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Key words: ankylosing spondylitis; hypercholesterolae-concentrations remained dramatically high (28 mmol/l and 20 mmol/l respectively). Simvastatin was therefore mia; hypertriglyceridaemia; LDL apheresis; priapism; minimal-change nephrotic syndrome; sulphasalazine stopped. The severity of the nephrotic syndrome and the renal insuÃciency made the use of fibric acid derivatives unsafe. The use of other lipid-lowering drugs was not considered because of their modest Case report eÃcacy in such severe dyslipidaemia. Subsequently we performed 10 LDL-A sessions to lower cholesterol concentration [1], whilst tapering the prednisone dose A 43 year-old-man presented in August 1992 with from 15 mg to 9 mg per day. The other drugs prescribed nephrotic syndrome. For the previous 3 months he were sulphasalazine 2 g/day until July 1995, and fruse-had been treated for ankylosing spondylitis with mide, which was given at a dose of 500 mg/day until sulphasalazine 2 g per day. Percutaneous renal biopsy September 1995; this treatment was then progressively showed normal glomeruli without mesangial hypercel-reduced and stopped; omeprazole 20 mg/day, cizapride lularity. The nephrotic syndrome was steroid-20 mg/day, nadroparine 0.6 ml b.i.d. and fenofibrate dependent with a high threshold (40 mg prednisone 67 mg/day from October 1995. per day). Between 1992 and 1995 the patient experi-LDL apheresis [1 ] was performed using haemofilter enced severe relapses despite continuous steroid treat-Sorin BT 900 with a surface of 1.10 m2 as the plasma ment (with serum albumin falling to 12 g/l). A second separator and a dextran sulphate cellulose column renal biopsy performed in September 1993 showed (Liposorber LA-40, Kaneka, Japan) as the LDL minimal-change disease. Successive concurrent therapy absorber. A double-lumen central vascular access was with cyclosporin A, chlorambucil, and quinolones used and 55 ml/kg of plasma processed at each session. failed to improve the condition. The duration of each procedure was about 2 h. We In April 1995, a massive relapse of the nephrotic performed 10 LDL-A in a period of 9 weeks. During syndrome was associated with deterioration of renal the LDL-A period, serum cholesterol decreased from function (plasma creatinine 180 mmol/l). A third renal 28 mmol/l to 9.5 mmol/l and serum triglycerides from biopsy was performed and showed minimal changes 20 mmol/l to 3.5 mmol/l (Figure 1). Proteinuria with global sclerosis of 3/9 glomeruli. Segmental glom-decreased to 1.26 g/day after the last LDL-A session, erular hyalinosis was not observed. There were some in parallel with the reduction in serum cholesterol r= focal areas of fibrosis with tubular …

Remission of a refractory nephrotic syndrome after low-density lipoprotein apheresis based on dextrane sulphate adsorption