LDL-apheresis (LDL-A) is a method to correct dyslipidemia rapidly. It is expected to alleviate the tissue toxicity of persistent dyslipidemia in this disease and to have a protective effect on the kidney. In addition, the effectiveness of apheresis therapy GF120918 cost including plasmapheresis to promote the remission of NS has been recognized [1], but that of LDL-A has been suggested not necessarily to be due to
the correction of abnormal lipid levels. At present, in Japan, LDL-A to control hyperlipidemia in patients with refractory NS associated with focal glomerulosclerosis FSGS is covered by national health insurance up to 12 times over 3 months, but clarification of the mechanism of the effect of this treatment and evidence for its effectiveness Transmembrane Transporters inhibitor to maintain
remission over a long period have been insufficient. Prospective cohort studies are being carried out, leading to the accumulation of evidence on its efficacy and clarification of cases in which the therapy is expected to be SC79 effective. Definition of refractory NS and characteristics of causative disorders The international and Japanese diagnostic criteria for NS are nearly the same. Urinary excretion of protein >3.5 g/day, together with serum albumin at 3 g/day or less or serum total protein level of 6 g/day or less (these are essential diagnostic conditions), is expected to be maintained in association with edema and hypercholesterolemia (not essential items). Concerning the criteria of remission, in Japan, categories of type I and II incomplete remission (ICR) have been established, in addition to the international criteria of urinary excretion of protein at 1 g/day or less and 1–3.5 g/day, Fossariinae respectively. In Japan, refractory NS is defined as an inability to achieve type I ICR or complete remission (CR) despite the continuation of various treatments over 6 months or longer. The outcome was internationally reported to have been significantly poorer in those who were not included in these
categories than in those who were, based on a survey of a large number of patients in Japan, and these categories are in wide clinical use and have been retained in diagnostic and therapeutic guidelines. Of the 3 major disorders considered to be causes of primary NS, FSGS and membranous nephropathy (MN) may develop into refractory NS. The pathological clarification of FSGS has advanced recently, and the nephrotoxicity of dyslipidemia associated with this disease has been reported. LDL-A was initiated against this disease in particular. Mechanism of occurrence of hyperlipidemia in NS and tissue toxicity of lipids Marked proteinuria due to NS causes severe hypoalbuminemia, promotes lipoprotein synthesis, and induces excessive albumin synthesis, resulting in hypercholesterolemia.