A case of chronic myeloid leukemia complicated with minimal change nephrotic syndrome

We present a 28-year-old patient with chronic myeloid leukemia (CML) in chronic phase complicated with nephrotic syndrome. The bone marrow cells revealed the presence of Philadelphia chromosome, the cytogenetic hallmark of CML, that results from a balanced, reciprocal translocation between the long arms of chromosomes 9 and 22, t(9;22)(q34;q11). This reciprocal translocation leads to the formation of the bcr/abl fusion gene, the presence of which was confirmed using the highly sensitive fluorescence in situ hybridization technique. The renal biopsy was compatible with minimal change nephrotic syndrome. To the best of our knowledge, this is the first case of minimal change nephrotic syndrome associated with CML before the administration of any therapy branoproliferative glomerulonephritis and glomerulonephritis. Of these, minimal change nephrotic syndrome is the more prevalent cause of nephrotic syndrome in children and young adults [1]. The occurrence of nephrotic syndrome has been reported in some hematopoietic malignancies, especially lymphoproliferative disorders like Hodgkin's lymphoma and chronic lymphocytic leukemia (CLL) [2-5]. In chronic myeloid leukemia (CML), nephrotic syndrome has been reported mainly as a complication associated with the administration of interferon-a therapy [6-10]. The association of CML with nephrotic syndrome prior to therapy has also been reported in 3 cases where renal pathologies revealed membranoproliferative glomerulonephritis or glomerulonephritis [ 11- 13]. We present the first case of minimal change nephrotic syndrome complicating CML in chronic phase prior to administration of any therapy. CML is characterized by the presence of Philadelphia (Ph-1) chromosome resulting from a balanced reciprocal translocation between the long arms of chromosomes 9 and 22, t(9;22)(q34;q11). This translocation leads to the repositioning of Abelson (abl) protooncogene from its normal position on 9q34 to the breakpoint cluster region on 22q11 resulting in the formation of a novel bcr/abl fusion gene that expresses an abnormal fusion protein with elevated tyrosine kinase activity. The Philadelphia chromosome was present in the patient's bone marrow cells and the molecular rearrangement resulting in the formation of the bcr/abl fusion gene was confirmed using molecular cytogenetic methods.