A 70-year-old white man had undergone a left total nephrectomy in 1999 for a clear-cell renal carcinoma, with a residual glomerular fi ltration rate (GFR) of 41 mL/min per 1·73m without proteinuria. In March, 2005, the patient was diagnosed with a pulmonary metastasis, and treatment with interferon alfa was started. Renal function remained stable with no proteinuria, but because of increasingly severe hypertension, treatment was stopped after 7 months. Treatment with bevacizumab was started a month later at a dose of 10 mg/kg every 2 weeks. After the second injection of bevacizumab, renal status changed abruptly with the presence of severe hypertension (210/130 mmHg), a nephrotic syndrome as defi ned by an albuminuria creatinuria ratio of 539 mg/mmol, and a GFR of 21 mL/min per 1·73m. There was evidence of a haemolytic-uraemic syndrome with intravascular haemolysis (haptoglobin <0.08 mg/L, lactic dehydro genase 389 UI/L, haemoglobin 102 g/L), and persistent thrombopenia. Coombs test, complement factors, and factor B, H, and I antigens were negative or normal, but the activity of von Willebrand protease factor was reduced to 53%. Viral, bacteriological, and immunological studies were all aetiologically negative. Transjugular renal biopsy revealed a glomerular thrombotic microangiopathy with many capillary-loop double contours, fi brin thrombi, zones of mesangiolysis (fi gure 1) strongly positive for anti fi brinogen, and endothelial lesions in an interlobular artery. Podocyte lesions were identifi ed by two specifi c markers: anti-vascular endothelial growth factor (antihuman VEGF monoclonal antibody, clone C1, Santa Cruz Biotechnology, Santa Cruz, CA, USA) and podocalyxin (MLC48A8, INSERM U702, Hopital Tenon, Paris, France). Staining showed that podocytes adjacent to the zones of mesangiolysis were diminished or absent altogether. Anti-VEGF staining further revealed the persistence of isolated pedicels on the glomerular wall, although the bodies of the podocytes had disappeared (fi gure 2). Response to stopping bevacizumab was favourable, with normalising blood pressure, disappearance of the stigmata of haemolysis, and return of renal function to previous baseline levels. However, there was persistence of proteinuria with an albuminuria creatinuria ratio of 232 mg/mmol. 2 months after the episode of haemolytic-uraemic syndrome, a second course of anti-VEGF was started, this time with sunitinib, which acts as an inhibitor of the intra cellular signalling pathway for VEGF. Sunitinib was stopped after 3 weeks of treatment as a result of the recurrence of a severe haemolytic-uraemic syndrome, with asthenia, severe hypertension (220/120 mmHg under triple treatment), nausea, oedema, and acute renal insuffi ciency with a GFR of 12 mL/min per 1·73m. Haptoglobin was undetectable and lactic dehydrogenase concentration was raised to 526 UI/L. Severe thrombopenia had a nadir of 19 000/mm of haemoglobin and anaemia had a nadir of 70 g/L. The activity of von Willebrand protease factor was lowered to 27%. Once again, the response of this second episode of haemolytic-uraemic syndrome was favourable in the days after stoppage of sunitinib, although ten courses of plasma exchange were initially needed. The advent of angiogenesis inhibitors has been a development that has brought hope for the treatment of metastatic solid tumours. Phase II and III trials have reported a regression in tumour mass and a signifi cant increase in patient survival. Treatment is aimed at blocking the activation of the VEGF receptor (VEGFR), which drives angiogenesis. This inhibition is partly achieved by blocking the binding of VEGF to its receptor by anti-VEGF antibodies (ie, bevacizumab), and partly by blocking the intracellular signalling pathway of VEGFR by inhibitors of receptor tyrosine kinases (ie, sunitinib). VEGF is the principal regulator of angiogenesis with several isoforms (A, B, C, D, and E) described. In the kidney, VEGF, especially VEGF-A, is predominantly expressed on podocytes and tubular epithelial cells, whereas its receptor is endothelial at the preglomerular, glomerular, and peritubular capillary levels. The role of VEGF in renal physiology is not completely understood, but it has been implicated in the pathophysiology of several renal diseases. We report the fi rst case to our knowledge of thrombotic microangiopathy occurring Lancet Oncol 2007; 8: 177–78