PMID- 10412778 OWN - NLM STAT- MEDLINE DCOM- 19990915 LR - 20220317 IS - 0098-6577 (Print) IS - 0098-6577 (Linking) VI - 71 DP - 1999 Jul TI - Rapid normalization of interleukin-8 production after low-density lipoprotein apheresis in steroid-resistant nephrotic syndrome. PG - S210-2 AB - BACKGROUND: Low-density lipoprotein apheresis (LDL-A) treatment combined with steroids demonstrated significant improvement of nephrotic proteinuria in steroid- or immunosuppressive-resistant patients from focal and segmental glomerulosclerosis (FGS). The mechanisms of the effect of LDL-A in nephrotic syndrome (NS) are unknown, but a reduction in inflammatory cytokines and chemokines secreted from macrophages has been supposed. METHODS: Serum levels of interleukin (IL)-8, tumor necrosis factor-alpha (TNF-alpha), and monocyte chemoattractant protein-1 (MCP-1) were measured by enzyme-linked immunosorbent assay in 27 patients with NS [13 with FGS and 14 with minimal change nephrotic syndrome (MCNS)] before and after LDL-A and in 13 age-matched, healthy controls. We also selected three FGS patients who were resistant to steroid therapy for at least one month and who had undergone six LDL-A procedures. The effects of steroids and LDL-A on the production of IL-8, TNF-alpha, and MCP-1 by peripheral blood mononuclear cells (PBMCs) were also determined in some patients. RESULTS: In NS, the serum levels of IL-8 and TNF-alpha, but not MCP-1, were significantly higher than in healthy controls. After LDL-A, IL-8 and TNF-alpha tended to decrease. IL-8 production by lipopolysaccharide (LPS)-stimulated PBMC, mainly adherent cells, was significantly reduced in both the steroid-resistant FGS group and nontreated NS group compared with controls, but TNF-alpha production was reduced in the only FGS group. After LDL-A, only IL-8 production recovered to the control group level. CONCLUSION: Significant amelioration of IL-8 production independent of any effect of steroids on LPS-stimulated PBMCs may reflect a beneficial effect of LDL-A in normalizing the function of circulating monocytes in steroid-resistant FGS. FAU - Sakurai, M AU - Sakurai M AD - Department of Cardiovascular Medicine, Kyoto University, Graduate School of Medicine, Japan. FAU - Muso, E AU - Muso E FAU - Matushima, H AU - Matushima H FAU - Ono, T AU - Ono T FAU - Sasayama, S AU - Sasayama S LA - eng PT - Clinical Trial PT - Controlled Clinical Trial PT - Journal Article PL - United States TA - Kidney Int Suppl JT - Kidney international. Supplement JID - 7508622 RN - 0 (Chemokine CCL2) RN - 0 (Interleukin-8) RN - 0 (Lipoproteins, LDL) RN - 0 (Steroids) RN - 0 (Tumor Necrosis Factor-alpha) SB - IM MH - *Blood Component Removal MH - Chemokine CCL2/blood MH - Drug Resistance MH - Female MH - Glomerulonephritis, Membranous/blood/therapy MH - Glomerulosclerosis, Focal Segmental/blood/therapy MH - Humans MH - Interleukin-8/*blood MH - Leukocytes, Mononuclear/cytology/drug effects/metabolism MH - Lipoproteins, LDL/*blood MH - Male MH - Nephrotic Syndrome/blood/pathology/*therapy MH - Steroids/*therapeutic use MH - Tumor Necrosis Factor-alpha/metabolism EDAT- 1999/07/21 00:00 MHDA- 1999/07/21 00:01 CRDT- 1999/07/21 00:00 PHST- 1999/07/21 00:00 [pubmed] PHST- 1999/07/21 00:01 [medline] PHST- 1999/07/21 00:00 [entrez] AID - S0085-2538(15)46642-6 [pii] PST - ppublish SO - Kidney Int Suppl. 1999 Jul;71:S210-2.