DOES LDL-APHERESIS IN STEROID-RESISTANT NEPHROTIC SYNDROME AFFECT PROGNOSIS

Citation
E. Muso et al., DOES LDL-APHERESIS IN STEROID-RESISTANT NEPHROTIC SYNDROME AFFECT PROGNOSIS, Nephrology, dialysis, transplantation, 9(3), 1994, pp. 257-264
Citations number
34
Categorie Soggetti
Urology & Nephrology
ISSN journal
09310509
Volume
9
Issue
3
Year of publication
1994
Pages
257 - 264
Database
ISI
SICI code
0931-0509(1994)9:3<257:DLISNS>2.0.ZU;2-C
Abstract
Low-density lipoprotein apheresis (LDL-A) was performed for nine episo des of steroid-resistant nephrotic syndrome in eight patients. The cli nical and immunohistological findings were analysed retrospectively. S ix of the patients had focal glomerular sclerosis (FGS), one had minim al-change nephrotic syndrome (MCNS), and one had membranous nephropath y (MN) with FGS. The LDL-A treatment, carried out 2-13 times (mean 7.3 3+/-4.05) for one nephrotic episode, at average intervals of 3-16 days (mean: 8.5+/-5.1 days) and combined with steroid pulse therapy and th e administration of an antihyperlipidaemic agent in some cases, led to rapid amelioration of hyperlipidaemia. In six nephrotic episodes (5 p atients) more than 50% reduction of proteinuria occurred(less than 3.5 g/day) (response-group). A significant elevation of serum albumin (mo re than 3.0 g/dl) was obtained in five of these episodes. The other th ree patients were resistant (resistant-group). The number of and inter vals between LDL-A treatments in the response group (5+/-2.8 times and 5.8+/-4.1 days) were significantly less than those in the resistant-g roup (12.0+/-0.8 times and 13.2+/-1.8 days) (P<0.05). After LDL-A, sig nificant reductions were observed in the serum total cholesterol (T-CH O), phospholipid (PL), triglyceride (TG), free-CHO (F-CHO), and beta-l ipoprotein (beta-lipo) (P<0.05). HDL-cholesterol (HDL-C) increased som ewhat after LDL-A. Further, C-cr was elevated in all nephrotic episode s, except in one patient who manifested renal failure after 6 months. An immunohistological study showed a reduction in the high intensity o f mesangial apoprotein B staining and intraglomerular macrophage infil tration after LDL-A in five of the six patients. Marked hyperlipidaemi a may be a cause of glomerular injury, probably mediated by glomerular macrophage infiltration, and the rapid improvement brought about by L DL-A may provide a therapeutic tool to induce remission in patients wi th this condition.