2016年 · 第32卷第03期

membranous nephropathy (MN) is one of the common pathological types of nephrotic syndrome in middle-aged and elderly people. The prognosis of natural course of MN varies greatly. About one third of patients can develop spontaneous remission, but 30% to 40% of patients still have poor efficacy and progress to end-stage renal disease within 5 to 15 years^[1]。 With the popularization and development of renal biopsy technique and registration system, the epidemiological characteristics of MN are gradually recognized, and many investigations show that the incidence of MN is on the rise. In order to systematically understand the epidemiology of MN, we reviewed the relevant literature of MN epidemiology at home and abroad in recent years, so as to comprehensively reveal the epidemiological characteristics of MN and provide data support for the prevention and treatment of MN.

Recently, many scholars have suggested that the mutation of APOL1, the gene encoding Apolipoprotein L1 (Apo L1), is associated with the susceptibility to chronic kidney disease (CKD) and the progression of renal insufficiency in African-American people, and have clarified the disease spectrum of APOL1-related kidney disease. This theory breaks through our inherent understanding of the cause of kidney disease from the genetic level, and opens a new window for the diagnosis and treatment of kidney disease. The relationship between APOL1 and nephropathy is reviewed as follows.

Chronic kidney disease (CKD) refers to structural and functional dysfunction of the kidney for ≥3 months due to various causes, including pathological damage to normal and abnormal glomerular filtration rate (GFR), abnormal blood or urine composition and abnormal imaging tests, or unexplained decrease in GFR (<60 ml/min) Over 3 months. The incidence of CKD has increased significantly globally over the past few decades, particularly in the elderly population^[1,2]The prevalence of CKD in China is 10.8%^[3]。 Sleep apnea can promote the progression of kidney disease, either directly by hypoxia or indirectly by increasing oxidative stress, endothelial dysfunction, inflammatory factor levels, sympathetic activity and systemic blood pressure^[4,5]。 This article will review the prevalence, clinical characteristics, effects of sleep apnea on renal function and possible mechanisms of sleep apnea in CKD patients, and the treatment of patients with CKD complicated with sleep apnea.