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Updated: May 29, 2025

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice
Published on: June 8, 2022
Low-density lipoprotein apheresis for refractory lupus nephritis: A case demonstrating marked improvement in
Narumichi Iwamura1, Yuta Matsukuma2, Kanako Tsutsumi1
1Department of Nephrology, Japanese Red Cross, Yamaguchi Hospital, Yamaguchi, Japan.
Abstract:
Systemic lupus erythematosus (SLE) predominantly involves the kidneys, causing lupus nephritis (LN). Patients with diffuse proliferative LN frequently experience poor outcomes despite advances in immunosuppressive therapies. Low-density lipoprotein apheresis (LDL-A) has been a potential therapeutic option for steroid-resistant nephrotic syndromes (NSs), but its efficacy in LN remains unknown. Here, we report the case of a 26-year-old female patient with SLE and LN classified as IV + V (G) A/C according to the renal pathology society, who developed refractory NS, severe haematuria, and declining renal function. The initial induction therapy, which included hydroxychloroquine, glucocorticoids, mycophenolate mofetil, and belimumab, proved to be ineffective. Consequently, LDL-A significantly improved proteinuria, haematuria, and kidney function. The urinary protein-to-creatinine ratio decreased from 7.15 to 0.61 g/gCr, and haematuria dropped from >100 to 10-19 erythrocytes per high-power field. Additionally, complement levels were improved and anti-double-stranded DNA antibody titres were reduced. Ascribing these improvements solely to LDL-A remains challenging, but the rapid proteinuria and haematuria reduction within 48 h indicates a substantial contribution of LDL-A to the clinical response. The effluent from LDL-A contained not only LDL cholesterol but also measurable amounts of immunoglobulin G and M, which may have contributed to the reduction in LN activity. This case represents the first report of a marked haematuria reduction following LDL-A in LN. LDL-A is a valuable adjunctive treatment in patients with refractory NS or highly active LN unresponsive to standard induction therapies.
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