BackgroundMultiple myeloma (MM) is a haematological malignancy associated with kidney injury resulting from cast nephropathy, which can be caused by monoclonal free light chains (FLC). It has been demonstrated that early reduction of FLC can lead to a higher proportion of patients recovering renal function with a better outcome, especially if high cut-off haemodialysis (HCO-HD) combined with chemotherapy is used.Patients and MethodsIn this study, four cases with MM nephropathy were treated with HCO-HD and chemotherapy at a single institution during the period from August 2009 to August 2011. All of the patients presented with acute renal failure and high serum FLC. All patients underwent a bone marrow biopsy to confirm the diagnosis of MM, according to the WHO criteria. Three patients had de novo MM and one patient had relapsed light chain myeloma disease. All patients underwent HCO-HD concomitantly with specific myeloma therapy once the diagnosis or relapse of MM was established.ResultsAfter a medial follow up of 26 months, (range, 13–36) our data showed that all patients had a significant decrease in serum FLC through HCO-HD, proving the effectiveness of HCO-HD in managing MM. De-novo MM patients restored their renal function and achieved low-level FLC early in the treatment and became dialysis-independent. One patient with relapsed myeloma remained dialysis-dependent.ConclusionIn summary, our study suggests that in myeloma nephropathy associated with light-chain MM, HCO-HD should be initiated as early as possible. At the same time a specific MM treatment should be initiated to gain control of the disease and salvage the kidneys in order to achieve dialysis-independency. Further randomized trials to confirm our results are warranted.

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A 58-year-old Caucasian female was known to have had autoimmune thrombocytopenia purpura (ITP) since childhood and had undergone splenectomy when she was 16 years old. She presented with a platelet count of 15 x 10 9 /l with bleeding manifestations and high dose intravenous immunoglobulin (IVIG) was therefore administered. The IVIG administered was Intragam-P (CSL Ltd., Parkville, Victoria, Australia). Her platelet count showed good improvement and had normalized by 48 h. However 48 h after a second dose of IVIG, the patient complained of reddish urine and her haemoglobin concentration (Hb) was found to have dropped from 122 g/l to 100 g/l, falling to 80 g/l after a further three days. Severe haemolysis was evidenced by polychromasia, spherocytes and nucleated red cells in her blood film (top). High lactate dehydrogenase (LDH), high bilirubin and low haptoglobin levels were also noted. A direct antiglobulin test (DAT) was strongly positive (4 + ), anti-IgG was strongly positive (4 + ) and anti-C3d was negative. Anti-A antibody was eluted from the red cells. The plasma was dark red in colour due to intravascular haemolysis (bottom left). Urine was also red in colour due to haemoglobinuria (bottom right), with no red cells on urine microscopy. There was no renal impairment. The patient's blood group was A RhD-positive. Tests for antinuclear antibody (ANA), anti-double stranded DNA and anti-extractable nuclear antigen were negative.The patient was managed conservatively and did not require transfusion. Urine colour became normal after four days. Hb and haemolytic markers started to show improvement after five days and had normalized within four weeks. The DAT became weak (1 + ) by four weeks and was negative by eight weeks. After the haemolysis had settled completely and the DAT had become negative, a small aliquot from the same batch of IVIG was cross-matched (using gel card technique) against the patient's red cells with A, B and O cells as controls. Strong agglutination was seen with the patient's and control A red cells up to 1:256 dilution confirming that anti-A antibody in IVIG was the cause of the haemolysis. IVIGinduced haemolysis is usually mild and self-limiting and can easily be un-noticed. Massive intravascular haemolysis due to anti-A antibody is a rare complication of high dose IVIG.