Lemerle1, Aline Schmidt2,3,4, Valérie Thepot-Seegers5, Achille Kouatchet6, Valérie Moal7, Melina Raimbault8, Corentin Orvain2,3,4, Jean-François Augusto1, Julien Demiselle9,10. 1. Service de Néphrologie, Dialyse, Transplantation, CHU Angers, Angers, France. 2. Service des Maladies du sang, CHU Angers, Angers, France. 3. Fédération Hospitalo-Universitaire Grand-Ouest Acute Leukemia, FHU-GOAL, Angers, France. 4. CRCINA, INSERM U1232, Université de Nantes, Université d'Angers, Angers, France. 5. Service de Biométrie, Institut de Cancérologie de l'Ouest, Centre Paul Papin, Angers, France. 6. Service de Médecine Intensive Réanimation, Médecine Hyperbare, CHU Angers, Angers, France. 7. Département de Biochimie, CHU Angers, Angers, France. 8. Département de Pharmacie, CHU Angers, Angers, France. 9. Service de Médecine Intensive Réanimation, Nouvel Hôpital Civil, CHU Strasbourg, 1 place de l'hôpital, 67 091, Strasbourg Cedex, France. julien.demiselle@chru-strasbourg.fr. 10. INSERM UMR 1260, Regenerative Nanomedecine (RNM), FMTS, Strasbourg, France. julien.demiselle@chru-strasbourg.fr.
Abstract
INTRODUCTION: Acute kidney injury (AKI) is a major cause of mortality in tumor lysis syndrome. The biochemical parameters and kinetics of tumor lysis syndrome remain poorly described. Particularly, whether blood serum phosphate variations may help in the identification and management of patients who will eventually develop AKI remains to be studied. METHODS: In this retrospective study, we included patients with tumor lysis syndrome episodes without AKI at diagnosis, and analyzed serum phosphate kinetic, clinical and tumor lysis syndrome biochemical variables to identify factors associated with AKI onset, and determine threshold values of phosphatemia associated with AKI development. RESULTS: One hundred thirty tumor lysis syndrome episodes occurred in 120 patients during an 11-year period at the University Hospital of Angers. AKI developed in 56 tumor lysis syndrome episodes. In multivariable analysis, among the analyzed factors, only an increase in serum phosphate levels (before AKI diagnosis), exposure to platinum salts and an increase in LDH levels were associated with AKI development. Before AKI onset, a serum phosphate cut-off of 2.1 mmol/L was not effective in predicting AKI development (sensitivity 48%, specificity 84%, area under the receiver operating characteristic curve (AUC) 0.63 [0.52-0.74]). No other biochemical parameters were effective to better predict AKI occurrence. CONCLUSION: This work suggests that increases in serum phosphate and LDH appear to be early and reliable biomarkers of AKI in tumor lysis syndrome. No valuable threshold value of serum phosphate was found to effectively predict AKI. This work is the basis for further prospective controlled studies on phosphate monitoring and phosphate lowering therapies to prevent AKI during tumor lysis syndrome.
INTRODUCTION: Acute kidney injury (AKI) is a major cause of mortality in tumor lysis syndrome. The biochemical parameters and kinetics of tumor lysis syndrome remain poorly described. Particularly, whether blood serum phosphate variations may help in the identification and management of patients who will eventually develop AKI remains to be studied. METHODS: In this retrospective study, we included patients with tumor lysis syndrome episodes without AKI at diagnosis, and analyzed serum phosphate kinetic, clinical and tumor lysis syndrome biochemical variables to identify factors associated with AKI onset, and determine threshold values of phosphatemia associated with AKI development. RESULTS: One hundred thirty tumor lysis syndrome episodes occurred in 120 patients during an 11-year period at the University Hospital of Angers. AKI developed in 56 tumor lysis syndrome episodes. In multivariable analysis, among the analyzed factors, only an increase in serum phosphate levels (before AKI diagnosis), exposure to platinum salts and an increase in LDH levels were associated with AKI development. Before AKI onset, a serum phosphate cut-off of 2.1 mmol/L was not effective in predicting AKI development (sensitivity 48%, specificity 84%, area under the receiver operating characteristic curve (AUC) 0.63 [0.52-0.74]). No other biochemical parameters were effective to better predict AKI occurrence. CONCLUSION: This work suggests that increases in serum phosphate and LDH appear to be early and reliable biomarkers of AKI in tumor lysis syndrome. No valuable threshold value of serum phosphate was found to effectively predict AKI. This work is the basis for further prospective controlled studies on phosphate monitoring and phosphate lowering therapies to prevent AKI during tumor lysis syndrome.
Authors: Anthony R Mato; Brett E Riccio; Li Qin; Daniel F Heitjan; Martin Carroll; Alison Loren; David L Porter; Alexander Perl; Edward Stadtmauer; Donald Tsai; Alan Gewirtz; Selina M Luger Journal: Leuk Lymphoma Date: 2006-05