Stroke-prone spontaneously hypertensive (SHRsp) rats develop severe hypertension resulting in renal injury. We investigated apoptosis inhibitor of macrophages (AIM) expression in nephrosclerotic rats and the involvement of AIM in olmesartan (OLM)-and azelnidipine (AZN)-induced decreases in the number of macrophages infiltrating the kidney. We randomly assigned 20-week-old male SHRsp rats to receive one of the following substances every day for 12 weeks: water (vehicle), hydralazine (HYD), OLM, or AZN. Renal damage was assessed by Masson trichrome staining. Expressions of ED-1, AIM, and oxidized low-density lipoprotein (oxLDL) were immunohistochemically detected. Apoptosis was analyzed by terminal deoxynucleotidyl transferase deoxyuridine triphosphate (dUTP) nick-end labeling (TUNEL) staining. All treatment groups showed significantly less renal interstitial fibrosis than the vehicle group. AZN and OLM groups had significantly fewer AIM-expressing cells than the HYD and vehicle groups. The ratios AIM-positive cells/ ED-1-positive macrophages and TUNEL-positive cells/ED-1-positive macrophages in the AZN and OLM groups were lower and higher, respectively, than the the HYD and vehicle groups. oxLDL expression in the renal interstitium was significantly lower in treatment groups compared to vehicle group. OLM and AZN inhibited interstitial fibrosis progression in SHRsp rats by suppressing AIM expression in macrophages, followed by reducing the number of infiltrating macrophages. Key words apoptosis; macrophage; nephrosclerosis; oxidized low-density lipoproteinThe number of patients with chronic kidney disease (CKD) has increased dramatically worldwide.1) A follow-up of the National Health and Nutrition Examination Surveys in the United States reported that the frequency of CKD (stages 1-4) increased from 10.0% in 1988-1994 to 13.1% in 1999-2004. 2) CKD is an independent risk factor (heart-and kidney-related) of cardiovascular disease, and is known to increase the risks for angina pectoris, myocardial infarction, cardiac arrest, cerebrovascular disorders, peripheral vascular disease, death due to cardiovascular disease, and sudden death. 3,4) Nephrosclerosis is one of the main diseases underlying CKD.5) It involves progressive arteriosclerosis at the level of the small arteries and arterioles in the kidneys, leading to ischemic changes in the glomeruli and interstitium, consequently compromising renal function.6) This increased arteriosclerosis due to long-term hypertension associated with aging has resulted in the increased global incidence of nephrosclerosis.Previous studies have reported that macrophages play a major role in the progression of arteriosclerosis in humans and in animal models. Further, macrophage infiltration is closely associated with the onset and progression of myocardial infarction, cerebrovascular disorders, and arteriosclerotic diseases such as nephrosclerosis. [7][8][9][10][11][12] Apoptosis inhibitor of macrophages (AIM) is a secretory protein comprising 3 scavenger receptor cystein-rich...

Reversible posterior leukoencephalopathy syndrome (RPLS) is a recently identified clinical and radiologic entity. The characteristic radiologic findings are bilateral gray and white matter edema in the posterior regions of the cerebral hemispheres. The typical clinical syndrome includes headache, confusion, visual symptoms, and seizures. RPLS most often occurs in the setting of hypertensive crisis, preeclampsia, or with cytotoxic immunosuppressive therapy, but many other clinical settings are described, such as cryoglobulinemia, hemolytic uremic syndrome, SLE, and the use of erythropoietin. A 24-year-old man, diagnosed as having anaphylactoid purpura nephritis at 12 years of age and who started peritoneal dialysis (PD) at 23 years of age, was admitted to our hospital with a seizure and a consciousness disturbance. His blood pressure (BP) and body fluid volume had not been controlled well because of poor compliance with medication and PD. T2-weighted magnetic resonance imaging (MRI) revealed high signal intensity changes restricted to the cortex and subcortical white matter of the cerebellum. On the other hand, diffusion-weighted imaging (DWI) showed an isointense signal.From these findings, he was diagnosed as having RPLS. With appropriate control of BP and volume control by PD and hemodialysis (HD), his symptoms improved, and a follow-up cranial MRI 1 month later was almost normal. To the best of our knowledge, this is the first report of RPLS in an adult PD patient.3

BackgroundEndocan is expressed in vascular endothelial cells, and its expression is enhanced following endothelial injury via inflammatory cytokines. Subsequently, endocan is secreted into the circulation. Thus, serum endocan levels are considered a marker of endothelial injury. However, to the best of our knowledge, no data on the serum endocan levels in peritoneal dialysis (PD) patients are available.Material/MethodsThis study included 21 PD patients who underwent peritoneal equilibration test (PET) more than once between 2011 and 2015. Serum samples were collected from each patient, and the 24-h urine volume was measured at the time of PET. Serum endocan levels were measured using enzyme-linked immunosorbent assay (ELISA) at the time of the first PET, and their relationship with clinical data or the extent of urine volume decline (mL/year) was analyzed retrospectively.ResultsSerum endocan levels were positively correlated with proteinuria level, serum creatinine level, serum tumor necrosis factor (TNF)-α level, β2-microglobulin level, and PD drainage volume, but not with urine volume at baseline. The extent of decline in urine volume was significantly associated with serum endocan level, proteinuria level, serum creatinine level, and serum TNF-α level at baseline in a simple linear regression analysis. Moreover, multiple linear regression analysis showed that the serum endocan level and proteinuria level at baseline were independent predictors for the extent of decline in urine volume.ConclusionsThe results of this study indicate that serum endocan level and proteinuria level may be useful predictive markers for decreased urine volume in PD patients.