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The role of TPE in lupus nephritis is controversial. TPE was reported to be effective in rapidly progressive lupus nephritis associated with high immunologic activity when the rise in serum creatinine was >88.4 ��mol/L (1.0 mg/dL) per month or when normal creatinine clearance decreased to [http://en.wikipedia.org/wiki/MERTK UNC2881] lupus nephritis who developed nephrotic syndrome within a year after diagnosis [3]. However, a randomized clinical trial of TPE in lupus nephritis showed no additional benefit beyond a combination therapy consisting of oral cyclophosphamide and glucocorticoids [4]. Therefore, it has been argued that TPE could serve as an adjunct treatment in patients with severe lupus nephritis who do not respond to the conventional therapy or those who demonstrate a rapidly progressive decline in renal function [3]. Our patient fulfilled the diagnostic criteria for the antiphospholipid syndrome (APS), and glomerular microthrombosis was associated with lupus anticoagulant. This raised the question whether concurrent APS can affect the renal outcome in proliferative lupus nephritis, and if so, what the treatment of choice would be. Lupus nephritis was accompanied by APS nephropathy in one-third of patients who underwent a renal biopsy [1]. APS nephropathy was associated with lupus anticoagulant and represented an independent risk factor for hypertension, interstitial fibrosis and diminished renal function. Zheng et al. [2] observed glomerular microthrombosis [http://www.selleckchem.com/products/Imatinib-Mesylate.html Selleckchem STI571] in 20% of renal biopsies demonstrating lupus nephritis. Glomerular microthrombosis directly correlated [http://www.selleckchem.com/products/AP24534.html AP24534] with systemic lupus activity as well as with the activity and chronicity of lupus nephritis. Furthermore, lupus anticoagulant and antibodies to ��2-glycoprotein I and thrombin were more prevalent in patients with lupus nephritis who demonstrated glomerular microthrombosis. It could be argued that resolving acute tubular necrosis (due to preceding sepsis) could have been the main reason for the recovery of renal function in our patient. However, shortly before TPE was initiated, an experienced pathologist (A.N.) examined the urine sediment under a microscope and observed numerous dysmorphic erythrocytes and erythrocyte casts, but no muddy brown granular casts to indicate ongoing acute tubular necrosis. In addition, our patient's serum creatinine level continued to rise following the final hemodialysis treatment and before the initiation of TPE. During the recovery phase of severe acute tubular necrosis, before serum creatinine level trends downwards, the degree of daily increase in serum creatinine level lessens followed by a plateau in serum creatinine of variable duration.